Noise-induced Hearing Loss Research Articles

Full of sound and fury.

The subject of noise in the operating theatre was recognized as early as 1972 and has been compared to noise levels on a busy highway. While noise-induced hearing loss in orthopaedic surgery specifically has been recognized as early as the 1990s, it remains poorly studied. As a result, there has been renewed focus in this occupational hazard. Noise level is typically measured in decibels (dB), whereas noise adjusted for human perception uses A-weighted sound levels and is expressed in dBA. Mean operating theatre noise levels range between 51 and 75 dBA, with peak levels between 80 and 119 dBA. The greatest sources of noise emanate from powered surgical instruments, which can exceed levels as high as 140 dBA. Newer technology, such as robotic-assisted systems, contribute a potential new source of noise. This article is a narrative review of the deleterious effects of prolonged noise exposure, including noise-induced hearing loss in the operating theatre team and the patient, intraoperative miscommunication, and increased cognitive load and stress, all of which impact the surgical team's overall performance. Interventions to mitigate the effects of noise exposure include the use of quieter surgical equipment, the implementation of sound-absorbing personal protective equipment, or changes in communication protocols. Future research endeavours should use advanced research methods and embrace technological innovations to proactively mitigate the effects of operating theatre noise.

Modulating the unfolded protein response with ISRIB mitigates cisplatin ototoxicity

Cisplatin is a commonly used chemotherapy agent with a nearly universal side effect of sensorineural hearing loss. The cellular mechanisms underlying cisplatin ototoxicity are poorly understood. Efforts in drug development to prevent or reverse cisplatin ototoxicity have largely focused on pathways of oxidative stress and apoptosis. An effective treatment for cisplatin ototoxicity, sodium thiosulfate (STS), while beneficial when used in standard risk hepatoblastoma, is associated with reduced survival in disseminated pediatric malignancy, highlighting the need for more specific drugs without potential tumor protective effects. The unfolded protein response (UPR) and endoplasmic reticulum (ER) stress pathways have been shown to be involved in the pathogenesis of noise-induced hearing loss and cochlear synaptopathy in vivo, and these pathways have been implicated broadly in cisplatin cytotoxicity. This study sought to determine whether the UPR can be targeted to prevent cisplatin ototoxicity. Neonatal cochlear cultures and HEK cells were exposed to cisplatin, and UPR marker gene expression and cell death measured. Treatment with ISRIB (Integrated Stress Response InhIBitor), a drug that activates eif2B and downregulates the pro-apoptotic PERK/CHOP pathway of the UPR, was tested for its ability to reduce apoptosis in HEK cells, hair-cell death in cochlear cultures, and hearing loss using an in vivo mouse model of cisplatin ototoxicity. Finally, to evaluate whether ISRIB might interfere with cisplatin chemoeffectiveness, we tested it in head and neck squamous cell carcinoma (HNSCC) cell-based assays of cisplatin cytotoxicity. Cisplatin exhibited a biphasic, non-linear dose–response of cell death and apoptosis that correlated with different patterns of UPR marker gene expression in HEK cells and cochlear cultures. ISRIB treatment protected against cisplatin-induced hearing loss and hair-cell death, but did not impact cisplatin’s cytotoxic effects on HNSCC cell viability, unlike STS. These findings demonstrate that targeting the pro-apoptotic PERK/CHOP pathway with ISRIB can mitigate cisplatin ototoxicity without reducing anti-cancer cell effects, suggesting that this may be a viable strategy for drug development.

Auditory decision-making deficits after permanent noise-induced hearing loss.

