CD36-mediated ROS/PI3K/AKT signaling pathway exacerbates cognitive impairment in APP/PS1 mice after noise exposure.

There is an association between noise exposure and cognitive impairment, and noise may have a more severe impact on patients with Alzheimer's disease (AD) and mild cognitive impairment; however, the mechanisms need further investigation. This study used the classic AD animal model APP/PS1 mice to simulate the AD population, and C57BL/6J mice to simulate the normal population. We compared their cognitive abilities after noise exposure, analyzed changes in Cluster of Differentiation (CD) between the two types of mice using transcriptomics, identified the differential CD molecule: CD36 in APP/PS1 after noise exposure, and used its pharmacological inhibitor to intervene to explore the mechanism by which CD36 affects APP/PS1 cognitive abilities. Our study shows that noise exposure has a more severe impact on the cognitive abilities of APP/PS1 mice, and that the expression trends of differentiation cluster molecules differ significantly between C57BL/6J and APP/PS1 mice. Transcriptomic analysis showed that the expression of CD36 in the hippocampus of APP/PS1 mice increased by 2.45-fold after noise exposure (p < 0.001). Meanwhile, Western Blot results from the hippocampus and entorhinal cortex indicated that CD36 protein levels increased by approximately 1.5-fold (p < 0.001) and 1.3-fold (p < 0.05) respectively, after noise exposure in APP/PS1 mice. The changes in CD36 expression elevated oxidative stress levels in the hippocampus and entorhinal cortex, leading to a decrease in PI3K/AKT phosphorylation, which in turn increased M1-type microglia and A1-type astrocytes while reducing the numbers of M2-type microglia and A2-type astrocytes. This increased neuroinflammation in the hippocampus and entorhinal cortex, causing synaptic and neuronal damage in APP/PS1 mice, ultimately exacerbating cognitive impairment. These findings may provide new insights into the relationship between noise exposure and cognitive impairment, especially given the different expression trends of CD molecules in the two types of mice, which warrants further research.

An Exploratory Study on Self-Reported Auditory Symptoms and Hearing Loss among Workers in a Small-Scale LPG Plant.

Background: Occupational noise is considered a factor contributing to acquired hearing loss (HL) in adults. Frequent noise exposure can cause cochlear damage, leading to sensorineural HL, tinnitus, vertigo, and other non auditory effects as well. Although it is well known that liquefied petroleum gas (LPG) plants in India have become a workplace source for occupational noise pollution exposure, there are not many studies that probe into the auditory effects of workplace noise in LPG plants. Aim: The study aims to document HL and self reported otological symptoms in employees with occupational noise exposure at a typical LPG plant in a suburban location in India. 53 employees who reported workplace noise exposure were assessed for HL and self reported auditory symptoms. Method: Self reported symptoms were collected using a custom made case history questionnaire, and auditory sensitivity was measured using air conduction audiometers. Results: Among the 53 participants, 27 tested positive for HL. A mild degree of HL was frequently observed, followed by a moderate and severe degree of HL. In the self reported otological complaints reported by 31 participants, HL and aural fullness were the most commonly reported auditory symptoms. Additionally, the use of ear protection devices and hearing conservation practices among the participants were poor. Conclusion: Hearing loss and self-reported auditory symptoms were present in the study group indicating the effect of occupational noise in the auditory system.

Noise exposure of the inner ear during robotic drilling.

