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International Journal of Occupational... Nov 2023Hearing loss is a major worldwide health issue affecting an estimated 1.5 billion people. Causes of hearing loss include genetics, chemicals, medications, lifestyle...
OBJECTIVES
Hearing loss is a major worldwide health issue affecting an estimated 1.5 billion people. Causes of hearing loss include genetics, chemicals, medications, lifestyle habits such as smoking, and noise. Noise is probably the largest contributing factor for hearing loss. Noise arises from the workplace, ambient environment, and leisure activities. The easiest noise sources to control are workplace and environmental. Workplace noise is unique in that the employer is responsible for the noise and the worker. Also, workers may be exposed to much higher levels of noise than they would accept elsewhere. Employers follow the traditional hierarchy of controls (substitution/engineering, administrative, personal protective equipment [PPE]). Substituting or engineering a lower noise level actually reduces the hazard present to the worker but demand more capital investment. Administrative and PPE controls can be effective, but enforcement and motivation are essential to reducing risk and there is still some hearing loss for a portion of the workers. The challenge is to estimate the costs more clearly for managers. A systems engineering approach can help visualize factors affecting hearing health.
MATERIAL AND METHODS
In this study, a systems engineering causal loop diagram (CLD) was developed to aid in understanding factors and their interrelationships. The CLD was then modeled in VenSim. The model was informed from the authors' expertise in hearing health and exposure science. Also, a case study was used to test the model. The model can be used to inform decision-makers of holistic costs for noise control options, with potentially better hearing health outcomes for workers.
RESULTS
The CLD and cost model demonstrated a 4.3 year payback period for the engineered noise control in the case study.
CONCLUSIONS
Systems thinking using a CLD and cost model for occupational hearing health controls can aid organizational managers in applying resources to control risk. Int J Occup Med Environ Health. 2023;36(5):672-84.
Topics: Humans; Hearing Loss, Noise-Induced; Noise, Occupational; Occupational Diseases; Workplace; Occupational Exposure; Systems Analysis
PubMed: 37767777
DOI: 10.13075/ijomeh.1896.02043 -
Frontiers in Behavioral Neuroscience 2023Noise-induced tinnitus is generally associated with hearing impairment caused by traumatic acoustic overexposure. Previous studies in laboratory animals and human...
Noise-induced tinnitus is generally associated with hearing impairment caused by traumatic acoustic overexposure. Previous studies in laboratory animals and human subjects, however, have observed differences in tinnitus susceptibility, even among individuals with similar hearing loss. The mechanisms underlying increased sensitivity or, conversely, resistance to tinnitus are still incompletely understood. Here, we used behavioral tests and ABR audiometry to compare the sound-evoked responses of mice that differed in the presence of noise-induced tinnitus. The aim was to find a specific pre-exposure neurophysiological marker that would predict the development of tinnitus after acoustic trauma. Noise-exposed mice were screened for tinnitus-like behavior with the GPIAS paradigm and subsequently divided into tinnitus (+T) and non-tinnitus (-T) groups. Both groups showed hearing loss after exposure, manifested by elevated audiometric thresholds along with reduced amplitudes and prolonged latencies of ABR waves. Prior to exposure, except for a slightly increased slope of growth function for ABR amplitudes in +T mice, the two groups did not show significant audiometric differences. Behavioral measures, such as the magnitude of the acoustic startle response and its inhibition by gap pre-pulse, were also similar before exposure in both groups. However, +T mice showed significantly increased suppression of the acoustic startle response in the presence of background noise of moderate intensity. Thus, increased modulation of startle by background sounds may represent a behavioral correlate of susceptibility to noise-induced tinnitus, and its measurement may form the basis of a simple non-invasive method for predicting tinnitus development in laboratory rodents.
PubMed: 38144362
DOI: 10.3389/fnbeh.2023.1321277 -
Hearing Research Mar 2024Hearing loss affects approximately 18% of the population worldwide. Hearing difficulties in noisy environments without accompanying audiometric threshold shifts likely... (Review)
Review
Hearing loss affects approximately 18% of the population worldwide. Hearing difficulties in noisy environments without accompanying audiometric threshold shifts likely affect an even larger percentage of the global population. One of the potential causes of hidden hearing loss is cochlear synaptopathy, the loss of synapses between inner hair cells (IHC) and auditory nerve fibers (ANF). These synapses are the most vulnerable structures in the cochlea to noise exposure or aging. The loss of synapses causes auditory deafferentation, i.e., the loss of auditory afferent information, whose downstream effect is the loss of information that is sent to higher-order auditory processing stages. Understanding the physiological and perceptual effects of this early auditory deafferentation might inform interventions to prevent later, more severe hearing loss. In the past decade, a large body of work has been devoted to better understand hidden hearing loss, including the causes of hidden hearing loss, their corresponding impact on the auditory pathway, and the use of auditory physiological measures for clinical diagnosis of auditory deafferentation. This review synthesizes the findings from studies in humans and animals to answer some of the key questions in the field, and it points to gaps in knowledge that warrant more investigation. Specifically, recent studies suggest that some electrophysiological measures have the potential to function as indicators of hidden hearing loss in humans, but more research is needed for these measures to be included as part of a clinical test battery.
