Search Results (12)

Background: Recreational noise exposure from personal listening devices (PLDs) may lead to hidden hearing loss (HHL), affecting auditory nerve function despite normal pure-tone audiometry (PTA) and otoacoustic emissions (OAE). Subclinical auditory damage at the synaptic level often goes undetected by conventional assessments, emphasizing the need for more sensitive measures. Recorded click ABR in the presence of various levels of ipsilateral maskers for the better identification of auditory damage at the synaptic level. These results could help to develop a better objective diagnostic tool that can detect hidden hearing loss. Objective: To examine the effects of PLD usage on extended high-frequency audiometric thresholds and on click-evoked auditory brainstem responses (ABR) with and without ipsilateral masking in individuals with normal hearing. Materials and Methods: Thirty-five young adults aged 18–35 years (18 PLD users, 17 controls) with clinically normal hearing were recruited. Extended high-frequency audiometry (EHFA) was conducted from 9 to 16 kHz. Click-evoked ABRs were recorded at 80 dB nHL under unmasked and ipsilateral broadband noise-masked conditions at 50, 60, and 70 dB SPL. ABR analyses included absolute and relative amplitude (V/I) and latencies of waves I, III, and V. Results: PLD users demonstrated significantly elevated extended high-frequency thresholds compared to controls. ABR analyses revealed reduced Wave I amplitudes across stimulus conditions in PLD users, while Wave V amplitudes were largely preserved, resulting in consistently higher V/I amplitude ratios under masked conditions. No group differences were observed for Wave III amplitudes or absolute/interpeak latencies, except for a modest prolongation of I–III latency at one masker level in PLD users. Conclusions: Conventional audiological tests may not detect early auditory damage; however, extended high-frequency audiometry and ABR with ipsilateral masking demonstrate greater sensitivity in identifying noise-induced functional changes within the auditory brainstem pathways. Full article

Hearing loss remains a significant but underexplored health challenge in individuals with HIV/AIDS, particularly those exposed to occupational noise. The ototoxic effects of antiretroviral therapy (ART) and comorbid conditions like tuberculosis (TB) further compound the risk. This narrative review examines the intersection of HIV/AIDS, ART, and occupational noise-induced hearing loss (ONIHL), emphasizing the South African and broader African contexts. The aim of the study was to map the existing literature on the association between HIV/AIDS, its treatments, and ONIHL, and to identify research gaps to inform policy and clinical practice. A narrative review approach was adopted, systematically searching databases including PubMed, Scopus, and Web of Science. Studies published between 2000 and 2024 were included, focusing on the effects of HIV/AIDS, ART, and occupational noise exposure on hearing health. Data extraction and thematic synthesis were performed to identify key findings and gaps. Twenty studies were included, covering diverse settings such as South Africa, Cameroon, Tanzania, and the USA. Three key themes emerged: (1) dual burden of HIV and occupational noise exposure: HIV-positive individuals in noise-intensive industries, such as mining, face amplified risks of hearing loss due to immunological compromise and ototoxic TB treatments; (2) ototoxicity of ART: older ART regimens, widely used in resource-limited settings, are associated with a higher prevalence of sensorineural hearing loss (SNHL); and (3) immunological susceptibility to ONIHL: HIV-related immune suppression exacerbates cochlear damage from noise and ototoxic agents, contributing to both peripheral and central auditory dysfunction. This review highlights the urgent need for integrated hearing health interventions in HIV care and occupational health frameworks, particularly in high-prevalence regions like South Africa. Routine audiological assessments, access to safer ART regimens, and enhanced workplace protections are essential to mitigate the dual burden of HIV/AIDS and ONIHL. Future research should prioritize longitudinal studies and innovative, low-cost solutions for resource-limited settings. Full article