INTRODUCTION: Preserving the cochlear structures and thus hearing preservation, has become a prominent topic of discussion in cochlear implant (CI) surgery. Various approaches and soft surgical techniques have been described when approaching the inner ear. Robot-assisted cochlear implant surgery (RACIS) reaches the round window in a minimally invasive manner by following a trajectory of minimal trauma. This involves the drilling of a keyhole trajectory to the round window, through the facial recess, with no need for a complete mastoidectomy. It involves less drilling, less drilling time and less structural damage. A lot of attention has been paid to the structural traumatic causes of hearing loss but acoustic trauma during the exposure of the inner ear appears to be neglected topic. AIM: The aim was to measure the noise exposure of the inner ear during the robotic drilling of the mastoid and bony overhang of the round window. The results were compared with the milling in conventional cochlear implantation surgery. INTERVENTION: RACIS on fresh frozen human cadavers. OUTCOME MEASUREMENTS: The equivalent frequency-weighted and time-averaged sound pressure level LAF in dB and the noise dose in % derived from a noise damage model, both obtained during RACIS. MATERIALS AND METHODS: The robotic drilling of 6 trajectories towards the inner ear were performed, including 4 trajectories through round window access and 2 trajectories through cochleostomy. The results were compared with the data of 7 cases of conventional CI surgery that have been described in literature. The induced equivalent sound pressure level LAF was determined via an accelleration sensor at the zygomatic arch and a calibration according to bone conduction audiometry. A noise dose for the whole procedure was calculated from the equivalent sound pressure level LAF and the exposure time using a noise damage model. A noise dose of 100% is considered a critical exposure limit and values above are considered potentially harmful, with the risk of hearing impairment. RESULTS: The maximum LAF was 82 dB during fiducial screw placement; 87 dB during middle ear access; 95 dB for the accesses through the round window and 88 dB for the accesses through cochleostomy. The noise dose due to the HEARO®-procedure was always far below the critical value of 100%. There was no acoustic trauma of the inner ear in all cases with the noise dose being smaller than 0.1% in five out of the six cases. The maximum LAF in the seven cases of conventional CI surgery was 118 dB with a maximum cumulative noise dose of 172.6%. The critical exposure limit of 100% was exceeded in three cases of conventional CI surgery. CONCLUSION: RACIS provokes significantly less acoustic trauma than conventional mastoid surgery in our findings. There were no observable differences in noise exposure levels between a cochleostomy or a round window approach where the bony overhang needed to be drilled.

Current limitations and opportunities for improvements of agent-based transport models for noise exposure assessment.

Agent-based models represent a promising approach for simulating transport systems and assessing their environmental noise impact, potentially enhancing standard noise exposure assessments. However, it is very important to understand the relevance of these assessments within the context of models initially designed for transport studies. Then, this research investigates the utilization of agent-based transport models when coupled with environmental models to assess individual exposure to transport-related noise. This is achieved by proposing a method to evaluate this approach across four dimensions: spatial, temporal, individual, and activity patterns. This evaluation is demonstrated and discussed with an exemplification model applied in the Lyon Metropolitan Area using open-source tools (MATSim, EQASim, NoiseModelling), which is a representative framework of the current literature. The findings encompass a range of issues, including the conceptualization of exposure contexts and activity spaces, the resolution of the acoustic content, the disaggregation of data at the individual level, the variability in noise reactions, and the correlation structures between social and exposure profiles. The study contributes to the advancement of exposure assessment with insights for future improvements in the field. Further, it underscores the need for more quantitative analyses and scientific research into momentary noise exposure and social epidemiology.

DNA Methylation Patterns Associated with Tinnitus in Young Adults-A Pilot Study.

