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International Journal of Environmental... Sep 2022Noise-induced hearing loss (NIHL) is the most prevalent occupational disease in the world and firefighters are at increased risk of NIHL due to their frequent exposure...
Noise-induced hearing loss (NIHL) is the most prevalent occupational disease in the world and firefighters are at increased risk of NIHL due to their frequent exposure to hazardous levels of noise during service. Adverse effects of NIHL include acceleration of age-related hearing loss and an increased risk of cognitive decline. A critical challenge in addressing NIHL is the delayed clinical presentation of symptoms and lack of sensitive tools for early detection. To study the early clinical symptoms of NIHL in this high-risk group, we collected hearing function data including behavioral audiometric thresholds and distortion product otoacoustic emissions (DPOAEs) in 176 firefighters during annual physical assessments. Results revealed significant deficits in cochlear outer hair cell function in the presence of normal audiograms. Additionally, 55% of firefighters self-reported changes in hearing, while 20% self-reported concerns about their balance. This study is the first to characterize DPOAEs in firefighters who display decreased DPOAE amplitudes with increasing years in the fire service. These effects were observed even when controlling for hearing loss and age and are suggestive of a link between hearing loss and occupational exposure to hazardous noise.
Topics: Firefighters; Hearing; Hearing Loss, Noise-Induced; Humans; Noise; Otoacoustic Emissions, Spontaneous
PubMed: 36078744
DOI: 10.3390/ijerph191711028 -
The Journal of the College of General... Mar 1964
Topics: Aging; Arteriosclerosis; Diuretics; Ethinyl Estradiol; Folic Acid; Geriatrics; Hearing Disorders; Hearing Loss, Noise-Induced; Humans; Hypertension; Methyltestosterone; Presbycusis; Smoking; Vasodilator Agents; Vitamin B Complex
PubMed: 14129699
DOI: No ID Found -
Revista Da Associacao Medica Brasileira... Sep 2022Noise-induced hearing loss is a preventable form of hearing loss that has serious social and economic impacts. This study aimed to investigate the protective effect of...
OBJECTIVE
Noise-induced hearing loss is a preventable form of hearing loss that has serious social and economic impacts. This study aimed to investigate the protective effect of berberine, a potent antioxidant and anti-inflammatory agent, against Noise-induced hearing loss.
METHODS
After applying distortion product otoacoustic emission, 28 female Sprague-Dawley rats were randomly divided into four groups. Group 1 was designated as acoustic trauma group, and rats in this group were exposed to white noise for 12 h at an intensity of 4 kHz 110 dB sound pressure level. Group 2 was the control group. Group 3 was designated as the berberine group, and 100 mg/kg of berberine was administered to rats in this group by intragastric lavage for five consecutive days. Group 4 was designated as the acoustic trauma+berberine group. distortion product otoacoustic emission was repeated on the 6th day of the study and cochlear tissues of rats were dissected for histopathological and immunohistochemical analyses after sacrificing rats.
RESULTS
The distortion product otoacoustic emission results showed a significant decrease in signal-noise ratio values at higher frequencies in rats of the trauma group compared to those in other groups. Acoustic trauma caused severe histopathological impairment at cochlear structures together with severe 8-hydroxy-2-deoxyguanosine expression. Rats in the acoustic trauma+berberine group showed mild histopathological changes with mild 8-hydroxy-2-deoxyguanosine expression and better signal-noise ratio values.
CONCLUSION
The histopathological and audiological findings of this experimental study showed that berberine provides protection in Noise-induced hearing loss and may have the potential for use in acoustic trauma-related hearing losses.
Topics: Animals; Antioxidants; Auditory Threshold; Berberine; Deoxyguanosine; Female; Hearing Loss, Noise-Induced; Otoacoustic Emissions, Spontaneous; Rats; Rats, Sprague-Dawley
PubMed: 36228267
DOI: 10.1590/1806-9282.20220758 -
ENeuro 2021Auditory stimuli travel from the cochlea to the brainstem through type I and type II cochlear afferents. While type I afferents convey information about the frequency,...