Topics: Animals; Humans; Hearing Loss, Noise-Induced; Noise; Auditory Threshold; Hearing Loss, Hidden; Auditory Perception; Cochlea; Synapses; Evoked Potentials, Auditory, Brain Stem
PubMed: 38335624
DOI: 10.1016/j.heares.2024.108967 -
Frontiers in Neurology 2024In addition to hearing loss, damage to the cochlea can lead to gain of function pathologies such as hyperacusis. It has been proposed that painful hyperacusis,... (Review)
Review
In addition to hearing loss, damage to the cochlea can lead to gain of function pathologies such as hyperacusis. It has been proposed that painful hyperacusis, noxacusis, may be carried to the central nervous system by type II cochlear afferents, sparse, unmyelinated neurons that share morphological and neurochemical traits with nociceptive C-fibers of the somatic nervous system. Also like in skin, damage elicits spreading calcium waves within cochlear epithelia. These are mediated by extracellular ATP combined with IP3-driven release from intracellular calcium stores. Type II afferents are excited by ATP released from damaged epithelia. Thus, the genesis and propagation of epithelial calcium waves is central to cochlear pathology, and presumably hyperacusis. Damage-evoked signals in type II afferents and epithelial cells have been recorded in cochlear explants or semi-intact otic capsules. These efforts have included intracellular electrical recording, use of fluorescent calcium indicators, and visualization of an activity-dependent, intrinsic fluorescent signal. Of relevance to hyperacusis, prior noise-induced hearing loss leads to the generation of prolonged and repetitive activity in type II neurons and surrounding epithelia.
PubMed: 38419694
DOI: 10.3389/fneur.2024.1361747 -
Scientific Reports Oct 2023Hearing loss and hearing disorders represent possible mediating pathways in the associations between noise exposures and non-auditory health outcomes. In this context,...
Hearing loss and hearing disorders represent possible mediating pathways in the associations between noise exposures and non-auditory health outcomes. In this context, we assessed whether the noise-obesity associations should consider hearing functions as possible mediators and applied Mendelian randomisation (MR) to investigate causal relationships between body constitution and hearing impairments. We obtained genetic associations from publicly available summary statistics from genome-wide association studies in European ancestry adult populations (N= from 210,088 to 360,564) for (i) body constitution: body mass index (BMI), waist circumference (WC) and body fat percentage (BFP), and (ii) hearing loss: sensorineural hearing loss, noise-induced hearing loss, and age-related hearing impairment (ARHI). We employed colocalisation analysis to investigate the genetic associations for BMI and ARHI liability within an FTO locus. We conducted bi-directional MR for the 'forward' (from body constitution to hearing) and 'reverse' directions. We applied the random effects inverse variance-weighted method as the main MR method, with additional sensitivity analyses. Colocalisation analysis suggested that BMI and ARHI shared a causal variant at the FTO gene. We did not find robust evidence for causal associations from body constitution to hearing loss and suggested that some associations may be driven by FTO variants. In the reverse analyses, ARHI was negatively associated with BMI [effect size - 0.22 (95% CI - 0.44 to - 0.01)] and BFP [effect size - 0.23 (95% CI - 0.45 to 0.00)], supporting the notion that ARHI may diminish body constitution. Finally, our data suggest that there is no strong evidence that hearing explains the association between noise exposure and body constitution.
Topics: Adult; Humans; Genome-Wide Association Study; Obesity; Body Constitution; Deafness; Body Mass Index; Mendelian Randomization Analysis; Polymorphism, Single Nucleotide; Alpha-Ketoglutarate-Dependent Dioxygenase FTO
PubMed: 37891192
DOI: 10.1038/s41598-023-44735-x -
The Annals of Otology, Rhinology, and... Aug 2023Molecular hydrogen (H) has shown therapeutic potential in several oxidative stress-related conditions in humans, is well-tolerated, and is easily administered via...