Loud noise exposure is one of the leading causes of permanent hearing loss. Individuals with noise-induced hearing loss (NIHL) suffer from speech comprehension deficits and experience impairments to cognitive functions such as attention and decision-making. Here, we tested whether a specific sensory deficit, NIHL, can directly impair auditory cognitive function. Gerbils were trained to perform an auditory decision-making task that involves discriminating between slow and fast presentation rates of amplitude-modulated (AM) noise. Decision-making task performance was assessed across pre-versus post-NIHL sessions within the same gerbils. A single exposure session (2 hours) to loud broadband noise (120 dB SPL) produced permanent NIHL with elevated threshold shifts in auditory brainstem responses (ABRs). Following NIHL, decision-making task performance was tested at sensation levels comparable to those prior to noise exposure in all animals. Our findings demonstrate NIHL diminished perceptual acuity, reduced attentional focus, altered choice bias, and slowed down evidence accumulation speed. Finally, video-tracking analysis of motor behavior during task performance demonstrates that NIHL can impact sensory-guided decision-based motor execution. Together, these results suggest that NIHL impairs the sensory, cognitive, and motor factors that support auditory decision-making.

NOISE-RELATED HEARING LOSS FREQUENCY AND RELATED FACTORS IN A UNIVERSITY HOSPITAL OCCUPATIONAL DISEASES CLINIC. Ege University Faculty of Medicine Hospital Occupational Diseases Clinic -2018

Objective: Noise is an important hazard that negatively affects hearing and perception in humans, causes physiological and psychological disorders, and reduces work performance. We wanted to determine the socio-demographic and occupational factors associated with the frequency of noise-induced hearing loss in patients who applied to the occupational diseases clinic and draw attention to what should be done to prevent its occurrence. Methods: The population of the cross-sectional study consisted of 463 workers who applied to a university hospital Occupational Diseases Policlinic between November 2015 and November 2018. General physical examination was performed and hearing problems were evaluated and than audiometric examination was performed with Madsen Itera II audiometry device. Chi-square test and descriptive statistics were used as statistical analysis. Results: 23.5% of the workers were diagnosed with hearing loss. 397 (85.7%) of the participants described that they were exposed to noise in the workplace. Noise exposure has been associated with hearing loss. 15 packs / year and above smoking, expressing noise exposure in the workplace and not using headphones, chemical substances in the work environment; Exposure to any of the lead, manganese and mercury made a significant difference in terms of hearing loss. Conclusion: The correct use of personal protective equipment such as earphones depends on individual factors. Incorrect and inadequate headphone use is an important factor in noise-induced hearing loss. For this reason, engineering measures are extremely important among the primary preventive methods. Smoking, chemical exposure are effective factors in noise-related hearing loss.

The role of GDF15 in attenuating noise-induced hidden hearing loss by alleviating oxidative stress

Noise-induced hidden hearing loss (HHL) is a newly uncovered form of hearing impairment that causes hidden damage to the cochlea. Patients with HHL do not have significant abnormalities in their hearing thresholds, but they experience impaired speech recognition in noisy environments. However, the mechanisms underlying HHL remain unclear. In this study, we developed single-cell transcriptome profiles of the cochlea of mice with HHL, detailing changes in individual cell types. Our study revealed a transient threshold shift, reduced auditory brainstem response wave I amplitude, and decreased number of ribbon synapses in HHL mice. Our findings suggest elevated oxidative stress and GDF15 expression in cochlear hair cells of HHL mice. Notably, the upregulation of GDF15 attenuated oxidative stress and auditory impairment in the cochlea of HHL mice. This suggests that a therapeutic strategy targeting GDF15 may be efficacious against HHL.Graphical HHL mice had a transient threshold shift, reduced ABR wave I amplitude, and decreased number of ribbon synapses.HHL mice's cochlear hair cells exhibited increased oxidative stress and elevated GDF15 expression.Upregulation of GDF15 attenuated oxidative stress and auditory damage in the cochlea of HHL mice, implying that GDF15-targeted treatment techniques may be useful for HHL.

The Role and Research Progress of Mitochondria in Sensorineural Hearing Loss.