PURPOSE: Tinnitus, the perception of sound without any external sound source, is a prevalent hearing health concern. Mounting evidence suggests that a confluence of genetic, environmental, and lifestyle factors can influence the pathogenesis of tinnitus. We hypothesized that alteration in DNA methylation, an epigenetic modification that occurs at cytosines of cytosine-phosphate-guanine (CpG) dinucleotide sites, where a methyl group from S-adenyl methionine gets transferred to the fifth carbon of the cytosine, could contribute to tinnitus. DNA methylation patterns are tissue-specific, but the tissues involved in tinnitus are not easily accessible in humans. This pilot study used saliva as a surrogate tissue to identify differentially methylated CpG regions (DMRs) associated with tinnitus. The study was conducted on healthy young adults reporting bilateral continuous chronic tinnitus to limit the influence of age-related confounding factors and health-related comorbidities. METHODS: The present study evaluated the genome-wide methylation levels from saliva-derived DNA samples from 24 healthy young adults with bilateral continuous chronic tinnitus (> 1 year) and 24 age, sex, and ethnicity-matched controls with no tinnitus. Genome-wide DNA methylation was evaluated for > 850,000 CpG sites using the Infinium Human Methylation EPIC BeadChip. The association analysis used the Bumphunter algorithm on 23 cases and 20 controls meeting the quality control standards. The methylation level was expressed as the area under the curve of CpG sites within DMRs.The FDR-adjusted p-value threshold of 0.05 was used to identify statistically significant DMRs associated with tinnitus. RESULTS: We obtained 25 differentially methylated regions (DMRs) associated with tinnitus. Genes within or in the proximity of the hypermethylated DMRs related to tinnitus included LCLAT1, RUNX1, RUFY1, NUDT12, TTC23, SLC43A2, C4orf27 (STPG2), and EFCAB4B. Genes within or in the proximity of hypomethylated DMRs associated with tinnitus included HLA-DPB2, PM20D1, TMEM18, SNTG2, MUC4, MIR886, MIR596, TXNRD1, EID3, SDHAP3, HLA-DPB2, LASS3 (CERS3), C10orf11 (LRMDA), HLA-DQB1, NADK, SZRD1, MFAP2, NUP210L, TPM3, INTS9, and SLC2A14. The burden of genetic variation could explain the differences in the methylation levels for DMRs involving HLA-DPB2, HLA-DQB1, and MUC4, indicating the need for replication in large independent cohorts. CONCLUSION: Consistent with the literature on comorbidities associated with tinnitus, we identified genes within or close to DMRs involved in auditory functions, chemical dependency, cardiovascular diseases, psychiatric conditions, immune disorders, and metabolic syndromes. These results indicate that epigenetic mechanisms could influence tinnitus, and saliva can be a good surrogate for identifying the epigenetic underpinnings of tinnitus in humans. Further research with a larger sample size is needed to identify epigenetic biomarkers and investigate their influence on the phenotypic expression of tinnitus.

'Cultural Insights into Adults' Hearing Awareness and Personal Listening Device Habits: A Survey Study.

Objective: The aim of this study was to investigate adults' habits regarding personal listening devices (PLDs), associated factors such as tinnitus and hearing threshold shift, and their knowledge of safety measures, including the use of hearing protectors in noisy environments. Design: A cross-sectional survey was designed and distributed online. Study Sample: Participants between the ages of 18 and 40 years were invited to complete the survey. The online survey was filled out by 274 individuals with an average age of 24.2 years (SD= 5.1 years). Based on age, the participants were grouped into young adults (18-23 years old, 151 participants) and adults (24-40 years old, 123 participants). The estimation of noise exposure was calculated based on self-reported responses of PLD use. Two categories emerged from this calculation: the participants with exposure lower than 80 dB were in the low exposure category (N: 196, 62.9 dB), while the participants with exposure higher than 80 dB were in the high exposure category (N: 78, 89.9 dB). Results: Based on the age categories, most of the questionnaire answers were similar between the young adults and the adults, revealing similar habits in using their PLDs. However, the investigation based on exposure revealed differences, as the participants with high exposure levels were more likely to have hobbies that involved noise, and they were less likely to obtain hearing evaluations. Among the participants, 30% used their devices at the maximum volume level and on a daily basis. 33.5% reported experiencing worsening in hearing, 2.4% reported persistent tinnitus, 94.1% knew that hearing protectors were available but only 20.7% reported using hearing protectors. Conclusion: The study concludes that adults are at risk of hearing loss due to unsafe listening habits. A discrepancy between knowledge and practice is apparent and needs to be addressed in young adults by increasing awareness of hearing loss, hearing protection and annual hearing evaluation.

Neurophysiological, structural, and molecular alterations in the prefrontal and auditory cortices following noise-induced hearing loss.

It is well established that hearing loss can lead to widespread plasticity within the central auditory pathway, which is thought to contribute to the pathophysiology of audiological conditions such as tinnitus and hyperacusis. Emerging evidence suggests that hearing loss can also result in plasticity within brain regions involved in higher-level cognitive functioning like the prefrontal cortex; findings which may underlie the association between hearing loss and cognitive impairment documented in epidemiological studies. Using the 40-Hz auditory steady state response to assess sound-evoked gamma oscillations, we previously showed that noise-induced hearing loss results in impaired gamma phase coherence within the prefrontal but not the auditory cortex. To determine whether region-specific structural or molecular changes accompany this differential plasticity following hearing loss, in the present study we utilized Golgi-Cox staining to assess dendritic organization and synaptic density, as well as Western blotting to measure changes in synaptic signaling proteins in these cortical regions. We show that following noise exposure, impaired gamma phase coherence within the prefrontal cortex is accompanied by alterations in pyramidal cell dendritic morphology and decreased expression of proteins involved in GABAergic (GAD65) and glutamatergic (NR2B) neurotransmission; findings that were not observed in the auditory cortex, where gamma phase coherence remained unchanged post-noise exposure. In contrast to the noise-induced effects we observed in the prefrontal cortex, plasticity in the auditory cortex was characterized by an increase in NR2B suggesting increased excitability, as well as increases in the synaptic proteins PSD95 and synaptophysin within the auditory cortex. Overall, our results highlight the disparate effect of noise-induced hearing loss on auditory and higher-level brain regions as well as potential structural and molecular mechanisms by which hearing loss may contribute to impaired cognitive and sensory functions mediated by the prefrontal and auditory cortices.

