Intense Noise Exposure Research Articles

Correlation between Occupational Noise Exposure and Renal Dysfunction in Male Workers

Objective: This study aimed to explore the relationship between occupational noise exposure and renal dysfunction in male workers. Methods: A total of 160 male workers (the number of people who met the inclusion criteria) who underwent health examinations in Qingdao Municipal Hospital from January 2023 to December 2023 were grouped into a noise group (80 cases) and a control group (80 cases) based on whether they engaged in noise work. We compared the differences in creatinine (CREA), cystatin C (CysC) and blood urea nitrogen (BUN) levels between the two groups. We also compared the differences in the above renal function indicators among workers with different working years in the noise group, as well as observed the relationship between renal dysfunction and noise exposure. Results: The levels of BUN, CREA and CysC in the noise group were significantly higher than those in the control group (P < 0.05). The overall abnormal rate of renal function in the noise group (42.50%) was significantly higher than that in the control group (11.25%, P < 0.05). The levels of BUN, CREA and CysC all significantly increased with the increase in working years (P < 0.05). The noise exposure intensity and cumulative noise exposure (CNE) of the group with renal dysfunction were higher than those of the group with normal renal function (P < 0.05). The area under the curve was 0.811 (95% confidence interval: 0.714–0.908), the optimal cut-off value of CNE was 96.53 dB (A) · year, the sensitivity was 89.29%, the specificity was 83.32% and the Youden index was 72.61%. Conclusion: There may be a correlation between long-term noise exposure and renal function. The intensity of noise exposure and CNE may have a certain correlation with renal function damage in occupational noise-exposed workers.

Vocalization-induced middle ear muscle reflex and auditory fovea do not contribute to the unimpaired auditory sensitivity after intense noise exposure in the CF-FM bat, Hipposideros pratti.

Behaviors and auditory physiological responses of some species of echolocating bats remain unaffected after exposure to intense noise, but information on the underlying mechanisms remains limited. Here, we studied whether the vocalization-induced middle ear muscle (MEM) contractions (MEM reflex) and auditory fovea contributed to the unimpaired auditory sensitivity of constant frequency-frequency modulation (CF-FM) bats after exposure to broad-band intense noise. The vocalizations of the CF-FM bat, Hipposideros pratti, were inhibited through anesthesia to eliminate the vocalization-induced MEM reflex. First, the anesthetized bats were exposed to intense broad-band noise, and the findings showed that the bats could still maintain their auditory sensitivities. However, auditory sensitivities were seriously impaired in CBA/Ca mice exposed to intense noise under anesthesia. This indicated that the unimpaired auditory sensitivity in H. pratti after exposure to intense noise under anesthesia was not due to anesthetization. The bats were further exposed to low-frequency band-limited noise, whose passband did not overlap with echolocation call frequencies. The results showed that the auditory responses to sound frequencies within the noise spectrum and one-half octave higher than the spectrum were also unimpaired. Taken together, the results indicate that both vocalization-induced MEM reflex and auditory fovea do not contribute to the unimpaired auditory sensitivity in H. pratti after exposure to intense noise. The possible mechanisms underlying the unimpaired auditory sensitivity after echolocating bats were exposed to intense noise are discussed.

Echolocating Bats Have Evolved Decreased Susceptibility to Noise-Induced Temporary Hearing Losses.

Glenis Long championed the application of quantitative psychophysical methods to understand comparative hearing abilities across species. She contributed the first psychophysical studies of absolute and masked hearing sensitivities in an auditory specialist, the echolocating horseshoe bat. Her data demonstrated that this bat has hyperacute frequency discrimination in the 83-kHz range of its echolocation broadcast. This specialization facilitates the bat's use of Doppler shift compensation to separate echoes of fluttering insects from concurrent echoes of non-moving objects. In this review, we discuss another specialization for hearing in a species of echolocating bat that contributes to perception of echoes within a complex auditory scene. Psychophysical and behavioral studies with big brown bats show that exposures to long duration, intense wideband or narrowband ultrasonic noise do not induce significant increases in their thresholds to echoes and do not impair their ability to orient through a naturalistic sonar scene containing multiple distracting echoes. Thresholds of auditory brainstem responses also remain low after intense noise exposures. These data indicate that big brown bats are not susceptible to temporary threshold shifts as measured in comparable paradigms used with other mammals, at least within the range of stimulus parameters that have been tested so far. We hypothesize that echolocating bats have evolved a decreased susceptibility to noise-induced hearing losses as a specialization for echolocation in noisy environments.

