Hearing loss, primarily caused by the irreversible loss of cochlear hair cells and spiral ganglion neurons, represents a major clinical challenge. Due to factors such as the blood-labyrinth barrier and the unique structure of the cochlea, there is still a lack of an effective and sustainable targeted drug delivery system. The development of inner ear drug delivery systems capable of sustaining therapeutic concentrations with site-specific localization remains a critical challenge in otopharmacology. In this paper, we engineered a magnetically navigable platform utilizing mesoporous silica nanoparticles (MMSNs) for precision-targeted cochlear drug administration. This system features a magnetic-responsive core and a permeable porous shell, combining the advantages of both nanomaterial carriers and Lycium barbarum glycopeptide (LbGP). The resultant MMSNs-LbGP nanocomposite exhibited good biocompatibility, antioxidant, and anti-inflammatory activities. In a guinea pig model of noise-induced hearing loss, MMSNs-LbGP treatment not only effectively restored auditory function and preserved cochlear hair cell structure but also significantly attenuated cochlear neuroinflammation and oxidative damage. This advancement establishes a novel framework for translational implementation of nanoparticle-mediated inner ear therapy, offering therapeutic solutions to rehabilitate or functionally augment auditory pathways in patients with sensorineural deficits.

Furosemide prevents noise-induced hearing loss and enhances the preventive effect of N-acetylcysteine.

Objectives: To quantify the global burden of occupational noise-induced hearing loss (ONHL) from 1990 to 2021 by sex, age, and Socio-demographic Index (SDI), and to project its future trends through 2035. Methods: Data on disability-adjusted life years (DALYs), age-standardized DALY rates (ASDRs), and summary exposure values (SEVs) of ONHL were extracted from the GBD 2021 study. Joinpoint regression was used to estimate annual percent changes in ASDRs. An age-period-cohort model assessed the effects of age, period, and cohort. Autoregressive integrated moving average (ARIMA) models forecasted DALY trends from 2025 to 2035. Results: Globally, ONHL-related DALYs increased from 3.84 million in 1990 to 7.85 million in 2021, with the highest relative increases in low- and middle-SDI regions. Males consistently had higher burden than females. DALYs peaked in midlife (ages 50-59), while age-specific DALY rates peaked at older ages (60-74). APC analysis revealed significant age effects across all SDI levels, while period and cohort effects were limited. ARIMA models predicted that global ONHL DALYs would reach 9.65 million by 2035, a 22.97% increase from 2021, with largest increases expected in those aged 55-59. Conclusions: Occupational noise–induced hearing loss remains a growing global public health challenge, particularly among male workers in lower-SDI regions. Continued increases are projected over the next decade. These results underscore the urgent need for strengthened hearing conservation strategies and targeted prevention policies to reduce ONHL burden worldwide.

Noise-induced sensorineural hearing loss is the consequence of multifactorial damage to the auditory structures, which is why the need for this work arose. Objective: To characterize hearing disorders due to exposure to industrial noise in generator set operators in Pinar del Río in the period 2021-2023. Methods: A longitudinal, prospective, descriptive and observational study was carried out, which was validated using theoretical, empirical and statistical methods. Results: a universe of (n-65) and a sample of (n-26) workers, with a predominance of the age group between 41 and 50 years, detecting 26 cases with hearing loss for 40% of the total workers exposed to noise, with a predominance of the male sex for 100%, the hearing impaired detected are directly exposed to noise with an intensity measured between 93 and 95 decibels. Mild hearing loss was present in 50% of the affected (n-13). The use of individual protection equipment against the harmful effects of noise was deficient; it was found that only 26.92% of the workers used them (n-7). Conclusions: all the generator sets were identified as sources of high noise emissions with measured levels higher than the internationally established values. Regarding the characteristics of the audiometric curves, there was a predominance of mild and moderate hearing loss, and the partial existence of the protective equipment was found, as well as their poor use by the workers.