Hearing loss is one of the most common human diseases, seriously affecting everyday lives. Mitochondria, as the energy metabolism center in cells, are also involved in regulating active oxygen metabolism and mediating the occurrence of inflammation and apoptosis. Mitochondrial defects are closely related to hearing diseases. Studies have shown that mitochondrial DNA mutations are one of the causes of hereditary hearing loss. In addition, changes in mitochondrial homeostasis are directly related to noise-induced hearing loss and presbycusis. This review mainly summarizes and discusses the effects of mitochondrial dysfunction and mitophagy on hearing loss. Subsequently, we introduce the recent research progress of targeted mitochondria therapy in the hearing system.

Recreational Noise and Hearing Loss. Systematic Review and Meta-Analysis

Background: Noise Induced Hearing Loss is a sensorineural hearing loss caused by exposure to loud noises within a long duration. In 2015, WHO predict that more than 1 billion teenagers and young adults are at risk of hearing loss due to unsafe listening practices. There is yet a concrete conclusion on how recreational noise effect hearing ability. This study aims to discover whether recreational noise can cause hearing loss. Purpose: To study the effect recreational activities, have on hearing ability. Method: The design of this study is a systematic review and meta-analysis method with a case-control approach. Of the 2072 studies identified, 3 studies passed the Intercollegiate Guidelines Network (SIGN) eligibility test and was proceed to a meta-analysis using the REVMAN MANAGER 5.4 software. Results: The result are there is no significant effect of recreational noise on hearing loss (OR 0.99, 95% CI 0.16, 06.26 P = 0.99). Conclusion: Statistically, there is no clinical significance of hearing loss caused by exposure from recreational activities, but there is a need for more variety of recreational activates sound exposure outside of the music sphere and need for more homogenous of methods amongst Noise Induced Hearing Loss caused by Recreational Activities.

Virally-Mediated Enhancement of Efferent Inhibition Reduces Acoustic Trauma in Wild Type Murine Cochleas.

Noise-induced hearing loss (NIHL) poses an emerging global health problem with only ear protection or sound avoidance as preventive strategies. In addition, however, the cochlea receives some protection from medial olivocochlear (MOC) efferent neurons, providing a potential target for therapeutic enhancement. Cholinergic efferents release ACh (Acetylycholine) to hyperpolarize and shunt the outer hair cells (OHCs), reducing sound-evoked activation. The (α9)2(α10)3 nicotinic ACh receptor (nAChR) on the OHCs mediates this effect. Transgenic knock-in mice with a gain-of-function nAChR (α9L9'T) suffer less NIHL. α9 knockout mice are more vulnerable to NIHL but can be rescued by viral transduction of the α9L9'T subunit. In this study, an HA-tagged gain-of-function α9 isoform was expressed in wildtype mice in an attempt to reduce NIHL. Synaptic integration of the virally-expressed nAChR subunit was confirmed by HA-immunopuncta in the postsynaptic membrane of OHCs. After noise exposure, α9L9'T-HA injected mice had less hearing loss (auditory brainstem response (ABR) thresholds and threshold shifts) than did control mice. ABRs of α9L9'T-HA injected mice also had larger wave1 amplitudes and better recovery of wave one amplitudes post noise exposure. Thus, virally-expressed α9L9'T combines effectively with native α9 and α10 subunits to mitigate NIHL in wildtype cochleas.

Cortical region-specific recovery of auditory temporal processing following noise-induced hearing loss

Noise-induced hearing loss (NIHL) studies have focused on the lemniscal auditory pathway, but little is known about how NIHL impacts different cortical regions. Here we compared response recovery trajectories in the auditory and frontal cortices (AC, FC) of mice following NIHL. We recorded EEG responses from awake mice (male n = 15, female n = 14) before and following NIHL (longitudinal design) to quantify event related potentials and gap-in-noise temporal processing. Hearing loss was verified by measuring the auditory brainstem response (ABR) before and at 1-, 10-, 23–, and 45-days after noise-exposure. Resting EEG, event related potentials (ERP) and auditory steady state responses (ASSR) were recorded at the same time-points after NIHL. The inter-trial phase coherence (ITPC) of the ASSR was measured to quantify the ability of AC and FC to synchronize responses to short gaps embedded in noise. Despite the absence of click-evoked ABRs up to 90 dB SPL and up to 45-days post-exposure, ERPs from the AC and FC showed full recovery in ∼ 50 % of the mice to pre-NIHL levels in both AC and FC. The ASSR ITPC was reduced following NIHL in AC and FC in all the mice on day 1 after NIHL. The AC showed full recovery of ITPC over 45-days. Despite ERP amplitude recovery, the FC does not show recovery of ASSR ITPC. These results indicate post-NIHL plasticity with similar response amplitude recovery across AC and FC, but cortical region-specific trajectories in temporal processing recovery.

