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British Journal of Hospital Medicine... Sep 2019Noise-induced hearing loss is sensory deafness caused by long-term exposure of the auditory system to a noisy environment. Auditory fatigue is an early symptom of... (Review)
Review
Noise-induced hearing loss is sensory deafness caused by long-term exposure of the auditory system to a noisy environment. Auditory fatigue is an early symptom of noise-induced hearing loss, and hearing can gradually recover after people leave a noisy environment. However, if people remain in a noisy environment for a prolonged period of time, their hearing will be permanently impaired. Societal changes mean that people are more likely to be exposed to noise. The hearing loss and tinnitus caused by noise seriously affect people's quality of life and lead to huge economic loss. The pathogenesis of noise-induced hearing loss is complex. Various theories try to explain this, such as the oxidative stress theory, but none perfectly explains the occurrence of noise-induced hearing loss. There is no treatment which can completely reverse the damage. More research is required to explore the pathogenesis and to better guide clinical practice. Preventative strategies, such as educating the public about hearing health, should be adopted to reduce the harm of noise-induced hearing loss.
Topics: Calcium; Cochlea; Health Education; Hearing Loss, Noise-Induced; Humans; Oxidative Stress; Potassium
PubMed: 31498679
DOI: 10.12968/hmed.2019.80.9.525 -
Neural Plasticity 2021Noise overexposure leads to hair cell loss, synaptic ribbon reduction, and auditory nerve deterioration, resulting in transient or permanent hearing loss depending on... (Review)
Review
Noise overexposure leads to hair cell loss, synaptic ribbon reduction, and auditory nerve deterioration, resulting in transient or permanent hearing loss depending on the exposure severity. Oxidative stress, inflammation, calcium overload, glutamate excitotoxicity, and energy metabolism disturbance are the main contributors to noise-induced hearing loss (NIHL) up to now. Gene variations are also identified as NIHL related. Glucocorticoid is the only approved medication for NIHL treatment. New pharmaceuticals targeting oxidative stress, inflammation, or noise-induced neuropathy are emerging, highlighted by the nanoparticle-based drug delivery system. Given the complexity of the pathogenesis behind NIHL, deeper and more comprehensive studies still need to be fulfilled.
Topics: Animals; Autophagy; Calcium; Clinical Trials, Phase II as Topic; DNA Repair; Drugs, Investigational; Energy Metabolism; Gap Junctions; Glutamic Acid; Hair Cells, Auditory; Hearing Loss, Noise-Induced; Humans; Inflammation; Isoindoles; Nanoparticles; Organoselenium Compounds; Oxidative Stress; Potassium Channels; Stereocilia
PubMed: 34306060
DOI: 10.1155/2021/4784385 -
Theranostics 2023Noise accounts for one-third of hearing loss worldwide. Regretfully, noise-induced hearing loss (NIHL) is deemed to be irreversible due to the elusive pathogenic... (Review)
Review
Noise accounts for one-third of hearing loss worldwide. Regretfully, noise-induced hearing loss (NIHL) is deemed to be irreversible due to the elusive pathogenic mechanisms that have not been fully elucidated. The complex interaction between genetic and environmental factors, which influences numerous downstream molecular and cellular events, contributes to the NIHL. In clinical settings, there are no effective therapeutic drugs other than steroids, which are the only treatment option for patients with NIHL. Therefore, the need for treatment of NIHL that is currently unmet, along with recent progress in our understanding of the underlying regulatory mechanisms, has led to a lot of new literatures focusing on this therapeutic field. The emergence of novel technologies that modify local drug delivery to the inner ear has led to the development of promising therapeutic approaches, which are currently under clinical investigation. In this comprehensive review, we focus on outlining and analyzing the basics and potential therapeutics of NIHL, as well as the application of biomaterials and nanomedicines in inner ear drug delivery. The objective of this review is to provide an incentive for NIHL's fundamental research and future clinical translation.
Topics: Humans; Hearing Loss, Noise-Induced; Ear, Inner; Drug Delivery Systems
PubMed: 37441605
DOI: 10.7150/thno.83383 -
Cell Reports Sep 2021Noise-induced hearing loss (NIHL) results from a complex interplay of damage to the sensory cells of the inner ear, dysfunction of its lateral wall, axonal retraction of...