OBJECTIVE
Molecular hydrogen (H) has shown therapeutic potential in several oxidative stress-related conditions in humans, is well-tolerated, and is easily administered via inhalation.The aim of this preclinical in vivo study was to investigate whether impulse noise trauma can be prevented by H when inhaled immediately after impulse noise exposure.
METHODS
Guinea pigs (n = 26) were subjected to impulse noise (n = 400; 156 dB SPL; 0.33/s; n = 11; the Noise group), to impulse noise immediately followed by H inhalation (2 mol%; 500 ml/min; 1 hour; n = 10; the Noise + H group), or to H inhalation (n = 5; the H group). The acoustically evoked ABR threshold at 3.15, 6.30, 12.5, 20.0, and 30.0 kHz was assessed before and 4 days after impulse noise and/or H exposure. The cochleae were harvested after the final ABR assessment for quantification of hair cells.
RESULTS
Noise exposure caused ABR threshold elevations at all frequencies (median 35, 35, 30, 35, and 35 dB SPL, the Noise group; 20, 25, 10, 13, and 20 dB SPL, the Noise + H group; < .05) but significantly less so in the Noise + H group ( < .05). Outer hair cell (OHC) loss was in the apical, mid, and basal regions 8.8%, 53%, and 14% in the Noise group and 3.5%, 22%, and 1.2% in the Noise + H group. The corresponding inner hair cell (IHC) loss was 0.1%, 14%, and 3.5% in the Noise group and 0%, 2.8%, and 0% in the Noise + H group. The difference between the groups was significant in the basal region for OHCs ( = .003) and apical ( = .033) and basal ( = .048) regions for IHCs.
CONCLUSIONS
Acute acoustic trauma can be reduced by H when inhaled immediately after impulse noise exposure.
Topics: Humans; Animals; Guinea Pigs; Hydrogen; Hearing Loss, Noise-Induced; Cochlea; Noise; Hair Cells, Auditory, Outer; Evoked Potentials, Auditory, Brain Stem; Auditory Threshold
PubMed: 35962590
DOI: 10.1177/00034894221118764 -
Noise & HealthExcessive noise is unpleasant and induces several physiological and psychological effects. Noise pollution is a potential threat to humans, particularly those... (Review)
Review
OBJECTIVE
Excessive noise is unpleasant and induces several physiological and psychological effects. Noise pollution is a potential threat to humans, particularly those continuously exposed for extended periods throughout the day over many years. This review aims to examine the various auditory and non-auditory outcomes associated with prolonged exposure to noise pollution.
MATERIALS AND METHODS
The review utilized a combination of relevant keywords to search the electronic databases. After screening based on the applied selection criteria for title, abstract, and full text, 44 articles were finally selected for critical review.
RESULTS
We identified and analyzed research findings related to noise-induced hearing loss, tinnitus, and sleep disturbances along with non-auditory issues such as annoyance, cognitive impairments, and mental stress associated with cardiovascular disorders. Furthermore, the existing studies were compared and collated to highlight the unique challenges and significance of noise pollution as a distinctive environmental concern and to explore the ongoing efforts in its research and prevention, including the early detection and potential reversal of noise-induced hearing loss.
CONCLUSION
The fundamental health consequences of noise pollution underscore the need for extensive research encompassing emerging noise sources and technologies to establish a health management system tailored to address noise-related health concerns and reduce noise exposure risk among populations. Finally, further research is warranted to ensure improved measurement of noise exposure and related health outcomes, especially in the context of occupational noise.
Topics: Humans; Hearing Loss, Noise-Induced; Tinnitus; Noise; Environmental Exposure; Sleep Wake Disorders; Noise, Occupational; Cardiovascular Diseases; Stress, Psychological; Cognitive Dysfunction
PubMed: 38904803
DOI: 10.4103/nah.nah_124_23 -
Journal of Otolaryngology - Head & Neck... Dec 2023Noise exposure is an important cause of acquired hearing loss. Studies have found that noise exposure causes dysregulated redox homeostasis in cochlear tissue, which has... (Review)
Review
Noise exposure is an important cause of acquired hearing loss. Studies have found that noise exposure causes dysregulated redox homeostasis in cochlear tissue, which has been recognized as a signature feature of hearing loss. Oxidative stress plays a pivotal role in many diseases via very complex and diverse mechanisms and targets. Reactive oxygen species are products of oxidative stress that exert toxic effects on a variety of physiological activities and are considered significant in noise-induced hearing loss (NIHL). Endogenous cellular antioxidants can directly or indirectly counteract oxidative stress and regulate intracellular redox homeostasis, and exogenous antioxidants can complement and enhance this effect. Therefore, antioxidant therapy is considered a promising direction for NIHL treatment. However, drug experiments have been limited to animal models of NIHL, and these experiments and related observations are difficult to translate in humans; therefore, the mechanisms and true effects of these drugs need to be further analyzed. This review outlines the effects of oxidative stress in NIHL and discusses the main mechanisms and strategies of antioxidant treatment for NIHL.