Endogenous glucocorticoids (GC) are known to modulate basic elements of cochlear physiology. These include both noise-induced injury and circadian rhythms. While GC signaling in the cochlea can directly influence auditory transduction via actions on hair cells and spiral ganglion neurons, evidence also indicates that GC signaling exerts effects via tissue homeostatic processes that can include effects on cochlear immunomodulation. GCs act at both the glucocorticoid receptor (GR) and the mineralocorticoid receptor (MR). Most cell types in the cochlea express both receptors sensitive to GCs. The GR is associated with acquired sensorineural hearing loss (SNHL) through its effects on both gene expression and immunomodulatory programs. The MR has been associated with age-related hearing loss through dysfunction of ionic homeostatic balance. Cochlear supporting cells maintain local homeostatic requirements, are sensitive to perturbation, and participate in inflammatory signaling. Here, we have used conditional gene manipulation techniques to target Nr3c1 (GR) or Nr3c2 (MR) for tamoxifen-induced gene ablation in Sox9-expressing cochlear supporting cells of adult mice to investigate whether either of the receptors sensitive to GCs plays a role in protecting against (or exacerbating) noise-induced cochlear damage. We have selected mild intensity noise exposure to examine the role of these receptors related to more commonly experienced noise levels. Our results reveal distinct roles of these GC receptors for both basal auditory thresholds prior to noise exposure and during recovery from mild noise exposure. Prior to noise exposure, auditory brainstem responses (ABRs) were measured in mice carrying the floxed allele of interest and the Cre recombinase transgene, but not receiving tamoxifen injections (defined as control (no tamoxifen treatment), versus conditional knockout (cKO) mice, defined as mice having received tamoxifen injections. Results revealed hypersensitive thresholds to mid- to low-frequencies after tamoxifen-induced GR ablation from Sox9-expressing cochlear supporting cells compared to control (no tamoxifen) mice. GR ablation from Sox9-expressing cochlear supporting cells resulted in a permanent threshold shift in mid-basal cochlear frequency regions after mild noise exposure that produced only a temporary threshold shift in both control (no tamoxifen) f/fGR:Sox9iCre⁺ and heterozygous f/+GR:Sox9iCre⁺ tamoxifen-treated mice. A similar comparison of basal ABRs measured in control (no tamoxifen) and tamoxifen-treated, floxed MR mice prior to noise exposure indicated no difference in baseline thresholds. After mild noise exposure, MR ablation was initially associated with a complete threshold recovery at 22.6 kHz by 3 days post-noise. Threshold continued to shift to higher sensitivity over time such that by 30 days post-noise exposure the 22.6 kHz ABR threshold was 10 dB more sensitive than baseline. Further, MR ablation produced a temporary reduction in peak 1 neural amplitude one day post-noise. While supporting cell GR ablation trended towards reducing numbers of ribbon synapses, MR ablation reduced ribbon synapse counts but did not exacerbate noise-induced damage including synapse loss at the experimental endpoint. GR ablation from the targeted supporting cells increased the basal resting number of Iba1-positive (innate) immune cells (no noise exposure) and decreased the number of Iba1-positive cells seven days following noise exposure. MR ablation did not alter innate immune cell numbers at seven days post-noise exposure. Taken together, these findings support differential roles of cochlear supporting cell MR and GR expression at basal, resting conditions and especially during recovery from noise exposure. Full article

Hyper-reactivity to sensory inputs is a common and debilitating symptom of autism spectrum disorder (ASD), but the underlying neural abnormalities remain unclear. Two of three patients in our clinical cohort screen harboring de novo SHANK2 mutations also exhibited high sensitivity to visual, auditory, and tactile stimuli, so we examined whether shank2 deficiencies contribute to sensory abnormalities and other ASD-like phenotypes by generating a stable shank2b-deficient zebrafish model (shank2b^−/−). The adult shank2b^−/− zebrafish demonstrated reduced social preference and kin preference as well as enhanced behavioral stereotypy, while larvae exhibited hyper-sensitivity to auditory noise and abnormal hyperactivity during dark-to-light transitions. This model thus recapitulated the core developmental and behavioral phenotypes of many previous genetic ASD models. Expression levels of γ-aminobutyric acid (GABA) receptor subunit mRNAs and proteins were also reduced in shank2b^−/− zebrafish, and these animals exhibited greater sensitivity to drug-induced seizures. Our results suggest that GABAergic dysfunction is a major contributor to the sensory hyper-reactivity in ASD, and they underscore the need for interventions that target sensory-processing disruptions during early neural development to prevent disease progression. Full article

