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.

Impact of Excessive Noise Generation in Orthopaedic Operating Theatres: A Comprehensive Review.

Excessive noise in the orthopaedic operating theatre (OT) is an underrecognized and often neglected health hazard noticed amongst surgeons, patients and theatre and scrub practitioners. A comprehensive search strategy was conducted using databases, such as PubMed, Scopus and Web of Science, with the search words 'noise', 'NIHL' and 'orthopaedics' to retrieve the significant data and generate this narrative review. We evaluated the typical causes, potential hazards and negative effects of noise-induced impacts on OT personnel and patients. Strategies to mitigate the effects of unnecessary, disproportionate noises in the OT environment were explored. Excessive noise generated in orthopaedic OTs can produce several negative effects on patients, surgeons and staff. Noise-induced hearing loss (NIHL) is a rare and under-noticed disorder. The orthopaedic OT environment, with the ever-increasing use of power tools and surgical instruments, contributes to detrimental noise generation. NIHL is an occupational hazard. Raising awareness, appropriate training and clinical governance in collaboration with the hospital risk management team amongst all the medical and paramedical fraternities working in orthopaedic theatres can mitigate challenges faced due to the deleterious effects of excessive noise. We propose recommendations and standard operating protocols that can be incorporated into hospital policies to prevent NIHL among the orthopaedic fraternity and patients alike.

Interactions of genetic variations in FAS, GJB2 and PTPRN2 are associated with noise-induced hearing loss: a case-control study in China.

BACKGROUND: This study aimed to screen and validate noise-induced hearing loss (NIHL) associated single nucleotide polymorphisms (SNPs), construct genetic risk prediction models, and evaluate higher-order gene-gene, gene-environment interactions for NIHL in Chinese population. METHODS: First, 83 cases and 83 controls were recruited and 60 candidate SNPs were genotyped. Then SNPs with promising results were validated in another case-control study (153 cases and 252 controls). NIHL-associated SNPs were identified by logistic regression analysis, and a genetic risk model was constructed based on the genetic risk score (GRS), and classification and regression tree (CART) analysis was used to evaluate interactions among gene-gene and gene-environment. RESULTS: Six SNPs in five genes were significantly associated with NIHL risk (p < 0.05). A positive dose-response relationship was found between GRS values and NIHL risk. CART analysis indicated that strongest interaction was among subjects with age ≥ 45 years and cumulative noise exposure ≥ 95 [dB(A)·years], without personal protective equipment, and carried GJB2 rs3751385 (AA/AB) and FAS rs1468063 (AA/AB) (OR = 10.038, 95% CI = 2.770, 47.792), compared with the referent group. CDH23, FAS, GJB2, PTPRN2 and SIK3 may be NIHL susceptibility genes. CONCLUSION: GRS values may be utilized in the evaluation of the cumulative effect of genetic risk for NIHL based on NIHL-associated SNPs. Gene-gene, gene-environment interaction patterns play an important role in the incidence of NIHL.

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.

Road tunnel noise: monitoring, prediction and evaluation of noise-induced hearing loss.

Incessant increases in vehicles and massive road networks lead to traffic-related problems and noise pollution. Road tunnels are considered a more feasible and effective solution for solving traffic problems. Compared to other traffic noise abatement strategies, road tunnels also offer enormous benefits to urban mass transit systems. However, the road tunnels that are non-complying with the design and safety standards negatively impact commuters' health of being exposed to the high noise level inside the tunnel, particularly for road tunnels above 500 m in length. The study aims to evaluate the applicability of the ASJ RTN-Model 2013 by validating predicted data with the measurement data at the tunnel portal. The study also investigates the acoustic characteristics of noise inside the tunnel by analysing octave frequencies to inspect the correlation of noise spectrum for noise-induced hearing loss (NIHL) and discussed the possible health effect on the pedestrian and vehicle riders passing through the tunnel. The result shows that people are exposed to a high noise level inside the tunnel. The equivalent sound pressure levels at different locations inside the tunnel along the length observed between 78.9 to 86.5 dB(A), which exceeded the CPCB, recommended permissible limits for road traffic noise. The locations L1, L5, L6 and L7 found higher sound pressure levels at 4 kHz and relates to NIHL. The observed average difference between the measurement and predicted LAeq value at the tunnel portal was 2.8 dB(A) which is highly acceptable and confirms the ASJ RTN-2013 prediction model applicability for predicting tunnel portal noise in the Indian road conditions. The study recommends complete restriction of honking inside the tunnel. Considering the commuter's safety perspective, the road tunnels above 500 m must have separate walk sides for pedestrians with a barrier.

