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.

UNASSIGNED: 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.
UNASSIGNED: A cross-sectional survey was designed and distributed online.
UNASSIGNED: 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).
UNASSIGNED: 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.
UNASSIGNED: 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.

BACKGROUND: 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.
OBJECTIVE: 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.
METHODS: RACIS on fresh frozen human cadavers.
METHODS: 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.
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.
CONCLUSIONS: 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.

UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: Self reported symptoms were collected using a custom made case history questionnaire, and auditory sensitivity was measured using air conduction audiometers.
UNASSIGNED: 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.
UNASSIGNED: Hearing loss and self-reported auditory symptoms were present in the study group indicating the effect of occupational noise in the auditory system.

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.

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.

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.
CONCLUSIONS: 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.
METHODS: Level 2.

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.

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.

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.