Hyaluronic acid-ibuprofen conjugation: a novel ototherapeutic approach protecting inner ear cells from inflammation-mediated damage.

There is a substantial need of effective drugs for the treatment of hearing loss, which affects nearly 500 million individuals globally. Hearing loss can be the result of intense or prolonged noise exposure, ototoxic drugs, infections, and trauma, which trigger inflammatory signaling cascades that lead to irreversible damage to cochlear structures. To address this, we developed and characterized a series of covalent conjugates of anti-inflammatory drugs to hyaluronic acid (HA), for potential use as topical ototherapeutics. These conjugates were tested in in vitro assays designed to mirror physiological processes typically observed with acoustic trauma. Intense noise exposure leads to macrophage recruitment to the cochlea and subsequent inflammatory damage to sensory cells. We therefore first tested our conjugates' ability to reduce the release of inflammatory cytokines in macrophages. This anti-inflammatory effect on macrophages also translated to increased cochlear cell viability. In our initial screening, one conjugate, ibuprofen-HA, demonstrated significantly higher anti-inflammatory potential than its counterparts. Subsequent cytokine release profiling of ibuprofen-HA further confirmed its ability to reduce a wider range of inflammatory markers, to a greater extent than its equivalent unconjugated drug. The conjugate's potential as a topical therapeutic was then assessed in previously developed tympanic and round window membrane tissue permeation models. As expected, our data indicate that the conjugate has limited tympanic membrane model permeability; however, it readily permeated the round window membrane model and to a greater extent than the unconjugated drug. Interestingly, our data also revealed that ibuprofen-HA was well tolerated in cellular and tissue cytocompatibility assays, whereas the unconjugated drug displayed significant cytotoxicity at equivalent concentrations. Moreover, our data highlighted the importance of chemical conjugation of ibuprofen to HA; the conjugate had improved anti-inflammatory effects, significantly reduced cytotoxicity, and is more suitable for therapeutic formulation. Overall, this work suggests that ibuprofen-HA could be a promising safe and effective topical ototherapeutic for inflammation-mediated cochlear damage.

The perception of ultrasonic vocalizations by laboratory mice following intense noise exposures.

Noise-induced hearing loss interacts with age, sex, and listening conditions to affect individuals' perception of ecologically relevant stimuli like speech. The present experiments assessed the impact of age and sex on vocalization detection by noise-exposed mice trained to detect a downsweep or complex ultrasonic vocalization in quiet or in the presence of a noise background. Daily thresholds before and following intense noise exposure were collected longitudinally and compared across several factors. All mice, regardless of age, sex, listening condition, or stimulus type showed their poorest behavioral sensitivity immediately after the noise exposure. There were varying degrees of recovery over time and across factors. Old-aged mice had greater threshold shifts and less recovery compared to middle-aged mice. Mice had larger threshold shifts and less recovery for downsweeps than for complex vocalizations. Female mice were more sensitive, had smaller post-noise shifts, and had better recovery than males. Thresholds in noise were higher and less variable than thresholds in quiet, but there were comparable shifts and recovery. In mice, as in humans, the perception of ecologically relevant stimuli suffers after an intense noise exposure, and results differ from simple tone detection findings.