Adult mice with noise-induced hearing loss exhibited temporal ordering memory deficits accompanied by microglia-associated neuroplastic changes in the medial prefrontal cortex.

Acquired peripheral hearing loss in midlife is considered the primary modifiable risk factor for dementia, while the underlying pathological mechanism remains poorly understood. Excessive noise exposure is the most common cause of acquired peripheral hearing loss in modern society. This study was designed to investigate the impact of noise-induced hearing loss (NIHL) on cognition, with a focus on the medial prefrontal cortex (mPFC), a brain region that is involved in both auditory and cognitive processes and is highly affected in patients with cognitive impairment. Adult C57BL/6 J mice were randomly assigned to a control group and seven noise groups: 0HPN, 12HPN, 1DPN, 3DPN, 7DPN, 14DPN, and 28DPN, which were exposed to broadband noise at a 123 dB sound pressure level (SPL) for 2 h and sacrificed immediately (0 h), 12 h, or 1, 3, 7, 14, or 28 days post-noise exposure (HPN, DPN), respectively. Hearing assessment, behavioral tests, and neuromorphological studies in the mPFC were performed in control and 28DPN mice. All experimental animals were included in the time-course analysis of serum corticosterone (CORT) levels and mPFC microglial morphology. The results illustrated that noise exposure induced early-onset transient serum CORT elevation and permanent moderate-to-severe hearing loss in mice. 28DPN mice, in which permanent NIHL has been verified, exhibited impaired performance in temporal order object recognition tasks concomitant with reduced structural complexity of mPFC pyramidal neurons. The time-course immunohistochemical analysis in the mPFC revealed significantly higher morphological microglial activation at 14 and 28 DPN, preceded by a remarkably higher amount of microglial engulfed postsynaptic marker PSD95 at 7 DPN. Additionally, lipid accumulation in microglia was observed in 7DPN, 14DPN and 28DPN mice, suggesting a driving role of lipid handling deficits following excessive phagocytosis of synaptic elements in delayed and sustained microglial abnormalities. These findings provide fundamentally novel information concerning mPFC-related cognitive impairment in mice with NIHL and empirical evidence suggesting the involvement of microglial malfunction in the mPFC neurodegenerative consequences of NIHL.

[Bibliometric and bioinformatics analysis of genetic literature on susceptibility to noise induced hearing loss].

Objective: To summarize and analyse of literature on the susceptibility genes of noise induced hearing loss (NIHL) , and the key genes were screened and obtained by bioinformatics method, so as to provide reference for the prevention research of NIHL. Methods: In September 2021, Based on CNKI, NCBI Pubmed database and Web of Science database, this paper conducted bibliometric analysis and bioinformatics analysis on the genetic literature related to the susceptibility to noise-induced hearing loss from 1999 to 2020. Endnote X9 software and the WPS office software were used for bibliometric analysis, and online software STRING and Cytoscape software were used for bioinformatics analysis. Results: A total of 131 literatures were included in the study, involving 40 genes in total. Bibliometric analysis shows that 131 papers which included 36 Chinese articles and 95 English articles were published in 63 biomedical journals; the highest number of published articles was 19 in 2020. Bioinformatics analysis suggests that GAPDH、SOD2、SOD1、CAT、CASP3、IL6 and other genes play a key role in the interaction network. The involved pathways mainly include MAP2K and MAPK activations, PTEN regulation, P53-depardent G1 DNA damage response, signaoling by BRAF and RAF fusions and soon. Conclusion: The study of noise induced hearing loss involves multi gene biological information, and bioinformatics analysis is helpful to predict the occurrence and development of noise induced hearing loss.