Moderate noise exposure is a common experience, yet its impact on central auditory synapses remains poorly understood. We study this issue at the first synapses in the central auditory pathway formed by auditory nerve afferents onto bushy cells in the cochlear nucleus, called endbulbs of Held. Non-traumatic noise exposure alters endbulb properties, decreasing the probability of vesicle release and enlarging the pool of releasable vesicles as assessed using electrophysiological methods and immunolabelling. These changes appear homeostatic, to maintain synaptic efficacy during periods of high activity. To identify structural changes underlying the larger vesicle pool, we used serial blockface electron microscopy of endbulbs from control and noise-exposed mice to quantitatively assess synaptic morphology. We observed no differences in the juxtapositional area between endbulbs and bushy cells, nor in the number or density of active zones and postsynaptic densities. Images of endbulb terminals were significantly darker after noise exposure, indicating an increase in the density of synaptic vesicles. These results suggest that moderate noise exposure induces an activity-dependent increase in presynaptic vesicle numbers, consistent with the observed physiological changes in neurotransmitter release. This work sets the stage for high-resolution studies to quantify docked and reserve vesicles.Significance statementNoise exposure is a fact of everyday life, and it is important to understand how noise affects function in the auditory pathway in the brain to understand the full consequences of noise exposure. Electrophysiological experiments indicate that noise triggers a homeostatic increase in the releasable pool of vesicles at auditory nerve synapses. We examined the cellular basis for this change using serial blockface electron microscopy of auditory nerve synapses with and without noise exposure. We reconstructed a number of bushy cells and their presynaptic auditory nerve terminals. After noise exposure, there was no significant increase in the area of synaptic contact or the number or density of synaptic release sites. There was an increase in the number of vesicles near release sites, which may account for the physiological changes. These results emphasize the importance of detailed anatomical studies to study the effects of noise exposure and thus determine the best mechanistic approach for therapies and treatments of noise-induced hearing loss.

Noise-induced hearing loss (NIHL) is widespread. Hearing protection devices (HPDs) are intended to reduce noise exposure and limit NIHL. However, rigorous HPD selection is complex as HPDs often impede auditory functions necessary to maintain situation awareness, and selection is dependent upon diverse user needs, environmental contexts, and behavioral factors. This research employs a modular ontology method to develop a knowledge representation to unify conceptual understanding and the availability of passive HPD data among industrial hygienists and experts across the United States Department of Defense and the National Institute of Occupational Safety and Health. The objective of the study was to harmonize standard terminology, identify a comprehensive set of metrics, and create a searchable repository to facilitate HPD selection. By capturing human, environmental, and device-related attributes in a structured, machine-readable format, the ontology lays the foundation for a sharable repository to support user-centered, and context-specific HPD selection. Unfortunately, detailed technical data to support selection is not readily available. Data collection efforts are recommended to populate the ontology, providing practitioners with access to metrics and data to support analytic HPD selection.

Although the effects of noise-induced hearing loss (NIHL) on cognitive functions have been widely investigated, the cognitive effects of noise-induced hidden hearing loss (NIHHL), particularly its impact on memory, remain poorly understood. The Dnah11 gene, which encodes a dynein motor protein involved in synaptic development, may play a role in NIHHL-related cognitive impairment. We aimed to investigate whether NIHHL induces memory impairment and explore the role of Dnah11 expression in this process. Behavioral experiments identified the peak of memory impairment at 1 month following noise exposure. To elucidate molecular changes, hippocampal gene expression was analyzed using transcriptomic sequencing, reverse transcription quantitative polymerase chain reaction (RT-qPCR), and immunofluorescence. RNA sequencing revealed significant Dnah11 upregulation, with immunofluorescence confirming DNAH11 overexpression in hyperactivated CaMKIIα-positive excitatory neurons. Stereotaxic injection of recombinant adeno-associated virus (rAAV) vectors to knock down hippocampal Dnah11 expression improved memory performance in NIHHL mice without improving hearing loss. This cognitive improvement was accompanied by partial restoration of synaptic plasticity-related proteins, including SYN and PSD95. These findings indicate that Dnah11 upregulation in hippocampal excitatory neurons contributes to NIHHL-induced memory impairment, and targeting Dnah11 may offer a therapeutic strategy for memory impairment associated with hidden hearing loss.Supplementary InformationThe online version contains supplementary material available at 10.1007/s10565-025-10124-5.