A longitudinal study investigating the effects of noise exposure on behavioural, electrophysiological and self-report measures of hearing in musicians with normal audiometric thresholds.

Musicians are at risk of hearing loss and tinnitus due to regular exposure to high levels of noise. This level of risk may have been underestimated previously since damage to the auditory system, such as cochlear synaptopathy, may not be easily detectable using standard clinical measures. Most previous research investigating hearing loss in musicians has involved cross-sectional study designs that may capture only a snapshot of hearing health in relation to noise exposure. The aim of this study was to investigate the effects of cumulative noise exposure on behavioural, electrophysiological, and self-report indices of hearing damage in early-career musicians and non-musicians with normal hearing over a 2-year period. Participants completed an annual test battery consisting of pure tone audiometry, extended high-frequency hearing thresholds, distortion product otoacoustic emissions (DPOAEs), speech perception in noise, auditory brainstem responses, and self-report measures of tinnitus, hyperacusis, and hearing in background noise. Participants also completed the Noise Exposure Structured Interview to estimate cumulative noise exposure across the study period. Linear mixed models assessed changes over time. The longitudinal analysis comprised 64 early-career musicians (female n = 34; age range at T0 = 18-26 years) and 30 non-musicians (female n = 20; age range at T0 = 18-27 years). There were few longitudinal changes as a result of musicianship. Small improvements over time in some measures may be attributable to a practice/test-retest effect. Some measures (e.g., DPOAE indices of outer hair cell function) were associated with noise exposure at each time point, but did not show a significant change over time. A small proportion of participants reported a worsening of their tinnitus symptoms, which participants attributed to noise exposure, or not using hearing protection. Future longitudinal studies should attempt to capture the effects of noise exposure over a longer period, taken at several time points, for a precise measure of how hearing changes over time. Hearing conservation programmes for "at risk" individuals should closely monitor DPOAEs to detect early signs of noise-induced hearing loss when audiometric thresholds are clinically normal.

Evaluation of the relationship between occupational noise exposure and stress levels in a healthcare facility.

Objectives. This study aimed to assess noise levels in various units in hospitals and explore the correlation between healthcare employees' daily noise exposure level (Lex,8h) and their stress and symptoms. Methods. A healthcare facility was selected to study noise pollution. Personal noise dosimeters were used during 8-h working shifts. Data were collected from 126 employees using the 36-item 'A stress scale' and a socio-demographic information form. Results. The results of noise measurements exceeded World Health Organization and US Environmental Protection Agency recommended limits at all sites. The lowest Lex,8h (52 dB) was detected in the endocrinology clinic, while the highest (91 dB) was recorded in the podology unit. According to the stress scale scores, the lowest mean psychological symptom score (PsSS), physiological symptom score (PhSS) and total scale score (TSS) were observed in diagnostic units with 35 ± 14, 41 ± 14 and 76 ± 27, respectively, while the highest mean PsSS, PhSS and TSS were observed in the polyclinics with 44 ± 6, 64 ± 10 and 107 ± 10, respectively. The PsSS of employees exposed to noise (Lex,8h) above 75 dB was found to be higher than for other employees. Conclusion. Lex,8h above 75 dB can increase psychological symptoms in healthcare employees.

Stereocilia fusion pathology in the cochlear outer hair cells at the nanoscale level.