Bibliometric and bioinformatics analysis of genetic literature on susceptibility to noise induced hearing loss / 中华劳动卫生职业病杂志

Objective: To summarize and analyse of literature on the susceptibility genes of noise induced hearing loss (NIHL) , and the key genes were screened and obtained by bioinformatics method, so as to provide reference for the prevention research of NIHL. Methods: In September 2021, Based on CNKI, NCBI Pubmed database and Web of Science database, this paper conducted bibliometric analysis and bioinformatics analysis on the genetic literature related to the susceptibility to noise-induced hearing loss from 1999 to 2020. Endnote X9 software and the WPS office software were used for bibliometric analysis, and online software STRING and Cytoscape software were used for bioinformatics analysis. Results: A total of 131 literatures were included in the study, involving 40 genes in total. Bibliometric analysis shows that 131 papers which included 36 Chinese articles and 95 English articles were published in 63 biomedical journals; the highest number of published articles was 19 in 2020. Bioinformatics analysis suggests that GAPDH、SOD2、SOD1、CAT、CASP3、IL6 and other genes play a key role in the interaction network. The involved pathways mainly include MAP2K and MAPK activations, PTEN regulation, P53-depardent G1 DNA damage response, signaoling by BRAF and RAF fusions and soon. Conclusion: The study of noise induced hearing loss involves multi gene biological information, and bioinformatics analysis is helpful to predict the occurrence and development of noise induced hearing loss.

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

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

Comparison of two behavioral tests for tinnitus assessment in mice.

Animal research focused on chronic tinnitus associated with noise-induced hearing loss can be expensive and time-consuming as a result of the behavioral training required. Although there exist a number of behavioral tests for tinnitus; there have been few formal direct comparisons of these tests. Here, we evaluated animals in two different tinnitus assessment methods. CBA/CaJ mice were trained in an operant conditioning, active avoidance (AA) test, and a reflexive, gap-induced pre-pulse inhibition of acoustic startle (GPIAS) test, or both. Tinnitus was induced in awake mice by unilateral continuous sound exposure using a 2-kHz- or 1 2 octave-wide noise centered at 16 kHz and presented at 113- or 116-dB SPL. Tinnitus was assessed 8 weeks after sound overexposure. Most mice had evidence of tinnitus behavior in at least one of the two behaviors. Of the mice evaluated in AA, over half (55%) had tinnitus positive behavior. In GPIAS, fewer animals (13%) were positive than were identified using the AA test. Few mice were positive in both tests (10%), and only one was positive for tinnitus behavior at the same spectral frequency in both tests. When the association between tinnitus behavior and spontaneous activity recorded in the inferior colliculus was compared, animals with tinnitus behavior in AA exhibited increased spontaneous activity, while those positive in GPIAS did not. Thus, it appears that operant conditioning tests, like AA, maybe more reliable and accurate tests for tinnitus than reflexive tests.

Contralateral Suppression of Transient-evoked Otoacoustic Emissions in Leisure Noise Exposed Individuals.

Background: Leisure noise may have a significant impact on hearing thresholds and young adults are often exposed to loud music during leisure activities. This behavior puts them at risk of developing noise-induced hearing loss (NIHL). A frequent initial indication of NIHL is reduced hearing acuity at 4 kHz. The objective of the current study was to assess the role of the medial olivocochlear reflex (MOCR) in leisure noise-exposed individuals with and without a 4-kHz notch. Materials and Methods: Audiological evaluation, including pure-tone and immittance audiometry, was performed for 156 college-going, young adults between May 2019 to December 2019. All participants had averaged pure-tone audiometric thresholds within normal limits, bilaterally. Annual individual exposure to personal listening devices (PLDs) was calculated using the Noise Exposure Questionnaire. The participants were then categorized into exposed (with and without audiometric 4 kHz notch) and nonexposed groups. Transient-evoked otoacoustic emission amplitude and its contralateral suppression were measured using linear and nonlinear click stimuli to study the effect of leisure noise exposure on MOCR. Results: A significantly reduced overall contralateral suppression effect in participants exposed to PLD usage (P = 0.01) in both linear and nonlinear modes. On the contrary, significantly increased suppression was observed in linear mode for the 4 kHz frequency band in the PLD-exposed group without an audiometric notch (P = 0.009), possibly suggesting an early biomarker of NIHL. Conclusion: Measuring contralateral suppression of otoacoustic emissions may be an effective tool to detect early NIHL in leisure noise-exposed individuals.

Evaluating the Effectiveness of Earplugs in Preventing Noise-Induced Hearing Loss in an Auto Parts Factory in China.