Neurodegeneration after repeated noise trauma in the mouse lower auditory pathway

High intensity noise exposure leads to a permanent shift in auditory thresholds (PTS), affecting both peripheral (cochlear) tissue and the central auditory system. Studies have shown that a noise-induced hearing loss results in significant cell loss in several auditory structures. Degeneration can be demonstrated within hours after noise exposure, particularly in the lower auditory pathway, and continues to progress over days and weeks following the trauma. However, there is limited knowledge about the effects of recurring acoustic trauma. Repeated noise exposure has been demonstrated to increase neuroplasticity and neural activity. Thus, the present study aimed to investigate the influence of a second noise exposure on the cytoarchitecture of key structures of the auditory pathway, including spiral ganglion neurons (SGN), the ventral and dorsal cochlear nucleus (VCN and DCN, respectively), and the inferior colliculus (IC). In the experiments, young adult normal hearing mice were exposed to noise once or twice (with the second trauma applied one week after the initial exposure) for 3 h, using broadband white noise (5 – 20 kHz) at 115 dB SPL. The cell densities in the investigated auditory structures significantly decreased in response to the initial noise exposure compared to unexposed control animals. These findings are consistent with earlier research, which demonstrated degeneration in the auditory pathway within the first week after acoustic trauma. Additionally, cell densities were significantly decreased after the second trauma, but this effect was only observed in the VCN, with no similar effects seen in the SGN, DCN, or IC. These results illustrate how repeated noise exposure influences the cytoarchitecture of the auditory system. It appears that an initial noise exposure primarily damages the lower auditory pathway, but surviving cellular structures may develop resistance to additional noise-induced injury.

Long-Term Hearing Loss after Acute Acoustic Trauma inthe French Military: A Retrospective Study.

Acute acoustic trauma (AAT) is characterized by cochlea-vestibular signs following intense noise exposure, often caused by impulse noise. French military faces a high risk of AAT because of the use of weapons with peak sound levels exceeding 150 dB. Hearing loss (HL) resulting from AAT can have a significant impact on quality of life and operational capacity. The aim of this study was to assess the prevalence of long-term hearing impairment after AAT. The study involved a retrospective review of computer-based patient records from four military medical centers in Northeast France between January 2016 and December 2021. The inclusion criteria required the presence of cochlea-vestibular signs following impulse acoustic exposure and the absence of other causes. Sociodemographic and clinical data were collected, including audiometric data before and after exposure. The primary end point was the presence of a threshold elevation greater than 10 dB between reference and late audiograms. A total of 419 patients were included in the analysis, with a majority of males (n = 419; 84.7%) and a mean age of 23.6 yrs. The most common causative agent was the 5.56-mm assault rifle (n = 327; 78.0%). Tinnitus was the most frequent symptom (n = 366; 87.4%), followed by hypoacusis (n = 147; 35.1%) and earache (n = 89; 21.2%). The initial audiograms showed no HL in 31.0% of cases, while the mean deficit across all frequencies was 15.4 dB. All patients received corticosteroid therapy, with a mean duration of 6.0 d. Late audiograms conducted at an average interval of 448.0 d after AAT revealed a prevalence of long-term HL exceeding 20%. Higher doses of corticosteroid therapy (>1 mg/kg) were associated with a reduced frequency of long-term HL. This study highlights the prevalence of long-term hearing impairment after AAT in the French military. The findings emphasize the importance of preventive measures, including proper use of hearing protection devices, and the need for timely diagnosis and treatment. Further research is warranted to explore gender susceptibility to AAT and evaluate the impact of different weapons on AAT characteristics. The study also underscores the potential benefits of higher doses of corticosteroid therapy in reducing the risk of long-term hearing impairment. Overall, the findings contribute to a better understanding of AAT and can inform strategies for its prevention and management in military settings.