Auditory stimuli travel from the cochlea to the brainstem through type I and type II cochlear afferents. While type I afferents convey information about the frequency, intensity, and timing of sounds, the role of type II afferents remains unresolved. Limited recordings of type II afferents from cochlear apex of prehearing rats reveal they are activated by widespread outer hair cell stimulation, ATP, and by the rupture of nearby outer hair cells. Altogether, these lines of evidence suggest that type II afferents sense loud, potentially damaging levels of sound. To explore this hypothesis further, calcium imaging was used to determine the impact of acoustic trauma on the activity of type II cochlear afferents of young adult mice of both sexes. Two known marker genes (, ) and one new marker gene (), expressed in type II afferents and some other cochlear cell types, drove GCaMP6f expression to reveal calcium transients in response to focal damage in the organ of Corti in all turns of the cochlea. Mature type II afferents responded to acute photoablation damage less often but at greater length compared with prehearing neurons. In addition, days after acoustic trauma, acute photoablation triggered a novel response pattern in type II afferents and surrounding epithelial cells, delayed bursts of activity occurring minutes after the initial response subsided. Overall, calcium imaging can report type II afferent responses to damage even in mature and noise-exposed animals and reveals previously unknown tissue hyperactivity subsequent to acoustic trauma.
Topics: Acoustic Stimulation; Animals; Cochlea; Female; Hair Cells, Auditory, Outer; Hearing Loss, Noise-Induced; Male; Mice; Neurons; Noise; Rats
PubMed: 34607806
DOI: 10.1523/ENEURO.0383-21.2021 -
European Archives of... Jul 2019Acute hearing loss can have a major impact on a patient's life. This holds true for both acute acoustic trauma (AAT) and idiopathic sudden sensorineural hearing loss... (Review)
Review
INTRODUCTION
Acute hearing loss can have a major impact on a patient's life. This holds true for both acute acoustic trauma (AAT) and idiopathic sudden sensorineural hearing loss (ISSHL), two devastating conditions for which no highly effective treatment options exist. This narrative review provides the rationale and evidence for HBOT in AAT and ISSHL.
METHODS
Narrative review of all the literature available on HBOT in acute hearing loss, studies were retrieved from systematic searches on PubMed and by cross referencing.
DISCUSSION
First, the etiological mechanisms of acute hearing loss and the mechanism of action of HBOT were discussed. Furthermore, we have provided an overview of 68 studies that clinically investigated the effect of HBOT in the last couple of decades. For future studies, it is recommend to start as early as possible with therapy, preferably within 48 h and to use combination therapy consisting of HBOT and corticosteroids.
IMPLICATIONS FOR PRACTICE
HBOT has been used quite extensively for acute hearing loss in the last couple of decades. Based on the amount of studies showing a positive effect, HBOT should be discussed with patients (shared decision making) as optional therapy in case of AAT and ISSHL.
Topics: Hearing Loss, Noise-Induced; Hearing Loss, Sudden; Humans; Hyperbaric Oxygenation; Treatment Outcome
PubMed: 31111252
DOI: 10.1007/s00405-019-05469-7 -
Hearing Research Jun 2017
Review
Topics: Acoustics; Auditory Pathways; Auditory Perception; Environmental Monitoring; Hearing; Hearing Loss, Noise-Induced; Humans; Noise, Occupational; Occupational Diseases; Occupational Exposure; Risk Assessment; Risk Factors; Tinnitus
PubMed: 27989948
DOI: 10.1016/j.heares.2016.10.020 -
International Journal of Occupational... Jan 2018The article shows 2 cases of unusual presentation of acute acoustic trauma and blast injury due to occupational exposure. In the case of both patients the range of...
The article shows 2 cases of unusual presentation of acute acoustic trauma and blast injury due to occupational exposure. In the case of both patients the range of impaired frequencies in pure tone audiograms was atypical for this kind of causative factor. Both patients had symmetrical hearing before the accident (which was confirmed by provided results of hearing controls during their employment). A history of noise/blast exposure, the onset of symptoms directly after harmful exposure, symmetrical hearing before the trauma documented with audiograms, directed initial diagnosis towards acoustic/blast trauma, however, of atypical course. Acute acoustic and blast trauma and coexisting acoustic neuroma (AN) contributed to, and mutually modified, the course of sudden hearing loss. In the literature there are some reports pointing to a higher sensitivity to acoustic trauma in the case of patients with AN and, on the other hand, indicating noise as one of the causative factors in AN. Int J Occup Med Environ Health 2018;31(3):361-369.
Topics: Adult; Audiometry; Explosions; Female; Hearing Loss, Noise-Induced; Hearing Loss, Sudden; Humans; Male; Middle Aged; Neuroma, Acoustic; Noise, Occupational; Occupational Exposure
PubMed: 29184217
DOI: 10.13075/ijomeh.1896.01156 -
International Journal of Molecular... Oct 2019Noise exposure affects the organ of Corti and the lateral wall of the cochlea, including the stria vascularis and spiral ligament. Although the inner ear vasculature and...