Objectives Farmworkers are at increased risk for noise-induced hearing loss. This scoping review aimed to summarise the evidence on interventions to prevent NIHL among farmworkers and to identify gaps and priorities for future research. Methods The review followed Arksey and O’Malley’s scoping review framework and was reported in accordance with PRISMA-ScR guidelines. Results Twenty-three studies published between 1999 and 2023 met the inclusion criteria. Most (88%) were conducted in the United States. The majority employed educational strategies targeting intent to use hearing protection or self-reported use. Although educational approaches were generally effective, interventions that increased access to hearing protection were linked to higher self-reported use. Nearly half of the studies (n = 11) focused solely on individual-level outcomes. Conclusions Although most existing NIHL prevention efforts have focused on education, structural approaches appear more promising for sustainable impact.

Noise-induced hearing loss (NIHL), a common sensory disorder, is traditionally thought to stem primarily from direct damage to sound-sensing hair cells (HCs). Here, we demonstrate that supporting cells (SCs), neighboring cells not previously implicated in NIHL pathogenesis, orchestrate hearing loss and HC degeneration through Gasdermin D (GSDMD) activation. Mechanistically, noise-induced oxidative stress in HCs triggers activation of epidermal growth factor receptor in SCs, leading to extracellular-regulated kinase phosphorylation and caspase-11-dependent cleavage of GSDMD, thereby establishing an HC-to-SC signaling cascade. Furthermore, GSDMD activation in SCs reciprocally exacerbates oxidative injury in HCs, creating a pathogenic positive feedback loop between the two cell types. Our findings uncover a central role for SCs in noise-induced hearing loss and identify GSDMD-mediated intercellular communication as a potential therapeutic target.

This study was conducted to determine whether occupational exposure to high sound levels, typical of an opera orchestra, can cause hearing loss. The orchestra professors at Teatro alla Scala in Milan underwent ear examinations, pure-tone audiometry, and other audiological tests. The hearing thresholds of these musicians were compared with those of populations not exposed to occupational noise and with populations exposed to industrial noise. Noise exposure levels were estimated through a phonometric survey conducted at our theater in 2011, which largely confirmed the exposure levels outlined in European guidelines. The average audiometric thresholds of the orchestra musicians were slightly worse than the median thresholds of a healthy, non-noise-exposed population. In three subjects (2.8%), bilateral hearing impairment (PTA 0.5, 1, 2, 3, 4 kHz > 25 dB HL) was observed; in four violinists (3.7%) left unilateral hearing impairment was found. This rate is lower than the expected risk from similar industrial noise exposures. Comparing these audiometries with those from about ten years earlier shows that the hearing threshold decline in the study group is comparable to that caused by presbycusis. The risk of noise-induced hearing loss among professional orchestra musicians appears lower than predicted by the UNI ISO 1999:2015 standard. A few cases of hearing loss due to chronic acoustic trauma were noted, particularly among violinists who demonstrated a higher incidence of left unilateral hearing loss. The high levels of sound exposure and the presence of some hearing loss cases highlight the need for targeted preventative measures in this work activity.