The hair bundle of cochlear hair cells comprises specialized microvilli, the stereocilia, which fulfil the role of mechanotransduction. Genetic defects and environmental noise challenge the maintenance of hair bundle structure, critically contributing to age-related hearing loss. Stereocilia fusion is a major component of the hair bundle pathology in mature hair cells, but its role in hearing loss and its molecular basis are poorly understood. Here, we utilized super-resolution expansion microscopy to examine the molecular anatomy of outer hair cell stereocilia fusion in mouse models of age-related hearing loss, heightened endoplasmic reticulum stress and prolonged noise exposure. Prominent stereocilia fusion in our model of heightened endoplasmic reticulum stress, Manf (Mesencephalic astrocyte-derived neurotrophic factor)-inactivated mice in a background with Cadherin 23 missense mutation, impaired mechanotransduction and calcium balance in stereocilia. This was indicated by reduced FM1-43 dye uptake through the mechanotransduction channels, reduced neuroplastin/PMCA2 expression and increased expression of the calcium buffer oncomodulin inside stereocilia. Sparse BAIAP2L2 and myosin 7a expression was retained in the fused stereocilia but mislocalized away from their functional sites at the tips. These hair bundle abnormalities preceded cell soma degeneration, suggesting a sequela from stereociliary molecular perturbations to cell death signalling. In the age-related hearing loss and noise-exposure models, stereocilia fusion was more restricted within the bundles, yet both models exhibited oncomodulin upregulation at the fusion sites, implying perturbed calcium homeostasis. We conclude that stereocilia fusion is linked with the failure to maintain cellular proteostasis and with disturbances in stereociliary calcium balance. KEY POINTS: Stereocilia fusion is a hair cell pathology causing hearing loss. Inactivation of Manf, a component of the endoplasmic reticulum proteostasis machinery, has a cell-intrinsic mode of action in triggering outer hair cell stereocilia fusion and the death of these cells. The genetic background with Cadherin 23 missense mutation contributes to the high susceptibility of outer hair cells to stereocilia fusion, evidenced in Manf-inactivated mice and in the mouse models of early-onset hearing loss and noise exposure. Endoplasmic reticulum stress feeds to outer hair cell stereocilia bundle pathology and impairs the molecular anatomy of calcium regulation. The maintenance of the outer hair cell stereocilia bundle cohesion is challenged by intrinsic and extrinsic stressors, and understanding the underlying mechanisms will probably benefit the development of interventions to promote hearing health.

Making a racket in America's fastest growing sport: Evaluation of noise exposure in pickleball.

OBJECTIVE: To measure noise exposure present on pickleball courts and assess the risk of noise-induced hearing loss (NIHL) per guidelines put forward by the National Institute of Occupational Safety and Health (NIOSH). METHODS: Observational study measuring noise levels at multiple recreational pickleball courts in the Richmond, VA area, documenting LAeq, LASmax, and LCpeak at courtside and waiting areas of pickleball courts. Measurements were completed using the NIOSH SLM application on an iPhone 13 with iMM-6 Calibrated Measurement Microphone (equivalent to IEC 61672-1 Class II) that was calibrated using ND-9 Sound Level Calibrator (IEC942 Class I). RESULTS: Average sound levels recorded at waiting areas adjacent to the courts, measured in LAeq, LASmax, and LCpeak, were 69.1 dBA, 92.0 dBA, and 112.1 dBC, respectively, while courtside measurements were 69.7 dBA, 92.2 dBA, and 115.6 dBC, respectively. These measurements were within NIOSH and OSHA recommendations. CONCLUSION: The data demonstrates that randomly sampled pickleball courts have noise levels that do not increase risk for NIHL for participants or bystanders alike based on NIOSH guidelines. However, prolonged noise exposure and ambient noise pollution may have other health implications and warrant further investigations. LEVEL OF EVIDENCE: Level 2.

Road traffic noise pollution and prevalence of ischemic heart disease: modelling potential association and abatement strategies in noise-exposed areas.

