Exposure to aircraft noise exacerbates cardiovascular and oxidative damage in three mouse models of diabetes.

BACKGROUND: Epidemiology links noise to increased risk of metabolic diseases like diabetes and obesity. Translational studies in humans and experimental animals showed that noise causes reactive oxygen species (ROS)-mediated cardiovascular damage. The interaction between noise and diabetes, specifically potential additive adverse effects, remains to be determined. METHODS AND RESULTS: C57BL/6 mice were treated with streptozotocin (i.p. injections, 50 mg/kg/d for 5d) to induce type-1 diabetes, with S961 (subcutaneous osmotic minipumps, 0.57 mg/kg/d for 7d) or fed a high-fat diet (HFD, 20 weeks) to induce type-2 diabetes. Control and diabetic mice were exposed to aircraft noise to an average sound pressure level of 72 dB(A) for 4d. While body weight was unaffected, noise reduced insulin production in all diabetes models. The oral glucose tolerance test showed only an additive aggravation by noise in the HFD model. Noise increased blood pressure and aggravated diabetes-induced aortic, mesenteric, and cerebral arterioles endothelial dysfunction. ROS formation in cerebral arterioles, the aorta, the heart, and isolated mitochondria was consistently increased by noise in all models of diabetes. Mitochondrial respiration was impaired by diabetes and noise, however without additive effects. Noise increased ROS and caused inflammation in adipose tissue in the HFD model. RNA sequencing data and alteration of gene pathway clusters also supported additive damage by noise in the setting of diabetes. CONCLUSION: In all three models of diabetes, aircraft noise exacerbates oxidative stress, inflammation, and endothelial dysfunction in mice with pre-existing diabetes. Thus, noise may potentiate the already increased cardiovascular risk in diabetic patients.

Traffic noise significantly contributes to an increased risk of cardiometabolic diseases (including diabetes and obesity) in the general population via stress hormones, inflammation and oxidative stress, all of which contribute to impaired vascular function and high blood pressure. However, the extent to which noise affects pre-existing diabetes is not sufficiently explained, which prompted us to investigate the molecular mechanisms responsible for noise-mediated exacerbation of cardiometabolic complications in three different animal models with diabetes mellitus: Noise exposure in diabetic mice caused further impairment of insulin signalling, increased blood pressure, and damage of small and large blood vessels as well as oxidative stress in the aorta, brain, and heart.Our functional observations were supported by gene analyses indicating combined effects of noise and diabetes on gene groups related to inflammation and metabolism, suggesting a need for further studies in humans to investigate how noise impacts cardiovascular risk in vulnerable groups such as patients with diabetes.

The Role of Connexin26 and Connexin30 in the Mouse Cochlea of Noise-Induced Hearing Loss.

OBJECTIVE: We aimed to explore the role of connexin26 (Cx26) and connexin30 (Cx30) in the cochlea in noise-induced permanent threshold shifts (PTS) and temporary threshold shift (TTS). STUDY DESIGN: Prospective, controlled. SETTING: Laboratory. METHODS: A mouse model of noise-induced PTS and TTS was constructed. Western blots were used to detect the expression of Cx26 and Cx30 in the cochlea. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were used to assess the potential biological pathways. RESULTS: Both the expression of Cx26 and Cx30 showed a trend of first rising and then falling in noise-induced PTS. The expression of Cx26 increased greatly in the 24 hours noise exposure (P < .05) and reached the highest level in the 4 hours after noise exposure (P < .05), then decreased gradually and returned to the control level on the seventh day after the noise exposure, when compared with the control group. The expression of Cx30 showed a similar trend in noise-induced PTS. However, both the expression of Cx26 and Cx30 showed a trend of first falling and then rising in noise induced TTS. The expression of Cx26/Cx30 reached its lowest level in the 4 hours after noise exposure (P < .05), and then increased to the control level on the second day after noise exposure (P > .05), compared with the control group. The first KEGG and GO pathway may be related with oxidative phosphorylation. CONCLUSION: Cx26 and Cx30 may have an effect in noise induced PTS and TTS. Future studies are needed to confirm the results.