To investigate diffusion changes suggestive of possible glymphatic alterations in patients with noise-induced hearing loss (NIHL), and to evaluate their relationships with free water (FW) and clinical characteristics. DTI scans were acquired from 48 NIHL patients and 40 healthy controls (HCs). The diffusion tensor imaging along perivascular spaces (DTI-ALPS) technique and FW diffusion model were used to calculate DTI-ALPS and FW values. Between-group differences were assessed using ANCOVA. Spearman correlation analysis was conducted between DTI-ALPS, FW, Hamilton Anxiety Scale (HAMA), and better-ear monaural threshold weighted value (MTWV). Compared with HCs, NIHL patients exhibited significantly reduced DTI-ALPS indices (mean: β = - 0.073, p = 0.008; left: β = - 0.081, p = 0.006; right: β = - 0.068, p = 0.026) and increased FW (β = 0.017, p = 0.019). Within the NIHL group, the left DTI-ALPS index was significantly lower than the right DTI-ALPS index (p < 0.001). Significant negative correlations were observed: mean DTI-ALPS with HAMA (r = - 0.406, p = 0.004) and FW (r = - 0.510, p < 0.001); left DTI-ALPS with HAMA (r = - 0.463, p < 0.001) and FW (r = - 0.459, p = 0.001); and right DTI-ALPS with FW (r = - 0.488, p < 0.001). All above results remained significant after FDR correction. Correlations of DTI-ALPS with MTWV (mean: r = - 0.311, p = 0.031; left: r = - 0.295, p = 0.042; right: r = - 0.287, p = 0.048) and right DTI-ALPS with HAMA (r = -0.308, p = 0.033) did not survive FDR correction. Patients with NIHL exhibited altered diffusion patterns suggestive of possible glymphatic alterations. These cross-sectional, correlational findings do not permit causal inferences. Longitudinal studies in larger and more diverse cohorts are needed for validation.

Noise-induced hearing loss (NIHL) is a major public health problem caused by damage to cochlear hair cells, synapses, and spiral ganglion neurons (SGNs). Since effective treatments are lacking, we investigated cellular stress responses induced by moderate and loud noise in a mouse model of cochlear synaptopathy. RNA sequencing and spatial transcriptomics revealed that noise exposure elicited a robust but transient upregulation of endoplasmic reticulum chaperones and proteasome subunits in SGNs and their supporting cells. To target this response, we administered TRC051384, a small-molecule activator of the heat shock transcription factor Hsf1, prior to noise exposure. TRC051384 crossed the blood–labyrinth barrier and reached the cochlea, induced heat shock protein gene expression, and restored ubiquitin–proteasome function in SGNs. Notably, TRC051384 treatment enhanced auditory brainstem response threshold recovery, preserved Wave I amplitudes, and maintained ribbon synapse density. These findings establish proteotoxic stress in SGNs as a key driver of NIHL and identify HSF1 activation as a promising therapeutic strategy.

Background: Noise-induced hearing loss (NIHL) stands as a significant health challenge that is both common and preventable. It calls for a profound understanding of exposure patterns, commitment to ear protection, and the influence of demographic factors. This cross-sectional study sets out to explore these elements among a varied group of participants. Methodology: A cross-sectional study engaged 252 individuals who provided demographic details and completed a structured questionnaire evaluating their noise exposure frequency, compliance with ear protection during various activities, and demographic variables. Data analysis utilized descriptive statistics, chi-square tests, and analysis of variance (ANOVA). Results: The demographic analysis revealed a notable representation of females 172 (68.3%) and diverse occupational backgrounds. Participants aged 20-30 years constituted the majority with 169 individuals (67.1%). Exposure frequency demonstrated variations across different scenarios, with a substantial percentage reporting never being exposed to loud noises. Adherence to ear protection varied, with low utilization reported in certain activities. The relationship between adherence and demographics indicate gender, age, marital status, and occupation-related differences. Conclusion: The study provides valuable insights into the demographic factors influencing noise exposure and adherence to ear protection. The observed patterns align with existing literature on NIHL, emphasizing the need for targeted interventions and educational campaigns to promote consistent hearing protection behaviors. Understanding demographic influences on hearing health is crucial for tailoring interventions and mitigating the risk of noise-induced hearing loss across diverse populations. The findings contribute to public health initiatives and workplace safety programs aimed at fostering a culture of proactive hearing health.

L-type calcium channel modulation reveals the relationship between neuronal synchrony and hyperactivity in the inferior colliculus following noise-induced hearing loss.