Dispensable role of Rac1 and Rac3 after cochlear hair cell specification

Rac small GTPases play important roles during embryonic development of the inner ear; however, little is known regarding their function in cochlear hair cells (HCs) after specification. Here, we revealed the localization and activation of Racs in cochlear HCs using GFP-tagged Rac plasmids and transgenic mice expressing a Rac1-fluorescence resonance energy transfer (FRET) biosensor. Furthermore, we employed Rac1-knockout (Rac1-KO, Atoh1-Cre;Rac1flox/flox) and Rac1 and Rac3 double KO (Rac1/Rac3-DKO, Atoh1-Cre;Rac1flox/flox;Rac3−/−) mice, under the control of the Atoh1 promoter. However, both Rac1-KO and Rac1/Rac3-DKO mice exhibited normal cochlear HC morphology at 13 weeks of age and normal hearing function at 24 weeks of age. No hearing vulnerability was observed in young adult (6-week-old) Rac1/Rac3-DKO mice even after intense noise exposure. Consistent with prior reports, the results from Atoh1-Cre;tdTomato mice confirmed that the Atoh1 promoter became functional only after embryonic day 14 when the sensory HC precursors exit the cell cycle. Taken together, these findings indicate that although Rac1 and Rac3 contribute to the early development of sensory epithelia in cochleae, as previously shown, they are dispensable for the maturation of cochlear HCs in the postmitotic state or for hearing maintenance following HC maturation.Key messagesMice with Rac1 and Rac3 deletion were generated after HC specification.Knockout mice exhibit normal cochlear hair cell morphology and hearing.Racs are dispensable for hair cells in the postmitotic state after specification.Racs are dispensable for hearing maintenance after HC maturation.

Noise exposure in pediatric otolaryngology clinic: A sound survey of a single-institution tertiary care facility

BackgroundThe Occupational Safety and Health Administration (OSHA) considers acoustic exposure of 90 decibels (dB) an occupational risk for noise-induced hearing loss. Pediatric healthcare clinicians are exposed to considerable noise especially during invasive procedures, predisposing them to noise-induced hearing loss, increased work-related stress, and increased complications associated with intense noise exposure. While there has been extensive research in noise exposure in dentistry, to date there has been no research on noise exposure in the pediatric otolaryngology clinic setting. The objective of this study is to quantify the degree of noise exposure that pediatric otolaryngologists encounter in the clinical setting. MethodsA sound survey was performed of 420 pediatric otolaryngology clinic visits within a single-institution tertiary care facility from January 2022 to March 2022, with a total of 409 visits included. At each visit, noise was measured using a calibrated National Institute for Occupational Safety and Health (NIOSH) Sound Meter application, an iPad, and a microphone. The Equivalent Continuous Sound Pressure Level (LAeq), peak sound pressure level (SPL), C-weighted peak noise level (LCpeak), and the 8-hour time-weighted average (TWA) sound level were recorded. ResultsThe average LAeq was 61.1 dB, the median LAeq was 60.3 dB, and the average peak SPL was 80.5 dB. Only 0.5 % of visits reached an LAeq above 80 dB, however, 51 % were above 60 dB and 99 % were above 45 dB. No clinicians were exposed to noise exceeding established limits of safety. Patients younger than ten years old (p < 0.001) and those who underwent procedures such as cerumen removal (p < 0.001) elicited higher ranges of elevated noise. Multivariate analysis confirmed that increased age decreased acoustic exposure while procedures increased acoustic exposure. ConclusionsThe results of this study suggest that pediatric otolaryngology clinicians do not exceed hazardous noise limit exposure. However, they are exposed to levels above those which have been linked to stress, poor productivity, and stress-related disorders. This analysis also reports that patients who are younger and those that undergo procedures, specifically cerumen removal, tend to expose their providers to the highest levels of noise. This is the first study examining noise exposure in pediatric otolaryngology, and further research should evaluate the risks of noise exposure in this environment.

Conditional Ablation of Glucocorticoid and Mineralocorticoid Receptors from Cochlear Supporting Cells Reveals Their Differential Roles for Hearing Sensitivity and Dynamics of Recovery from Noise-Induced Hearing Loss.

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.