Noise exposure affects the organ of Corti and the lateral wall of the cochlea, including the stria vascularis and spiral ligament. Although the inner ear vasculature and spiral ligament fibrocytes in the lateral wall consist of a significant proportion of cells in the cochlea, relatively little is known regarding their functional significance. In this study, 6-week-old male C57BL/6 mice were exposed to noise trauma to induce transient hearing threshold shift (TTS) or permanent hearing threshold shift (PTS). Compared to mice with TTS, mice with PTS exhibited lower cochlear blood flow and lower vessel diameter in the stria vascularis, accompanied by reduced expression levels of genes involved in vasodilation and increased expression levels of genes related to vasoconstriction. Ultrastructural analyses by transmission electron microscopy revealed that the stria vascularis and spiral ligament fibrocytes were more damaged by PTS than by TTS. Moreover, mice with PTS expressed significantly higher levels of proinflammatory cytokines in the cochlea (e.g., IL-1β, IL-6, and TNF-α). Overall, our findings suggest that cochlear microcirculation and lateral wall pathologies are differentially modulated by the severity of acoustic trauma and are associated with changes in vasoactive factors and inflammatory responses in the cochlea.
Topics: Animals; Blood Flow Velocity; Cochlea; Cytokines; Disease Models, Animal; Hearing Loss, Noise-Induced; Male; Mice; Wounds and Injuries
PubMed: 31731459
DOI: 10.3390/ijms20215316 -
Hearing Research Jun 2017For decades, we have presumed the death of hair cells and spiral ganglion neurons are the main cause of hearing loss and difficulties understanding speech in noise, but... (Review)
Review
For decades, we have presumed the death of hair cells and spiral ganglion neurons are the main cause of hearing loss and difficulties understanding speech in noise, but new findings suggest synapse loss may be the key contributor. Specifically, recent preclinical studies suggest that the synapses between inner hair cells and spiral ganglion neurons with low spontaneous rates and high thresholds are the most vulnerable subcellular structures, with respect to insults during aging and noise exposure. This cochlear synaptopathy can be "hidden" because this synaptic loss can occur without permanent hearing threshold shifts. This new discovery of synaptic loss opens doors to new research directions. Here, we review a number of recent studies and make suggestions in two critical future research directions. First, based on solid evidence of cochlear synaptopathy in animal models, it is time to apply molecular approaches to identify the underlying molecular mechanisms; improved understanding is necessary for developing rational, effective therapies against this cochlear synaptopathy. Second, in human studies, the data supporting cochlear synaptopathy are indirect although rapid progress has been made. To fully identify changes in function that are directly related this hidden synaptic damage, we argue that a battery of tests including both electrophysiological and behavior tests should be combined for diagnosis of "hidden hearing loss" in clinical studies. This new approach may provide a direct link between cochlear synaptopathy and perceptual difficulties.
Topics: Animals; Auditory Perception; Hair Cells, Auditory, Inner; Hearing; Hearing Loss, Noise-Induced; Hearing Tests; Humans; Noise; Predictive Value of Tests; Psychoacoustics; Spiral Ganglion; Synapses; Synaptic Transmission
PubMed: 28007526
DOI: 10.1016/j.heares.2016.12.008 -
Neural Plasticity 2016Recent studies on animal models have shown that noise exposure that does not lead to permanent threshold shift (PTS) can cause considerable damage around the synapses... (Review)
Review
Recent studies on animal models have shown that noise exposure that does not lead to permanent threshold shift (PTS) can cause considerable damage around the synapses between inner hair cells (IHCs) and type-I afferent auditory nerve fibers (ANFs). Disruption of these synapses not only disables the innervated ANFs but also results in the slow degeneration of spiral ganglion neurons if the synapses are not reestablished. Such a loss of ANFs should result in signal coding deficits, which are exacerbated by the bias of the damage toward synapses connecting low-spontaneous-rate (SR) ANFs, which are known to be vital for signal coding in noisy background. As there is no PTS, these functional deficits cannot be detected using routine audiological evaluations and may be unknown to subjects who have them. Such functional deficits in hearing without changes in sensitivity are generally called "noise-induced hidden hearing loss (NIHHL)." Here, we provide a brief review to address several critical issues related to NIHHL: (1) the mechanism of noise induced synaptic damage, (2) reversibility of the synaptic damage, (3) the functional deficits as the nature of NIHHL in animal studies, (4) evidence of NIHHL in human subjects, and (5) peripheral and central contribution of NIHHL.
Topics: Acoustic Stimulation; Animals; Cochlea; Hearing Loss, Noise-Induced; Humans; Noise; Synapses
PubMed: 27738526
DOI: 10.1155/2016/6143164