A survey was administered to 385 noise-exposed workers from an auto parts factory and 1268 non-noise-exposed health department employees in China. Individual 8 h A-weighted equivalent sound levels (LAeq,8h), earplug personal attenuation ratings (PARs), and pure-tone audiometric tests were performed. The average LAeq,8h of noise-exposed workers was 87 dB (A) with a mean PAR of 7 dB. The prevalence of high-frequency hearing loss was 65% for noise-exposed workers and 33% for the non-noise-exposed employees. The use of earplugs had no observable effect on the prevalence of high-frequency hearing loss of the study participants (OR 0.964, 95% CI 0.925-1.005, p = 0.085). No significant relationship between the effectiveness offered by earplug use and high-frequency hearing thresholds at 3, 4, and 6 kHz was found (t = -1.54, p = 0.125). The mandatory requirement of earplug use without individualized training on how to wear HPDs correctly had no detectable effect on the prevention of hearing loss at the auto parts factory. The hearing conservation program at the surveyed factory was not effective. Periodic hearing tests, earplug fit testing, expanding the offer of different types of hearing protection, and employee education about the importance of protecting their hearing were recommended to the occupational health and safety program.

Patterns of noise exposure and prevalence of hearing loss amongst Cape Town Minstrel Carnival musicians.

BACKGROUND: Cape Town Minstrel Carnival is one of the oldest and most authentic indigenous New Year's customs in South Africa. Musicians who perform at this carnival are exposed to excessively loud music and therefore at a risk of acquiring noise-induced hearing loss (NIHL). OBJECTIVES: This study aimed to determine patterns of exposure to loud music and prevalence of hearing loss amongst Cape Town Minstrel Carnival musicians. METHOD: A descriptive, observational exploratory survey design was used and 43 participants (21 males and 22 females; mean age, 21 ± 9 years) took part in this study. Sound level measurements were conducted to assess musicians' sound exposure during rehearsals and performances. All participants underwent the following audiological test battery at least 2 h before music exposure: Case history, otoscopic examination, tympanometry, pure tone audiometry and distortion products otoacoustic emission (DPOAE). RESULTS: Average noise levels recorded were 86 dBA during rehearsals and 98.7 dBA at performances and average durations of exposure were 240 and 10 min at rehearsals and performances, respectively. One out of 43 (1/43) participants presented with sensorineural hearing loss. Audiometric results of the remaining participants were normal and did not show a pattern suggestive of NIHL. A high proportion of participants (21/43) reported experiencing tinnitus. CONCLUSION: Despite being exposed to high levels of noise, there was a low prevalence of hearing loss amongst these musicians. However, a high proportion of them reported tinnitus, which could be an indication that they were at a high risk of NIHL from the music that they played.

The Immediate and Long-Term Impact of Military Aircraft Noise on Hearing: A Cross-Sectional Comparison of Fighter Pilots and Ground Staff.

We examined the immediate and long-term impacts of military aircraft noise exposure on noise-induced hearing loss (NIHL) in fighter pilots and ground staff. We recruited 40 pilots, 40 ground staff, and 136 age-matched controls; all participants underwent hearing tests, including conventional pure-tone audiometry (PTA) (0.25-8.0 kHz), extended high-frequency (EHF) audiometry (9.0-18.0 kHz), and distortion-product otoacoustic emission (DPOAE) as a recent reference. A subsequent hearing test immediately after flight-mission noise exposure was requested. The results revealed higher recent hearing thresholds in pilots and ground staff than in controls. Threshold shifts at many octave band frequencies were also significantly elevated in ground staff. The grouped frequency threshold was significantly elevated in the 4-8 kHz high-frequency range. After a single flight-mission noise exposure, both ground staff and pilots showed decreased signal-to-noise ratios for DPOAE (1-8 kHz), whereas only ground staff showed significantly elevated left-ear hearing thresholds at 3, 11.2, and 12.5 kHz by conventional and EHF PTA. Fighter pilots and ground staff serve in hazardous noise-exposed environments that cause hearing damage and subsequent NIHL, but ground staff may be more vulnerable. A comprehensive hearing conservation program should be implemented to protect high-risk service members, and especially ground staff, from high-intensity noise exposure.

Endogenous Pituitary Adenylate Cyclase-Activating Polypeptide (PACAP) Plays a Protective Effect Against Noise-Induced Hearing Loss.