In many developing countries with surging vehicular traffic and inadequate traffic management, excessive road traffic noise exposure poses substantial health concerns, linked to increased stress, insomnia and other metabolic disorders. This study aims to assess the linkage between sociodemographic factors, traffic noise levels in residential areas and health effects using a cross-sectional study analyzing respondents' perceptions and reports. Noise levels were measured at 57 locations in Srinagar, India, using noise level meter. Sound PLAN software was employed to generate noise contour maps, enabling the visualization of noise monitoring locations and facilitating the assessment of noise levels along routes in proximity to residential areas. Correlation analysis showed a strong linear relationship between field-measured and modelled noise (r2 = 0.88). Further, a questionnaire-based survey was carried out near the sampling points to evaluate the association of ischemic heart disease with traffic noise. Residents exposed to noise levels (Lden > 60 dB(A)) were found to have a 2.24 times higher odds ratio. Compared to females, males reported a 16% higher prevalence of the disease. Multi-faceted policy strategies involving noise mapping initiatives, source noise standards, traffic flow urban mobility optimization, smart city initiatives and stringent litigatory measures could significantly reduce its detrimental impact on public health. Finally, this study envisions a region-specific strong regulatory framework for integrating noise pollution mitigation strategies into the public health action plans of developing nations.

Association between exposure to metalworking fluid aerosols, occupational noise and chronic kidney disease: a cross-sectional study in China.

BACKGROUND: Chronic kidney disease (CKD) carries a high public health burden yet little is known about the relationship between metalworking fluid (MWF) aerosols, occupational noise and CKD. We aimed to explore the relationship between occupational MWF aerosols, occupational noise and CKD. METHODS: A total of 2,738 machinists were sampled from three machining companies in Wuxi, China, in 2022. We used the National Institute for Occupational Safety and Health (NIOSH) method 5524 to collect individual samples for MWF aerosols exposure, and the Chinese national standard (GBZ/T 189.8-2007) method to test individual occupational noise exposure. The diagnostic criteria for CKD were urinary albumin/creatinine ratio (UACR) of ≥ 30 mg/g and reduced renal function (eGFR < 60 mL.min- 1. 1.73 m- 2) lasting longer than 3 months. Smooth curve fitting was conducted to analyze the associations of MWF aerosols and occupational noise with CKD. A segmented regression model was used to analyze the threshold effects. RESULTS: Workers exposed to MWF aerosols (odds ratio [OR] = 2.03, 95% confidence interval [CI]: 1.21-3.41) and occupational noise (OR = 1.77, 95%CI: 1.06-2.96) had higher prevalence of CKD than nonexposed workers. A nonlinear and positive association was found between increasing MWF aerosols and occupational noise dose and the risk of CKD. When daily cumulative exposure dose of MWF aerosols exceeded 8.03 mg/m3, the OR was 1.24 (95%CI: 1.03-1.58), and when occupational noise exceeded 87.22 dB(A), the OR was 1.16 (95%CI: 1.04-1.20). In the interactive analysis between MWF aerosols and occupational noise, the workers exposed to both MWF aerosols (cumulative exposure ≥ 8.03 mg/m3-day) and occupational noise (LEX,8 h ≥ 87.22 dB(A)) had an increased prevalence of CKD (OR = 2.71, 95%CI: 1.48-4.96). MWF aerosols and occupational noise had a positive interaction in prevalence of CKD. CONCLUSIONS: Occupational MWF aerosols and noise were positively and nonlinearly associated with CKD, and cumulative MWF aerosols and noise exposure showed a positive interaction with CKD. These findings emphasize the importance of assessing kidney function of workers exposed to MWF aerosols and occupational noise. Prospective and longitudinal cohort studies are necessary to elucidate the causality of these associations.

Power saw noise levels during steel stud cutting tasks on commercial construction sites: a tool characterization from a worker exposure standpoint.

Construction framers who cut and install steel studs as part of their daily tasks are exposed to hazardous noise levels during their work shift in large part due to the power saws they use to cut steel studs. This investigation characterized the sound pressure levels of power saws used to cut steel studs on active construction sites. Further, the length of time it took to cut various studs on a construction site was investigated to understand worker exposure times to saw noise. In general, power saws used on the study sites to cut steel studs had a mean A-weighted equivalent continuous sound pressure level (LAeq) of 107.2 dB and a C-weighted peak sound pressure level (LCpeak) of 120.1 dB. Three of the saws-the chopsaw, the cut-off saw, and the grinder-had similar noise levels, whereas the cordless circular saw had higher noise levels. It took an average of 13.2 s to cut each stud, and workers in the study used power saws to cut steel studs for an average of 371.5 s per day. This average exposure time at the average recorded sound pressure levels (SPLs) suggests these saws can increase the risk of occupational noise-induced hearing loss, according to National Institute for Occupational Safety and Health (NIOSH) recommendations.