Topics: Animals; Humans; Hearing Loss, Noise-Induced; Antioxidants; Oxidative Stress; Oxidation-Reduction; Homeostasis
PubMed: 38082455
DOI: 10.1186/s40463-023-00686-x -
Seminars in Hearing Nov 2023Workers rely on hearing protection devices to prevent occupational noise-induced hearing loss. This study aimed to evaluate changes in attenuation over time for properly... (Review)
Review
Workers rely on hearing protection devices to prevent occupational noise-induced hearing loss. This study aimed to evaluate changes in attenuation over time for properly fit devices when worn by workers exposed to hazardous noise. Earplug fit testing was accomplished on 30 workers at a brewery facility with three types of foam and three types of premolded earplugs. The personal attenuation ratings (PARs) were measured before and after a 2-hour work period while exposed to hazardous noise levels. The minimum acceptable initial PAR was 15 dB. Average decreases in PAR ranged from -0.7 to -2.6 dB across all six earplug types. Significant changes in PAR were observed for the Foam-1 ( = 0.009) and Premold-3 ( = 0.004) earplugs. A linear mixed regression model using HPD type and study year as fixed effects and subject as random effect was not significant for either fixed effect ( = 0.05). Ninety-five percent of the final PAR measurements maintained the target attenuation of 15 dB. Properly fitting earplugs can be effective at reducing worker's noise exposures over time. The potential for a decrease in attenuation during the work shift should be considered when training workers and establishing the adequacy of protection from hazardous noise exposures.
PubMed: 37818150
DOI: 10.1055/s-0043-1769586 -
Biomedicine & Pharmacotherapy =... Oct 2023Over-production of reactive oxygen species (ROS) in the inner ear can be triggered by a variety of pathological events identified in animal models after traumatic noise...
Over-production of reactive oxygen species (ROS) in the inner ear can be triggered by a variety of pathological events identified in animal models after traumatic noise exposure. Our previous research found that inhibition of the AMP-activated protein kinase alpha subunit (AMPKα) protects against noise-induced cochlear hair cell loss and hearing loss by reducing ROS accumulation. However, the molecular pathway through which AMPKα exerts its antioxidative effect is still unclear. In this study, we have investigated a potential target of AMPKα and ROS, cystic fibrosis transmembrane conductance regulator (CFTR), and the protective effect against noise-induced hair cell loss of an FDA-approved CFTR potentiator, ivacaftor, in FVB/NJ mice, mouse explant cultures, and HEI-OC1 cells. We found that noise exposure increases phosphorylation of CFTR at serine 737 (p-CFTR, S737), which reduces wildtype CFTR function, resulting in oxidative stress in cochlear sensory hair cells. Pretreatment with a single dose of ivacaftor maintains CFTR function by preventing noise-increased p-CFTR (S737). Furthermore, ivacaftor treatment increases nuclear factor E2-related factor 2 (Nrf2) expression, diminishes ROS formation, and attenuates noise-induced hair cell loss and hearing loss. Additionally, inhibition of noise-induced AMPKα activation by compound C also diminishes p-CFTR (S737) expression. In line with these in-vivo results, administration of hydrogen peroxide to cochlear explants or HEI-OC1 cells increases p-CFTR (S737) expression and induces sensory hair cell or HEI-OC1 cell damage, while application of ivacaftor halts these effects. Although ivacaftor increases Nrf2 expression and reduces ROS accumulation, cotreatment with ML385, an Nrf2 inhibitor, abolishes the protective effects of ivacaftor against hydrogen-peroxide-induced HEI-OC1 cell death. Our results indicate that noise-induced sensory hair cell damage is associated with p-CFTR. Ivacaftor has potential for treatment of noise-induced hearing loss by maintaining CFTR function and increasing Nrf2 expression for support of redox homeostasis in sensory hair cells.
Topics: Animals; Mice; NF-E2-Related Factor 2; Reactive Oxygen Species; Cystic Fibrosis Transmembrane Conductance Regulator; Oxidative Stress; Hair Cells, Auditory; AMP-Activated Protein Kinases; Alopecia; Antibodies; Oxidation-Reduction
PubMed: 37657258
DOI: 10.1016/j.biopha.2023.115399