The Effects of Green Spaces and Noise Exposure on the Risk of Ischemic Stroke: A Case-Control Study in Lebanon.

BACKGROUND: Environmental surroundings reduce the rate of several diseases, especially those related to stressful events. Ischemic stroke can be affected by such events, either directly or through its risk factors. Therefore, the present study evaluates the effects of green spaces and noise exposure on the risk of ischemic stroke. METHODS: A case-control study was carried out, including 200 ischemic stroke cases within the first 48 h of diagnosis and 200 controls, divided equally into hospitalized and non-hospitalized participants. Controls were matched to cases based on age and gender. Socio-demographic characteristics were assessed, in addition to environmental surroundings and noise exposure at home and at workplaces. RESULTS: Living in a house, having a house garden, and taking care of the garden were associated with a lower risk of suffering an ischemic stroke (p < 0.001, p < 0.001, and p = 0.009, respectively). However, having buildings as the view from home led to a higher stroke rate (p < 0.001). Working in an urban area, the workplace being surrounded by buildings, and the workplace not being surrounded by green spaces were also associated with a higher risk of suffering an ischemic stroke (p = 0.002, p = 0.001, and p = 0.03, respectively). As for noise exposure, being exposed to traffic noise, human noise, and other types of noise was significantly associated with a higher risk of ischemic stroke, while being exposed to higher levels of natural noise was significantly associated with a lower risk of ischemic stroke. Higher levels of noise were also associated with higher risks of ischemic stroke in homes and workplaces (p < 0.001 and p = 0.008, respectively). CONCLUSIONS: Environmental surroundings and noise exposure were found to affect the risk of ischemic stroke. Greater green spaces and lower noise exposure play a protective role against ischemic stroke, suggesting a possible prevention strategy through environmental modifications at home and workplaces.

Effects of Ultrasonic Use on Hearing Loss in Dental Hygienists: A matched pairs design study.

Purpose Dental professionals are exposed to hazardous noise levels on a daily basis in clinical practice. The purpose of this study was to compare the hearing status of dental hygienists who utilize ultrasonic scalers in the workplace compared to age-matched control participants (non-dental hygienists) who were not exposed to ultrasonic noise.Methods A convenience sample of nineteen dental hygienists (experimental) and nineteen non-dental hygienists (control) was recruited for this study. A matched pairs design was utilized; participants in each group were matched based on age and gender to eliminate confounding variables. The testing procedure consisted of an audiologist performing a series of auditory tests including otoacoustic emissions test, pure-tone audiometry, and tympanometry on the experimental and control groups.Results In the right ear, there were notable differences from 1000 Hz - 10,000 Hz and in the left ear from 6000 Hz - 10,000 Hz, with higher hearing thresholds in the experimental group of dental hygienists. While 56% of the univariate tests conducted on how many days were worked per week showed statistical significance, the regression line slope indicated those that worked more days had better hearing statuses. The variables for years in practice for dental hygienists, how many of those years were full-time employment, and how many years the dental hygienist had used an ultrasonic scaling device, also had many significant univariate tests for the experimental group only. These variables were more likely to serve as proxies representing true noise exposure. The paired t-test between the groups demonstrated statistically significant differences between the experimental and control group at 9000 Hz in both ears.Conclusion While results from this study demonstrated various qualitative differences in hearing status of the control group (non-dental hygienists) and experimental group (dental hygienists), age was found to be the most critical variable. Furthermore, this data demonstrated differences in hearing status based on various frequencies between dental hygienists and age-matched controls that should be further explored with a larger population.

Association between residential noise exposure and burnout among healthcare workers in Taiwan: a cross-sectional study.