Activation of Src Kinase Mediates the Disruption of Adherens Junction in the Blood-labyrinth Barrier after Acoustic Trauma.

BACKGROUND: Adherens junction in the blood-labyrinth barrier is largely unexplored because it is traditionally thought to be less important than the tight junction. Since increasing evidence indicates that it actually functions upstream of tight junction adherens junction may potentially be a better target for ameliorating the leakage of the blood-labyrinth barrier under pathological conditions such as acoustic trauma. AIMS: This study was conducted to investigate the pathogenesis of the disruption of adherens junction after acoustic trauma and explore potential therapeutic targets. METHODS: Critical targets that regulated the disruption of adherens junction were investigated by techniques such as immunofluorescence and Western blottingin C57BL/6J mice. RESULTS: Upregulation of Vascular Endothelial Growth Factor (VEGF) and downregulation of Pigment Epithelium-derived Factor (PEDF) coactivated VEGF-PEDF/VEGF receptor 2 (VEGFR2) signaling pathway in the stria vascularis after noise exposure. Downstream effector Src kinase was then activated to degrade VE-cadherin and dissociate adherens junction which led to the leakage of the blood-labyrinth barrier. By inhibiting VEGFR2 or Src kinase VE-cadherin degradation and blood-labyrinth barrier leakage could be attenuated but Src kinase represented a better target to ameliorate blood-labyrinth barrier leakage as inhibiting it would not interfere with vascular endothelium repair neurotrophy and pericytes proliferation mediated by upstream VEGFR2. CONCLUSION: Src kinase may represent a promising target to relieve noise-induced disruption of adherens junction and hyperpermeability of the blood-labyrinth barrier.

Association of noise exposure with lipid metabolism among Chinese adults: mediation role of obesity indices.

PURPOSE: Noise exposure in the workplace has been linked to a number of health consequences. Our objectives were to explore the relationship between occupational noise and lipid metabolism and evaluate the possible mediating effect of obesity indices in those relationships with a cross-sectional study design. METHODS: Cumulative noise exposure (CNE) was used to measure the level of noise exposure. Logistic regression models or generalized linear models were employed to evaluate the association of occupational noise and obesity with lipid metabolism markers. Cross-lagged analysis was conducted to explore temporal associations of obesity with lipid metabolism. RESULTS: A total of 854 participants were included, with each one-unit increase in CNE, the values of total cholesterol/high-density lipoprotein cholesterol and low-density lipoprotein cholesterol/high-density lipoprotein cholesterol increased by 0.013 (95% confidence interval: 0.006, 0.020) and 0.009 (0.004, 0.014), as well as the prevalence of dyslipidemia increased by 1.030 (1.013, 1.048). Occupational noise and lipid metabolism markers were all positively associated with body mass index (BMI), waist circumference (WC), a Body Shape Index (ABSI) and a Body Shape Index and Body Roundness Index (BRI) (all P < 0.05). Moreover, BMI, WC, ABSI and BRI could mediate the associations of occupational noise with lipid metabolism; the proportions ranged from 21.51 to 24.45%, 23.84 to 30.14%, 4.86 to 5.94% and 25.59 to 28.23%, respectively (all P < 0.05). CONCLUSIONS: Our study demonstrates a positive association between occupational noise and abnormal lipid metabolism, and obesity may partly mediate the association. Our findings reinforce the need to take practical steps to reduce or even eliminate the health risks associated with occupational noise.

Effects of age and noise exposure history on auditory nerve response amplitudes: A systematic review, study, and meta-analysis.