Pituitary adenylyl cyclase-activating polypeptide (PACAP) is a member of the vasoactive intestinal polypeptide (VIP)-the secretin-glucagon family of neuropeptides. They act through two classes of receptors: PACAP type 1 (PAC1) and type 2 (VPAC1 and VPAC2). Among their pleiotropic effects throughout the body, PACAP functions as neuromodulators and neuroprotectors, rescuing neurons from apoptosis, mostly through the PAC1 receptor. To explore the potential protective effect of endogenous PACAP against Noise-induced hearing loss (NIHL), we used a knockout mouse model lacking PAC1 receptor expression (PACR1-/-) and a transgenic humanized mouse model expressing the human PAC1 receptor (TgHPAC1R). Based on complementary approaches combining electrophysiological, histochemical, and molecular biological evaluations, we show PAC1R expression in spiral ganglion neurons and in cochlear apical cells of the organ of Corti. Wild-type (WT), PAC1R-/-, and TgHPAC1R mice exhibit similar auditory thresholds. For most of the frequencies tested after acute noise damage, however, PAC1R-/- mice showed a larger elevation of the auditory threshold than did their WT counterparts. By contrast, in a transgene copy number-dependent fashion, TgHPAC1R mice showed smaller noise-induced elevations of auditory thresholds compared to their WT counterparts. Together, these findings suggest that PACAP could be a candidate for endogenous protection against noise-induced hearing loss.

Epac1 Signaling Pathway Mediates the Damage and Apoptosis of Inner Ear Hair Cells after Noise Exposure in a Rat Model.

To investigate the role of the exchange protein directly activated by cAMP (Epac) signaling pathway in inner ear hair cell damage and apoptosis after noise exposure, we analyzed the expression level of Epac1 in a rat model of noise-induced hearing loss (NIHL), based on rat exposure to a 4-kHz and 106-dB sound pressure level (SPL) for 8 h. Loss of outer hair cells (OHCs), mitochondrial lesions, and hearing loss were examined after treatment with the Epac agonist, 8-CPT, or the Epac inhibitor, ESI-09. The effects of 8-CPT and ESI-09 on cell proliferation and apoptosis were examined by CCK-8 assays, holographic microscopy imaging, and Annexin-V FITC/PI staining in HEI-OC1 cells. The effects of 8-CPT and ESI-09 on Ca2+ entry were evaluated by confocal Ca2+ fluorescence measurement. We found that the expression level of Epac1 was significantly increased in the cochlear tissue after noise exposure. In NIHL rats, 8-CPT increased the loss of OHCs, mitochondrial lesions, and hearing loss compared to control rats, while ESI-09 produced the opposite effects. Oligomycin was used to induce HEI-OC1 cell damage in vitro. In HEI-OC1 cells treated with oligomycin, 8-CPT and ESI-09 increased and reduced cell apoptosis, respectively. Moreover, 8-CPT promoted Ca2+ uptake in HEI-OC1 cells, while ESI-09 inhibited this process. In conclusion, our data provide strong evidence that the Epac1 signaling pathway mediates early pathological damage in NIHL, and that Epac1 inhibition protects from NIHL, identifying Epac1 as a new potential therapeutic target for NIHL.

Inhibition of Cochlear HMGB1 Expression Attenuates Oxidative Stress and Inflammation in an Experimental Murine Model of Noise-Induced Hearing Loss.

Noise-induced hearing loss (NIHL) is a common inner ear disease but has complex pathological mechanisms, one of which is increased oxidative stress in the cochlea. The high-mobility group box 1 (HMGB1) protein acts as an inflammatory mediator and shows different activities with redox modifications linked to the generation of reactive oxygen species (ROS). We aimed to investigate whether manipulation of cochlear HMGB1 during noise exposure could prevent noise-induced oxidative stress and hearing loss. Sixty CBA/CaJ mice were divided into two groups. An intraperitoneal injection of anti-HMGB1 antibodies was administered to the experimental group; the control group was injected with saline. Thirty minutes later, all mice were subjected to white noise exposure. Subsequent cochlear damage, including auditory threshold shifts, hair cell loss, expression of cochlear HMGB1, and free radical activity, was then evaluated. The levels of HMGB1 and 4-hydroxynonenal (4-HNE), as respective markers of reactive nitrogen species (RNS) and ROS formation, showed slight increases on post-exposure day 1 and achieved their highest levels on post-exposure day 4. After noise exposure, the antibody-treated mice showed markedly less ROS formation and lower expression of NADPH oxidase 4 (NOX4), nitrotyrosine, inducible nitric oxide synthase (iNOS), and intercellular adhesion molecule-1 (ICAM-1) than the saline-treated control mice. A significant amelioration was also observed in the threshold shifts of the auditory brainstem response and the loss of outer hair cells in the antibody-treated versus the saline-treated mice. Our results suggest that inhibition of HMGB1 by neutralization with anti-HMGB1 antibodies prior to noise exposure effectively attenuated oxidative stress and subsequent inflammation. This procedure could therefore have potential as a therapy for NIHL.