Pathogenesis and New Pharmacological Approaches to Noise-Induced Hearing Loss: A Systematic Review.

Noise-induced hearing loss (NIHL) is responsible for significant adverse effects on cognition, quality of life and work, social relationships, motor skills, and other psychological aspects. The severity of NIHL depends on individual patient characteristics, sound intensity, and mainly the duration of sound exposure. NIHL leads to the production of a reactive oxygen (ROS) inflammatory response and the activation of apoptotic pathways, DNA fragmentation, and cell death. In this situation, antioxidants can interact with free radicals as well as anti-apoptotics or anti-inflammatory substances and stop the reaction before vital molecules are damaged. Therefore, the aim of this study was to analyze the effects of different pharmacological treatments, focusing on exogenous antioxidants, anti-inflammatories, and anti-apoptotics to reduce the cellular damage caused by acoustic trauma in the inner ear. Experimental animal studies using these molecules have shown that they protect hair cells and reduce hearing loss due to acoustic trauma. However, there is a need for more conclusive evidence demonstrating the protective effects of antioxidant/anti-inflammatory or anti-apoptotic drugs' administration, the timeline in which they exert their pharmacological action, and the dose in which they should be used in order to consider them as therapeutic drugs. Further studies are needed to fully understand the potential of these drugs as they may be a promising option to prevent and treat noise-induced hearing loss.

Investigation of Noise Induced Hearing Loss Among Power Loom Industry Workers in Tamil Nadu, India

Investigation of Noise Induced Hearing Loss Among Power Loom Industry Workers in Tamil Nadu, India

Novel Clinical Manifestation and Favorable Treatment Outcome of Cochlear Implant in a Chinese Family With Likely Pathogenic Variant of the P2RX2 Gene.

The rapid development and clinical application of sequencing technologies enable the genetic diagnosis of inherited deafness. P2RX2, as the gene responsible for autosomal dominant non-syndromic deafness-41 (DFNA41), has been proven to be essential for life-long normal hearing and for the protection of noise-induced hearing loss (NIHL). Our present study reports a missense variant in the P2RX2 gene (c.178G > T (p.V60L)), for the second time worldwide, in a five-generation kindred living in Henan, China. Despite carrying the same variant, the affected members in this family appear to present with earlier-onset hearing loss and poorer hearing compared to the original DFNA41 families. In addition, this study supplements some content that was not covered in previous reports. We quantitatively evaluated the pain perception ability of some members using the Pain Vision PS-2100 system, and further found an interesting clinical manifestation, that is, hyperalgesia, in heterozygotes for P2RX2 p.V60L. The cochlear implant (CI) was also provided for the proband of profound deafness, resulting in satisfactory clinical outcomes. Finally, we carried out a systematic review of recently published articles on the P2RX2 gene, which is beneficial for better understanding the role of the P2RX2 gene in the auditory system and the pathogenic mechanisms in sensorineural hearing loss (SNHL).

Activated tissue-resident macrophages contribute to hair cell insults in noise-induced hearing loss in mice

Macrophages serve as the primary immune cell population and assume a pivotal role in the immune response within the damaged cochleae. Yet, the origin and role of macrophages in response to noise exposure remain controversial. Here, we take advantage of Ccr2RFP/+ Cx3cr1GFP/+ dual-reporter mice to identify the infiltrated and tissue-resident macrophages. After noise exposure, we reveal that activated resident macrophages change in morphology, increase in abundance, and migrate to the region of hair cells, leading to the loss of outer hair cells and the damage of ribbon synapses. Meanwhile, peripheral monocytes are not implicated in the noise-induced hair cell insults. These noise-induced activities of macrophages are abolished by inhibiting TLR4 signaling, resulting in alleviated insults of hair cells and partial recovery of hearing. Our findings indicate cochlear resident macrophages are pro-inflammatory and detrimental players in acoustic trauma and introduce a potential therapeutic target in noise-induced hearing loss.