Few studies have explored the association between residential noise exposure and burnout. In this study, we investigated the association between residential noise exposure and burnout prevalence among 5416 health-care workers in Taiwan from 2012 to 2017. Burnout was evaluated using the Mandarin version of the Copenhagen Burnout Inventory by considering both continuous and binary measures. We applied ordinary Kriging models to calculate the annual average residential noise exposure at an individual level. Multivariable linear regression models and logistic regression models were employed. Restricted cubic splines were used to explore dose-response relationships. The median age of the health-care workers was 31.5 years. In the multivariable linear regression models, exposure to residential noise (per 1 dBA) was associated with increases in personal burnout and work-related burnout scores by 1.59 ± 0.25 and 1.38 ± 0.20, respectively. In the multivariable logistic regression models, the adjusted odds ratios were 1.24 (95% confidence interval [CI]: 1.16, 1.32) for personal burnout and 1.19 (95% CI: 1.13, 1.26) for work-related burnout per 1-dBA increase in residential noise exposure. Linear dose-response associations of burnout with residential noise level were detected. Our findings suggest that exposure to residential noise may increase the risk of burnout among health-care workers.

Audiological Profile of Yakshagana Artists.

Yakshagana is an India's traditional folk theatre musical dance drama. The purpose of the study is to profile audiological characteristics and document hearing-related symptoms in Yakshagana artists. A cross-sectional study was performed on 96 Yakshagana artists. Participants' demographic data were captured, and audiological evaluations, including high frequency audiometry (HFA), tympanometry, acoustic reflex threshold and transient evoked otoacoustic emission (TEOAE), were performed. The majority of the individuals had minimal and mild hearing loss. The mean scores of pure tone thresholds were greater at 4 kHz and 8 kHz. The majority of the HFA thresholds at 10 kHz, 12.5 kHz, and 16 kHz indicated no responses, which can be accredited to the fact that noise-induced hearing loss (NIHL) first affects the higher frequencies. TEOAE analysis showed a greater percentage of failures in the higher frequencies, particularly at 3 and 4 kHz in both ears, which can be an indicator of bilateral cochlear damage. These findings indicate that Yakshagana artists are at risk of hearing loss due to noise exposure. Hearing evaluation and regular monitoring of hearing thresholds is advisable for this population as it can impact their careers.

Noise Exposure in the Workplace, Genetic Susceptibility, and Incidence of Atrial Fibrillation: A Prospective Cohort Study.

BACKGROUND: No study explored the association of noise exposure in the workplace and genetic susceptibility with incidence of atrial fibrillation (AF). We aimed to assess the separate and joint relationship of noise exposure in the workplace and genetic susceptibility with the risk of AF. METHODS AND RESULTS: We included 167 577 participants without AF at baseline in UK Biobank. Cox proportional hazards models were used to assess the separate and joint association of noise exposure in the workplace and genetic susceptibility with the risk of AF. During a median follow-up of 11.83 years, we observed 9355 AF cases. Compared with no noise exposure in the workplace, the hazard ratios (HRs) and were 1.08 (95% CI, 0.99-1.18) for noise exposure in the workplace of <1 year, 1.03 (95% CI, 0.95-1.12) for noise exposure in the workplace of around 1 to 5 years, and 1.08 (95% CI, 1.02-1.14) for noise exposure in the workplace of >5 years, respectively, after adjusting for potential confounders. Genetic risk was positively associated with AF, compared with low genetic risk (tertile 1), the HRs were 1.50 (95% CI, 1.41-1.59) for medium genetic risk (tertile 2) and 2.51 (95% CI, 2.38-2.65) for high genetic risk (tertile 3). However, no interaction between noise exposure in the workplace and genetic susceptibility was observed (P>0.05). CONCLUSIONS: Long-term noise exposure in the workplace is positively associated with a higher incidence of AF regardless of genetic background.

Individual-level noise exposure and its association with sleep quality and duration: A cross-sectional study using real-time data.