High-Frequency Audiometry for Early Detection of Hearing Loss: A Narrative Review.

The WHO considers hearing loss to be a major global problem. A literature search was conducted to see whether high-frequency audiometry (HFA) could be used for the early detection of hearing loss. A further aim was to see whether any differences exist in the hearing threshold using conventional audiometry (CA) and HFA in workers of different age groups exposed to workplace noise. Our search of electronic databases yielded a total of 5938 scientific papers. The inclusion criteria were the keywords "high frequency" and "audiometry" appearing anywhere in the article and the participation of unexposed people or a group exposed to workplace noise. Fifteen studies met these conditions; the sample size varied (51-645 people), and the age range of the people studied was 5-90 years. Commercial high-frequency audiometers and high-frequency headphones were used. In populations unexposed to workplace noise, significantly higher thresholds of 14-16 kHz were found. In populations with exposure to workplace noise, significantly higher statistical thresholds were found for the exposed group (EG) compared with the control group (CG) at frequencies of 9-18 kHz, especially at 16 kHz. The studies also showed higher hearing thresholds of 10-16 kHz in respondents aged under 31 years following the use of personal listening devices (PLDs) for longer than 5 years. The effect of noise-induced hearing loss (NIHL) first became apparent for HFA rather than CA. However, normative data have not yet been collected. Therefore, it is necessary to establish a uniform evaluation protocol accounting for age, sex, comorbidities and exposures, as well as for younger respondents using PLDs.

Accelerated age-related decline in hippocampal neurogenesis in mice with noise-induced hearing loss is associated with hippocampal microglial degeneration.

Large-scale epidemiological surveys suggest that hearing loss (HL) is a significant risk factor for dementia. We previously showed that noise-induced HL (NIHL) impairs hippocampal cognitive function and decreases hippocampal neurogenesis and neuronal complexity, suggesting a causal role of HL in dementia. To further investigate the influence of acquired peripheral HL on hippocampal neurogenesis with the aging process as well as the underlying mechanism, we produced NIHL in male CBA/J mice and assessed hippocampal neurogenesis and microglial morphology in the auditory brain and hippocampus at 4 days post-noise exposure (DPN) or 1, 3, 6, or 12 months post-noise exposure (MPN) by immunofluorescence labeling. We found that the age-related decline in hippocampal neurogenesis was accelerated in mice with NIHL. Furthermore, in mice with NIHL, prolonged microglial activation occurred from 1 MPN to 12 MPN across multiple auditory nuclei, while aggravated microglial deterioration occurred in the hippocampus and correlated with the age-related decline in hippocampal neurogenesis. These results suggest that acquired peripheral HL accelerates the age-related decline in hippocampal neurogenesis and that hippocampal microglial degeneration may contribute to the development of neurodegeneration following acquired peripheral HL.

The evaluation of in-chamber sound levels during hyperbaric oxygen applications: Results of 41 centres.

INTRODUCTION: Noise has physical and psychological effects on humans. Recommended exposure limits are exceeded in many hospital settings; however, information about sound levels in hyperbaric oxygen treatment chambers is lacking. This study measured in-chamber sound levels during treatments in Turkish hyperbaric centres. METHODS: Sound levels were measured using a sound level meter (decibel meter). All chambers were multiplace with similar dimensions and shapes. Eight measurements were performed in each of 41 chambers; three during compression, three during decompression, and two at treatment pressure, one during chamber ventilation (flushing) and one without ventilation. At each measurement a sound sample was collected for 25 seconds and A-weighted equivalent (LAeq) and C-weighted peak (LCpeak) levels were obtained. Recorded values were evaluated in relation to sound level limits in regulations. RESULTS: The highest sound level measured in the study was 100.4 dB(A) at treatment pressure while ventilation was underway and the lowest was 40.5 dB(A) at treatment pressure without ventilation. Most centres had sound levels between 70 dB and 85 dB throughout the treatment. Ventilation caused significant augmentation of noise. CONCLUSIONS: The chambers were generally safe in terms of noise exposure. Nevertheless, hyperbaric chambers can be very noisy environments so could pose a risk for noise-related health problems. Therefore, they should be equipped with appropriate noise control systems. Silencers are effective in reducing noise in chambers. Thus far, hyperbaric noise research has focused on chambers used for commercial diving. To our knowledge, this is the first study to investigate noise in hospital-based chambers during medical treatments.