Protocol of health screening related to occupational diseases in 100 000 workers in critical sectors: a cross-sectional study with worksite risk assessment

BackgroundOccupational diseases are one of the most important health problems related to employment However, in Malaysia, there are few epidemiological studies discussing these issues, especially among workers in the industry....

Calcitriol alleviates noise-induced hearing loss by regulating the ATF3/DUSP1 signalling pathway

BackgroundCalcitriol (Cal) is the most active metabolite of vitamin D and has antioxidant and anti-inflammatory properties. The aim of this study was to investigate the role of Cal in noise-induced hearing loss (NIHL) to further elucidate the mechanism of noise-induced oxidative stress in the mouse cochlea. MethodsC57BL/6 J mice were given six intraperitoneal injections of Cal (500 ng/kg/d). After 14 days of noise exposure, auditory brainstem response (ABR) thresholds, and the cochlear outer hair cell loss rate were analysed to evaluate auditory function. Real-time fluorescence quantitative PCR, immunofluorescence and western blotting were performed in vitro after the treatment of cochlear explants with 100 µM tert-butyl hydroperoxide (TBHP) for 2.5 h and HEI-OC1 cells with 250 µM TBHP for 1.5 h. ResultsIn vivo experiments confirmed that Cal pretreatment mitigated NIHL and outer hair cell death. The in vitro results demonstrated that Cal significantly reduced TBHP-induced cochlear auditory nerve fibre degradation and spiral ganglion neuron damage. Moreover, treatment with Cal inhibited the expression of oxidative stress-related factors (3-NT and 4-HNE) and DNA damage-related factors (γ-H2A.X) and attenuated TBHP-induced apoptosis in cochlear explants and HEI-OC1 cells. A total of 1479 upregulated genes and 1443 downregulated genes were screened in cochlear tissue 1 h after noise exposure. The level of transcription factor 3 (ATF3) was significantly elevated in HEI-OC1 cells after TBHP stimulation. Gene Transcription Regulation Database （GTRD）and Cistrome database analyses revealed that the downstream target gene of ATF3 is dual specificity phosphatase 1 (DUSP1). Cistrome DB Toolkit database results showed that the transcription factor of DUSP1 was ATF3. In addition, the ChIP-PCR results indicated that ATF3 might be a direct transcription factor of DUSP1. ConclusionThe results of our study suggest that Cal attenuates NIHL and inhibits noise-induced apoptosis by regulating the ATF3/DUSP1 signalling pathway.

Surgeons Who Perform Total Hip Arthroplasty Are at Risk for Noise-Induced Hearing Loss, Especially When Using Automated Broaching.

Noise-induced hearing loss (NIHL) is a serious concern for orthopedic surgeons. The National Institute for Occupational Safety and Health (NIOSH) sets the safe exposure limit at 85 dB for 8 hours, yet operating rooms often surpass this limit. This study investigated if using an automated broaching system exposes orthopedic surgeons to dangerous decibel (dB) levels. A prospective study analyzed 138 intraoperative sound recordings from 92 total hip arthroplasty (THA) surgeries and 46 baseline measurements at an academic-affiliated private practice, using the NIOSH Sound Level Meter (SLM) application and a microphone. The surgeries were categorized into manual and automated broaching. Key metrics measured included maximal dB level (MDL), peak sound pressure (LCpeak), average continuous sound (LAeq), and average weighted sound in an 8-hour period (TWA), along with dose representations, to identify hazardous noise levels. Of the 92 THA sound recordings, 50 used manual broaching and 42 employed automated broaching. Automated broaching exhibited higher noise levels, with an average MDL of 109.92 dBA, a LAeq of 86.09 dBA, a TWA of 76.48 dBA, and a projected noise dose of 137.74%. In contrast, manual broaching exhibited an average MDL of 105.87 dBA, a LAeq of 83.06 dBA, a TWA of 72.82 dBA, and a projected noise dose of 82.02%. This study highlights the auditory risks from automated broach and manual THA surgeries that orthopedic surgeons experience. Manufacturers should focus on reducing instrument noise when designing surgical tools and orthopedic surgeons and operating room staff should take measures to protect themselves from NIHL during surgery. [Orthopedics. 202x;4x(x):xx-xx.].