Nitrative stress is increasingly recognized as a critical mediator of apoptotic cell death in many pathological conditions. The accumulation of nitric oxide along with superoxide radicals leads to the generation of peroxynitrite that can eventually result in the nitration of susceptible proteins. Nitrotyrosine is widely used as a biomarker of nitrative stress and indicates oxidative damage to proteins. Ototoxic insults, such as exposure to noise and ototoxic drugs, enhance the generation of 3-nitrotyrosine in different cell types in the cochlea. Nitrated proteins can disrupt critical signaling pathways and eventually lead to apoptosis and loss of sensory receptor cells in the cochlea. Accumulating evidence shows that selective targeting of nitrative stress attenuates cellular damage. Anti-nitrative compounds, such as peroxynitrite decomposition catalysts and inducible nitric oxide synthase inhibitors, prevent nitrative stress-mediated auditory damage. However, the role of nitrative stress in acquired hearing loss and its potential significance as a promising interventional target is yet to be fully characterized. This review provides an overview of nitrative stress mechanisms, the induction of nitrative stress in the auditory tissue after ototoxic insults, and the therapeutic value of targeting nitrative stress for mitigating auditory dysfunction. Full article

Recent studies demonstrated that reversible continuous noise exposure may induce a temporary threshold shift (TTS) with a permanent degeneration of auditory nerve fibers, although hair cells remain intact. To probe the impact of TTS-inducing impulse noise exposure on hearing, CBA/J Mice were exposed to noise impulses with peak pressures of 145 dB SPL. We found that 30 min after exposure, the noise caused a mean elevation of ABR thresholds of ~30 dB and a reduction in DPOAE amplitude. Four weeks later, ABR thresholds and DPOAE amplitude were back to normal in the higher frequency region (8–32 kHz). At lower frequencies, a small degree of PTS remained. Morphological evaluations revealed a disturbance of the stereociliary bundle of outer hair cells, mainly located in the apical regions. On the other hand, the reduced suprathreshold ABR amplitudes remained until 4 weeks later. A loss of synapse numbers was observed 24 h after exposure, with full recovery two weeks later. Transmission electron microscopy revealed morphological changes at the ribbon synapses by two weeks post exposure. In addition, increased levels of oxidative stress were observed immediately after exposure, and maintained for a further 2 weeks. These results clarify the pathology underlying impulse noise-induced sensory dysfunction, and suggest possible links between impulse-noise injury, cochlear cell morphology, metabolic changes, and hidden hearing loss. Full article

The high level noise caused by intense acoustic weapons and blasting is a common source of acute acoustic trauma faced by some special environmental personnel. Studies have shown that high level noise can cause auditory and non-auditory effects. However, there are few reports on the biological effects, especially the non-auditory effects of acute high level noise exposure in simulated special working environments, and the great differences between experimental animals and human beings make it difficult to extrapolate from research conclusions. In this study, macaque monkeys were used to detect the effects of acute high level noise exposure on hearing, cognition, and cardiovascular function. Auditory brainstem response, auditory P300, and electrocardiogram (ECG) of macaque monkeys were measured. Results showed that acute high level noise exposure caused permanent hearing threshold shifts; partial hearing loss which couldn’t recover to normal levels in the detection period; pathological changes in T wave and QRS complexes; and large fluctuations in cognitive ability after exposure, which finally recovered to normal. These alterations may be a combination of effects caused by stress-induced neuroendocrine dysfunction and mechanical damage of auditory organs. To elaborate the exact mechanism, further studies are still needed. Meanwhile, positive measures should be taken to reduce the incidence of acute high level noise injury. Full article

Pollutants that contaminate the natural or built environment adversely affect the health of living organisms. Although exposure to many of them could be avoided or minimized by careful preventive measures, it is impossible to totally avoid exposure to all pollutants. Ototraumatic agents, such as noise, chemicals, and heavy metals, are pervasive pollutants, mostly produced by human activity, and are critical factors in inducing acquired hearing loss. More importantly, exposure to these pollutants often occurs concurrently and, therefore, the synergistic interactions potentiate auditory dysfunction in susceptible individuals. Epidemiological studies have provided compelling data on the incidence of auditory dysfunction after exposure to a number of ototraumatic agents in the environment, while animal studies have offered crucial insights for understanding the underlying molecular mechanisms. Together, they provide a framework for developing effective interventional approaches for mitigating the adverse impacts of environmental or occupational exposure to ototraumatic agents. This article provides a brief overview of the common pollutants that cause hearing loss. Full article