Background: Noise-induced hearing loss (NIHL) is one of the most common types of hearing impairment, even though it is preventable. However, awareness and protective behaviors among young adults remain limited. This study explored the knowledge, attitudes, and behaviors of young adults in Greece regarding exposure to high-noise environments and the risk of NIHL. Methods: A cross-sectional survey was conducted with 104 participants aged 18–30 years in Patras, Greece. A 27-item questionnaire was used to collect data on demographics, patterns of noise exposure, use of personal listening devices, auditory symptoms, and preventive behaviors. Descriptive statistics and chi-square tests were used to examine relationships between demographic variables and participants’ responses. Results: Most participants (93.3%) recognized that prolonged exposure to high noise levels can harm hearing. However, only 6.7% reported having regular hearing checks, and almost half (45.2%) had never been tested. Remarkably, 19.2% of participants experienced tinnitus, while more than half (54.8%) reported fatigue after exposure to loud sounds. Younger participants (aged 18–22 years) were significantly more likely to listen at high volumes compared to older groups (p < 0.05). Males reported higher rates of tinnitus and ear discomfort, whereas females more often experienced headaches. Although general awareness of NIHL was high, preventive behaviors such as using hearing protection were rarely practiced. Conclusions: These findings highlight the need for targeted educational campaigns and preventive screening programs to promote safe listening practices and reduce the overall prevalence of NIHL.

Emerging evidence in animal models and humans suggests that statins may provide partial protection against noise-induced and drug-induced hearing loss. However, evidence for protection against age-related hearing loss (ARHL) is mixed, and longitudinal studies in large adult cohorts from the general population are limited. This study examined the association between statin use and ARHL in a diverse, community-based longitudinal cohort of adults across the lifespan. The 1239 participants, aged ≥ 55 years, are from the MUSC Longitudinal Cohort Study of Age-Related Hearing Loss (1988-present). Following a comprehensive baseline examination, participants attended annual examinations during which audiometric and statin use data were collected. Multivariable linear regression models were performed on baseline data for cross-sectional analyses, and general linear mixed models were performed on longitudinal data to assess the association between statin use, two types of statins, and hearing over time. Hearing outcomes include four pure-tone averages (PTA): narrow (0.5, 1.0, 2.0, and 4.0 kHz), low frequency (0.25, 0.5, and 1.0 kHz), broad (0.5, 1.0, 2.0, 3.0, 4.0, 6.0, and 8.0 kHz), and high frequency (2.0, 3.0, 4.0, 6.0, and 8.0 kHz). Missing covariate data were imputed with multiple imputation using chain equations (MICE). Statin use (versus no use) was associated with better hearing at baseline for the broad and high-frequency PTAs for adults aged 55-64 and 65-74 years. However, this statin benefit was not observed for the 75+-year age group and for all participants when hearing was examined over time. Without age stratification, similar results were observed for atorvastatin use but not for simvastatin use. Overall, the findings suggest statin benefits for mid-to-high frequency hearing for middle-aged to older adults at early stages of ARHL. On the basis of evidence suggesting that some statins have beneficial effects on hearing, well-controlled clinical trials are needed to examine effects of statin use and statin types on ARHL in the general population.

Occupational noise induced hearing loss in orthopaedic theatre nurses: Exposing the silent threat and outlining interventions to prevent it.

The occupational deafness is one the most frequent diseases recognized in occupational medicine. This paper recalls how noxious the noise in working places can be; it describes how to measure it by the definition of the notion of decibel and the evaluation rules within the scope of labour laws. It draws attention to the principle of «globalization», which implies that the expert in charge of the evaluation takes into account the distinction between occupational deafness and other disorders such as age-related hearing loss or transmission defects in the hearing apparatus.

Insights into early cochlear damage induced by potassium channel deficiency.

Calpain2-mediated downregulation of apoptosis-inducing factors impairs mitochondrial function in noise-induced spiral ganglion neuron degeneration.