Factors Related to Dizziness in Workers With Noise-Induced Hearing Loss in Brazil.

The purpose of this study was to describe the factors related to dizziness in workers with noise-induced hearing loss in Brazil. A cross-sectional study was carried out with a sample from noise-induced hearing loss reports (2007-2019). The dependent variable in this study was dizziness, and the independent variables were sociodemographic characteristics, comorbidities, symptoms, and noise characteristics in the work environment. Logistic regression analysis was performed. A total of 3,824 individuals with noise-induced hearing loss in Brazil were analyzed. The prevalence of dizziness was 23.4% in the sample. Factors associated with dizziness were women (odds ratio [OR]: 2.10; 95% confidence interval [CI] [1.64, 2.69]), hypertension (OR: 1.68; 95% CI [1.38, 2.06]), headache (OR: 6.31; 95% CI [5.26, 7.57]), tinnitus (OR: 3.46; 95% CI [2.82, 4.25]), and continuous noise at the work environment (OR: 1.54; 95% CI [1.22, 1.94]). The factors associated with the outcome-dizziness-were gender (female), systemic arterial hypertension, headache, tinnitus, and continuous exposure to workplace noise. Such findings demonstrate the importance of promoting a multifactorial approach to understanding dizziness among workers exposed to occupational noise.

Effects of Castanopsis echinocarpa on Sensorineural Hearing Loss via Neuronal Gene Regulation.

Sensorineural hearing loss (SNHL), characterized by damage to the inner ear or auditory nerve, is a prevalent auditory disorder. This study explores the potential of Castanopsis echinocarpa (CAE) as a therapeutic agent for SNHL. In vivo experiments were conducted using zebrafish and mouse models. Zebrafish with neomycin-induced ototoxicity were treated with CAE, resulting in otic hair cell protection with an EC50 of 0.49 µg/mL and a therapeutic index of 1020. CAE treatment improved auditory function and protected cochlear sensory cells in a mouse model after noise-induced hearing loss (NIHL). RNA sequencing of NIHL mouse cochleae revealed that CAE up-regulates genes involved in neurotransmitter synthesis, secretion, transport, and neuronal survival. Real-time qPCR validation showed that NIHL decreased the mRNA expression of genes related to neuronal function, such as Gabra1, Gad1, Slc32a1, CaMK2b, CaMKIV, and Slc17a7, while the CAE treatment significantly elevated these levels. In conclusion, our findings provide strong evidence that CAE protects against hearing loss by promoting sensory cell protection and enhancing the expression of genes critical for neuronal function and survival.

Noise Induced Hearing Loss among Industrial Workers in North India: A Tale of Various Influencing Factors

Noise Induced Hearing Loss among Industrial Workers in North India: A Tale of Various Influencing Factors

Airbag Deployment and Tinnitus Emergence Following Car crash, a Case Report and a Brief Literature Review

Automatic airbag deployment during car accidents undoubtedly plays a vital role in preventing injuries. However, it may occasionally lead to aural damage, including noise-induced hearing loss, tympanic membrane perforation, and tinnitus. Here, we present a case of left curtain airbag deployment immediately following a low-speed car accident, which resulted in the driver experiencing tinnitus. In addition to the case presentation, we have included a brief literature review on potential otologic and nonotologic injuries caused by airbags