Firefighters are susceptible to auditory dysfunction due to long-term exposure to noise from sirens, air horns, equipment, and tools used in forcible entry, ventilation, and extrication. In addition, they are exposed to ototoxic chemicals, particularly, during overhaul operations. Studies indicate that 40% of firefighters have hearing loss in the noise-sensitive frequencies of 4 and 6 kHz. Noise-induced hearing loss (NIHL) is often accompanied by tinnitus, which is characterized by ringing noise in the ears. The presence of phantom sounds can adversely affect the performance of firefighters. However, there has been limited research conducted on the prevalence of tinnitus in firefighters. We enrolled firefighters from Michigan, with at least 5 years of continuous service. The hearing handicap inventory for adults (HHIA) was used to determine the difficulty in hearing perceived by the firefighters and the tinnitus functional index (TFI) was used to determine the severity of tinnitus. Self-perceived hearing handicap was reported by 36% of the participants, while tinnitus was reported by 48% of the participants. The TFI survey indicated that 31% perceived tinnitus as a problem. More importantly, self-perceived hearing handicap was significantly associated with the incidence of tinnitus in firefighters, suggesting a potential link between occupational exposure to ototraumatic agents and tinnitus in firefighters. Full article

Mitochondrial dysfunction is associated with the etiologies of sensorineural hearing loss, such as age-related hearing loss, noise- and ototoxic drug-induced hearing loss, as well as hearing loss due to mitochondrial gene mutation. Mitochondria are the main sources of reactive oxygen species (ROS) and ROS-induced oxidative stress is involved in cochlear damage. Moreover, the release of ROS causes further damage to mitochondrial components. Antioxidants are thought to counteract the deleterious effects of ROS and thus, may be effective for the treatment of oxidative stress-related diseases. The administration of mitochondria-targeted antioxidants is one of the drug delivery systems targeted to mitochondria. Mitochondria-targeted antioxidants are expected to help in the prevention and/or treatment of diseases associated with mitochondrial dysfunction. Of the various mitochondria-targeted antioxidants, the protective effects of MitoQ and SkQR1 against ototoxicity have been previously evaluated in animal models and/or mouse auditory cell lines. MitoQ protects against both gentamicin- and cisplatin-induced ototoxicity. SkQR1 also provides auditory protective effects against gentamicin-induced ototoxicity. On the other hand, decreasing effect of MitoQ on gentamicin-induced cell apoptosis in auditory cell lines has been controversial. No clinical studies have been reported for otoprotection using mitochondrial-targeted antioxidants. High-quality clinical trials are required to reveal the therapeutic effect of mitochondria-targeted antioxidants in terms of otoprotection in patients. Full article

Autophagy is a natural catabolic process of the cell that dismantles the useless or dysfunctional components. Autophagy allows the systematic and the lysosomal-mediated deterioration of cellular organelles. During the embryonic development, autophagy plays a critical role by remodeling the tissue and organs of the body, and the deletion of some of the autophagy related genes results in the defective embryonic development. Inner ear is the most sophisticated organ of the body responsible for the sound perception. In mammalian inner ear, autophagy protects the hair cells (HCs) from drug and noise induced damage. In this review, we particularly discuss how autophagy implicates during the auditory system development in mammals and presents its role in age-related hearing loss. Moreover, we discuss the protecting effects of autophagy after noise and drug induced auditory trauma. Full article

Exposure to some chemicals in the workplace can lead to occupational chemical-induced hearing loss. Attention has mainly focused on the adverse auditory effects of solvents. However, other chemicals such as heavy metals have been also identified as ototoxic agents. The aim of this work was to review the current scientific knowledge about the adverse auditory effects of heavy metal exposure with and without co-exposure to noise in humans. PubMed and Medline were accessed to find suitable articles. A total of 49 articles met the inclusion criteria. Results from the review showed that no evidence about the ototoxic effects in humans of manganese is available. Contradictory results have been found for arsenic, lead and mercury as well as for the possible interaction between heavy metals and noise. All studies found in this review have found that exposure to cadmium and mixtures of heavy metals induce auditory dysfunction. Most of the studies investigating the adverse auditory effects of heavy metals in humans have investigated human populations exposed to lead. Some of these studies suggest peripheral and central auditory dysfunction induced by lead exposure. It is concluded that further evidence from human studies about the adverse auditory effects of heavy metal exposure is still required. Despite this issue, audiologists and other hearing health care professionals should be aware of the possible auditory effects of heavy metals. Full article