Noise-induced hearing loss (NIHL) results from a complex interplay of damage to the sensory cells of the inner ear, dysfunction of its lateral wall, axonal retraction of type 1C spiral ganglion neurons, and activation of the immune response. We use RiboTag and single-cell RNA sequencing to survey the cell-type-specific molecular landscape of the mouse inner ear before and after noise trauma. We identify induction of the transcription factors STAT3 and IRF7 and immune-related genes across all cell-types. Yet, cell-type-specific transcriptomic changes dominate the response. The ATF3/ATF4 stress-response pathway is robustly induced in the type 1A noise-resilient neurons, potassium transport genes are downregulated in the lateral wall, mRNA metabolism genes are downregulated in outer hair cells, and deafness-associated genes are downregulated in most cell types. This transcriptomic resource is available via the Gene Expression Analysis Resource (gEAR; https://umgear.org/NIHL) and provides a blueprint for the rational development of drugs to prevent and treat NIHL.
Topics: Animals; Cochlea; Ear, Inner; Evoked Potentials, Auditory, Brain Stem; Hair Cells, Auditory; Hearing Loss, Noise-Induced; Mice; Neurons; Noise; Spiral Ganglion
PubMed: 34592158
DOI: 10.1016/j.celrep.2021.109758 -
Environmental Health and Preventive... Oct 2020Occupational noise-induced hearing loss (ONIHL) is the most prevalent occupational disease in the world. The goal of this study was to review the epidemiology,... (Review)
Review
Occupational noise-induced hearing loss (ONIHL) is the most prevalent occupational disease in the world. The goal of this study was to review the epidemiology, pathogenesis, and preventive measures of ONIHL among workers and provide evidence for the implementation of control measures. Literature studies were identified from the MEDLINE, PubMed, Embase, Web of Science, and Google Scholar using the search terms "noise-induced hearing loss" "prevalence", "pathogenesis", and "preventive measures". The articles reviewed in this report were limited from 2000 to 2020. Articles that were not published in the English language, manuscripts without an abstract, and opinion articles were excluded. After a preliminary screening, all of the articles were reviewed and synthesized to provide an overview of the current status of ONIHL among workers. The mechanism of ONIHL among workers is a complex interaction between environmental and host factors (both genetic and acquired factors). The outcomes of noise exposure are different among individual subjects. Clinical trials are currently underway to evaluate the treatment effect of antioxidants on ONIHL. Noise exposure may contribute to temporary or permanent threshold shifts; however, even temporary threshold shifts may predispose an individual to eventual permanent hearing loss. Noise prevention programs are an important preventive measure in reducing the morbidity of ONIHL among workers.
Topics: Adult; Aged; Female; Hearing Loss, Noise-Induced; Humans; Male; Middle Aged; Noise; Occupational Diseases; Prevalence; Young Adult
PubMed: 33129267
DOI: 10.1186/s12199-020-00906-0 -
The Journal of Neuroscience : the... Mar 2023Resident cochlear macrophages rapidly migrate into the inner hair cell synaptic region and directly contact the damaged synaptic connections after noise-induced...
Resident cochlear macrophages rapidly migrate into the inner hair cell synaptic region and directly contact the damaged synaptic connections after noise-induced synaptopathy. Eventually, such damaged synapses are spontaneously repaired, but the precise role of macrophages in synaptic degeneration and repair remains unknown. To address this, cochlear macrophages were eliminated using colony stimulating factor 1 receptor (CSF1R) inhibitor, PLX5622. Sustained treatment with PLX5622 in mice of both sexes led to robust elimination of resident macrophages (∼94%) without significant adverse effects on peripheral leukocytes, cochlear function, and structure. At 1 day (d) post noise exposure of 93 or 90 dB SPL for 2 hours, the degree of hearing loss and synapse loss were comparable in the presence and absence of macrophages. At 30 d after exposure, damaged synapses appeared repaired in the presence of macrophages. However, in the absence of macrophages, such synaptic repair was significantly reduced. Remarkably, on cessation of PLX5622 treatment, macrophages repopulated the cochlea, leading to enhanced synaptic repair. Elevated auditory brainstem response thresholds and reduced auditory brainstem response Peak 1 amplitudes showed limited recovery in the absence of macrophages but recovered similarly with resident and repopulated macrophages. Cochlear neuron loss was augmented in the absence of macrophages but showed preservation with resident and repopulated macrophages after noise exposure. While the central auditory effects of PLX5622 treatment and microglia depletion remain to be investigated, these data demonstrate that macrophages do not affect synaptic degeneration but are necessary and sufficient to restore cochlear synapses and function after noise-induced synaptopathy. The synaptic connections between cochlear inner hair cells and spiral ganglion neurons can be lost because of noise over exposure or biological aging. This loss may represent the most common causes of sensorineural hearing loss also known as hidden hearing loss. Synaptic loss results in degradation of auditory information, leading to difficulty in listening in noisy environments and other auditory perceptual disorders. We demonstrate that resident macrophages of the cochlea are necessary and sufficient to restore synapses and function following synaptopathic noise exposure. Our work reveals a novel role for innate-immune cells, such as macrophages in synaptic repair, that could be harnessed to regenerate lost ribbon synapses in noise- or age-linked cochlear synaptopathy, hidden hearing loss, and associated perceptual anomalies.