Auditory nerve (AN) function has been hypothesized to deteriorate with age and noise exposure. Here, we perform a systematic review of published studies and find that the evidence for age-related deficits in AN function is largely consistent across the literature, but there are inconsistent findings among studies of noise exposure history. Further, evidence from animal studies suggests that the greatest deficits in AN response amplitudes are found in noise-exposed aged mice, but a test of the interaction between effects of age and noise exposure on AN function has not been conducted in humans. We report a study of our own examining differences in the response amplitude of the compound action potential N1 (CAP N1) between younger and older adults with and without a self-reported history of noise exposure in a large sample of human participants (63 younger adults 18-30 years of age, 103 older adults 50-86 years of age). CAP N1 response amplitudes were smaller in older than younger adults. Noise exposure history did not appear to predict CAP N1 response amplitudes, nor did the effect of noise exposure history interact with age. We then incorporated our results into two meta-analyses of published studies of age and noise exposure history effects on AN response amplitudes in neurotypical human samples. The meta-analyses found that age effects across studies are robust (r = -0.407), but noise exposure effects are weak (r = -0.152). We conclude that noise exposure effects may be highly variable depending on sample characteristics, study design, and statistical approach, and researchers should be cautious when interpreting results. The underlying pathology of age-related and noise-induced changes in AN function are difficult to determine in living humans, creating a need for longitudinal studies of changes in AN function across the lifespan and histological examination of the AN from temporal bones collected post-mortem.

Sources of noise exposure across Australian workplaces: cross-sectional analysis and modelling the impact of a targeted noise-source reduction initiative.

CONTEXT: Workplace noise regulations and guidance follow the hierarchy of control model that prioritizes eliminating or reducing noise at its source. OBJECTIVES: To determine the main sources of workplace noise exposure in the Australian working population and estimate the reduction of workers exposed over the noise limit (LAeq,8h > 85 dB) if noise levels of specific tools or equipment were reduced by 10 dB. METHODS: Information on the tools used and tasks performed during each participant's last working shift was collected from 4,977 workers via telephone survey. Using a predetermined database of task-based noise levels, partial noise exposures (Pa2h) were determined for each noisy activity performed by the workers and their daily noise exposure level (LAeq,8h) was estimated. Partial exposures were categorized into 15 tool/task groups and the tally, average, and sum (Pa2h) for each group were calculated. The impacts of 5 different scenarios that simulated a reduction of 10 dB in noise emissions for specific tool groups were modelled. RESULTS: Powered tools and equipment were responsible for 59.3% of all noise exposure (Pa2h); vehicles for 10.6%; mining, refineries, and plant equipment for 5.1%; and manufacturing and food processing for 4.2%. Modelling demonstrated that a 10 dBA noise-level reduction of all powered tools and equipment would lead to a 26.4% (95% confidence interval: 22.7% to 30.3%) reduction of workers with an LAeq,8h > 85 dB. This could represent over 350,000 Australian workers no longer exposed above the workplace limit daily. CONCLUSIONS: A universal reduction of 10 dB to power tools and equipment would substantially reduce the future burden of hearing loss, tinnitus, workplace injuries, and other health effects. Initiatives to reduce the noise emissions of specific powered tool groups are warranted.

Effects of Age and Noise Exposure History on Auditory Nerve Response Amplitudes: A Systematic Review, Study, and Meta-Analysis.

Auditory nerve (AN) function has been hypothesized to deteriorate with age and noise exposure. Here, we perform a systematic review of published studies and find that the evidence for age-related deficits in AN function is largely consistent across the literature, but there are inconsistent findings among studies of noise exposure history. Further, evidence from animal studies suggests that the greatest deficits in AN response amplitudes are found in noise-exposed aged mice, but a test of the interaction between effects of age and noise exposure on AN function has not been conducted in humans. We report a study of our own examining differences in the response amplitude of the compound action potential N1 (CAP N1) between younger and older adults with and without a self-reported history of noise exposure in a large sample of human participants (63 younger adults 18-30 years of age, 103 older adults 50-86 years of age). CAP N1 response amplitudes were smaller in older than younger adults. Noise exposure history did not appear to predict CAP N1 response amplitudes, nor did the effect of noise exposure history interact with age. We then incorporated our results into two meta-analyses of published studies of age and noise exposure history effects on AN response amplitudes in neurotypical human samples. The meta-analyses found that age effects across studies are robust (r=-0.407), but noise-exposure effects are weak (r=-0.152). We conclude that noise-exposure effects may be highly variable depending on sample characteristics, study design, and statistical approach, and researchers should be cautious when interpreting results. The underlying pathology of age-related and noise-induced changes in AN function are difficult to determine in living humans, creating a need for longitudinal studies of changes in AN function across the lifespan and histological examination of the AN from temporal bones collected post-mortem.