As urban populations grow, the problem of noise pollution becomes more significant. The limited number of epidemiological studies linking individual-level dynamic noise exposure to sleep highlights a gap in our understanding of how individual-level noise exposure impact sleep quality and duration. A cross-sectional survey was conducted in Hong Kong, and portable noise sensors were used to record participants' real-time noise exposure. The Pittsburgh Sleep Quality Index was used to assess their sleep quality. Logistic regression was used to examine the relationship of individual-level noise exposure with sleep quality and sleep duration. Among a total of 763 subjects included in the analysis, and a-weighted decibels [dB(A)] 24-h average exposure (L24) was 63.21 (58.85-67.85) dB(A) for workday and 63.52 (59.03-67.86) dB(A) for non-workday. A significant decrease in individual noise level was observed closer to bedtime (P < 0.05). Compared with the lowest noise exposure, exposure to the highest noise level was positively associated with the presence of poor sleep quality for L24, Ld and Ln, with an odds ratio (OR) and 95 % confidential interval (CI) of 1.53 (1.04-2.24), 1.65 (1.12-2.43), and 1.51 (1.03-2.21), respectively. Exposure to elevated noise level was associated with increased risk of shorter nocturnal sleep duration (< 7 h), the OR and 95 % CI was 1.87 (1.29-2.73) for L24, 1.58 (1.09-2.30) for Ld, 1.50 (1.03-2.18) for Le, and 1.60 (1.10-2.32) for Ln in the highest noise exposure group. Similar findings were observed both on workdays and non-workdays, respectively. Furthermore, the results showed that each 10 dB(A) increment in L24 and Ln was associated with a probable 29 % and 27 % increase in poor sleep quality and a 24 % and 24 % reduction in sleep duration. This study demonstrates that environmental noise exposure was associated with poor sleep quality and shorter sleep duration, posing a significant public health issue in Hong Kong.

The role of NLRP3 inflammasome-mediated neuroinflammation in chronic noise-induced impairment of learning and memory ability.

BACKGROUND: Noise pollution pervades daily working and living environment, becoming a serious public health problem. In addition to causing auditory impairment, noise independently contributes to cognitive decline as a risk factor. Though neuroinflammation plays an important role in noise-induced cognitive deficits, the mechanisms underlying noise-induced neuroinflammation in the hippocampus are still poorly understood. Glial hyperactivation of the NLRP3 inflammasome contributes to various neurodegenerative diseases, including Alzheimer's disease (AD) and Parkinson's disease (PD). However, whether the NLRP3 inflammasome plays a role in noise-induced cognitive impairment remains to be further investigated. METHODS: Adult male Wistar rats were exposed to 100 dB white noise (4 h/day) for 30 days with or without injection of the NLRP3 inhibitor MCC950 (10 mg/kg/day). The Morris water maze (MWM) test and the open field test (OFT) were performed to evaluate learning and memory ability of rats. HE staining was used to explore hippocampal pathological changes, while immunohistochemical staining was employed to evaluate the number and morphology of microglia and astrocytes. The mRNA levels of the NLRP3 inflammasome in the hippocampus were examined by Real-time PCR. The protein levels of NLRP3 inflammasome, inflammatory cytokines, p-Tau-S396, and amyloid-ß (Aß) 42 in the hippocampus were examined by Western blot. Immunofluorescence was used to observe the distribution of NLRP3 in glial cells and neurons, and the assembly of the NLRP3 inflammasome. RESULTS: We found that noise exposure induced learning and memory impairment in rats, mainly related to the activation of microglia and astrocytes in hippocampus region. Noise exposure increased the protein levels of p-Tau-S396, Aß42, ionized calcium binding adapter molecule 1 (Iba-1), glial fibrillary acidic protein (GFAP), interleukin (IL)-1ß, IL-18, and tumor necrosis factor-α (TNF-α) in hippocampus. Furthermore, the hippocampus of noise-exposed rats showed elevated protein levels of NLRP3, ASC and cleaved caspase-1. The co-labeled immunofluorescence levels of Iba-1 or GFAP with NLRP3 significantly increased in the dentate gyrus (DG) region of the hippocampus. NLRP3 inhibitor MCC950 intervention reversed chronic noise-induced activation of NLRP3 inflammasome, AD-like pathologies and impairment of learning and memory in rats. CONCLUSIONS: The NLRP3 inflammasome-mediated neuroinflammation played an essential role in chronic noise-induced cognitive dysfunction. These results provide novel strategies for the prevention and treatment of cognitive deficits caused by chronic noise.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.