Topics: Male; Female; Animals; Mice; Hair Cells, Auditory, Inner; Hearing Loss, Noise-Induced; Acoustic Stimulation; Auditory Threshold; Cochlea; Synapses; Evoked Potentials, Auditory, Brain Stem; Macrophages
PubMed: 36810227
DOI: 10.1523/JNEUROSCI.1273-22.2023 -
Scientific Reports Nov 2023Acoustic overexposure can eliminate synapses between inner hair cells (IHCs) and auditory nerve fibers (ANFs), even if hair-cell function recovers. This synaptopathy has...
Acoustic overexposure can eliminate synapses between inner hair cells (IHCs) and auditory nerve fibers (ANFs), even if hair-cell function recovers. This synaptopathy has been extensively studied by confocal microscopy, however, understanding the nature and sequence of damage requires ultrastructural analysis. Here, we used focused ion-beam scanning electron microscopy to mill, image, segment and reconstruct ANF terminals in mice, 1 day and 1 week after synaptopathic exposure (8-16 kHz, 98 dB SPL). At both survivals, ANF terminals were normal in number, but 62% and 53%, respectively, lacked normal synaptic specializations. Most non-synapsing fibers (57% and 48% at 1 day and 1 week) remained in contact with an IHC and contained healthy-looking organelles. ANFs showed a transient increase in mitochondrial content (51%) and efferent innervation (34%) at 1 day. Fibers maintaining synaptic connections showed hypertrophy of pre-synaptic ribbons at both 1 day and 1 week. Non-synaptic fibers were lower in mitochondrial content and typically on the modiolar side of the IHC, where ANFs with high-thresholds and low spontaneous rates are normally found. Even 1 week post-exposure, many ANF terminals remained in IHC contact despite loss of synaptic specializations, thus, regeneration efforts at early post-exposure times should concentrate on synaptogenesis rather than neurite extension.
Topics: Mice; Animals; Cochlea; Noise; Hearing Loss, Noise-Induced; Hair Cells, Auditory; Hair Cells, Auditory, Inner; Synapses; Cochlear Nerve; Auditory Threshold
PubMed: 37945811
DOI: 10.1038/s41598-023-46859-6 -
International Journal of Environmental... Jul 2020Pollutants that contaminate the natural or built environment adversely affect the health of living organisms. Although exposure to many of them could be avoided or...
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.
Topics: Animals; Environmental Exposure; Environmental Pollutants; Hearing Loss, Noise-Induced; Humans; Noise; Occupational Exposure
PubMed: 32645823
DOI: 10.3390/ijerph17134879 -
Indian Journal of Otolaryngology and... Dec 2022Noise in human societies is unavoidable, but it tends to become a modern epidemic that induces various detrimental effects to several organs and functions in humans....
Noise in human societies is unavoidable, but it tends to become a modern epidemic that induces various detrimental effects to several organs and functions in humans. Increased cardiovascular danger, anxiety and sleep disturbance are just few of these effects. It is noteworthy that children, even neonates and their developing organism are especially vulnerable to noise-related health problems. Noise is measured with special noise-meters. These devices express results in decibels by transforming random noise to a continuous sound. This sound is characterized by equivalent acoustic energy to the random noise for a defined time interval. Human auditory apparatus is principally endangered by acute noises but also by chronic noise exposure, in the context of both occupational and recreational activities. Various mechanisms are implicated in the pathogenesis of noise-induced hearing loss that can cause either temporary or permanent damage. Among them, emphasis is given to the impairment by free radicals and inflammatory mediators, to the activation of apoptotic molecular pathways, but also to glutamate excitotoxicity. A hidden hearing loss, synaptopathy, is attributed to the latter. The irreversible nature of hearing loss, as well as the idiosyncratic sensitivity of individuals, imposes the necessity of early diagnosis of auditory impairment by noise. Super high frequency audiograms, otoacoustic emissions and electrophysiological examinations can address diagnosis. Thankfully, there is extensive research on acoustic trauma therapeutic approaches. However, until we succeed in regenerating the sensory organ of hearing, chronic noise-induced hearing loss cannot be treated. Thus, it is fundamental that society protects people from noise, by laws and regulations.
PubMed: 36742745
DOI: 10.1007/s12070-021-02797-1 -
International Journal of Environmental... Feb 2022The best protectors are those that are worn (Aram Glorig) [...].
The best protectors are those that are worn (Aram Glorig) [...].
Topics: Ear Protective Devices; Hearing; Hearing Loss, Noise-Induced; Humans
PubMed: 35206353
DOI: 10.3390/ijerph19042165