Noise exposure and hearing loss among tractor drivers in India.

Tractors emit high intensity noise and prolonged exposure to high intensity noise causes hearing loss to the drivers. The aim of this study was to measure noise intensity at the tractor drivers' ear level and hearing loss among tractor drivers. Noise intensity was measured on 6 models of tractors which were operated with 5 different tillage implements. In order to assess hearing loss, audiometric test was performed at 7 frequencies, i.e. 250, 500, 1000, 2000, 4000, 6000, and 8000 Hz, among 30 tractor drivers and 30 control group subjects. All the selected tractor drivers and control group subjects were also interviewed to obtain personal information and noise exposure details. The tractor drivers were exposed to noise intensity in the range of 91.7-97.5 dB(A). Audiogram analysis shows that the hearing threshold levels were significantly (p < 0.05) higher among the tractor drivers as compared with the control group subjects. The effect was significantly (p < 0.05) more on the left ear as compared with the right ear among the tractor drivers. Increase in age has significant (p < 0.05) effect on the hearing threshold levels on the left ear. Prevalence of high frequency hearing loss was 50% among tractor drivers as compared with 10% among control group subjects. Hearing loss was significantly (p < 0.05) more in the low frequency as compared with the high frequency among the tractor drivers. Indian tractor operators are exposed to high noise levels which may result in hearing loss. It is recommended that hearing conservation programs should be initiated to prevent noise hazards and hearing loss among the tractor drivers.

Contralateral inhibition of distortion product otoacoustic emissions in young noise-exposed Veterans.

Although animal models show a clear link between noise exposure and damage to afferent cochlear synapses, the relationship between noise exposure and efferent function appears to be more complex. Animal studies indicate that high intensity noise exposure reduces efferent medial olivocochlear (MOC) reflex strength, whereas chronic moderate noise exposure is associated with a conditioning effect that enhances the MOC reflex. The MOC reflex is predicted to improve speech-in-noise perception and protects against noise-induced auditory damage by reducing cochlear gain. In humans, MOC reflex strength can be estimated by measuring contralateral inhibition of distortion product otoacoustic emissions (DPOAEs). The objective of this study was to determine the impact of military noise exposure on efferent auditory function by measuring DPOAE contralateral inhibition in young Veterans and non-Veterans with normal audiograms. Compared with non-Veteran controls, Veterans with high levels of reported noise exposure demonstrated a trend of reduced contralateral inhibition across a broad frequency range, suggesting efferent damage. Veterans with moderate noise exposure showed trends of reduced inhibition from 3 to 4 kHz but greater inhibition from 1 to 1.5 kHz, consistent with conditioning. These findings suggest that, in humans, the impact of noise exposure on the MOC reflex differs depending on the noise intensity and duration.

Low Intensity Noise Exposure Enhanced Auditory Loudness and Temporal Processing by Increasing Excitability of DCN.

Sound stimulation is generally used for tinnitus and hyperacusis treatment. Recent studies found that long-term noise exposure can change synaptic and firing properties in the central auditory system, which will be detected by the acoustic startle reflex. However, the perceptual consequences of long-term low-intensity sound exposure are indistinct. This study will detect the effects of moderate-level noise exposure (83 dB SPL) on auditory loudness, and temporal processing was evaluated using CBA/CaJ mice. C-Fos staining was used to detect neural activity changes in the central auditory pathway. With two weeks of 83 dB SPL noise exposure (8 hours per day), no persistent threshold shift of the auditory brainstem response (ABR) was identified. On the other hand, noise exposure enhanced the acoustic startle response (ASR) and gap-induced prepulse inhibition significantly (gap-PPI). Low-level noise exposure, according to the findings, can alter temporal acuity. Noise exposure increased the number of c-Fos labeled neurons in the dorsal cochlear nucleus (DCN) and caudal pontine reticular nucleus (PnC) but not at a higher level in the central auditory nuclei. Our results suggested that noise stimulation can change acoustical temporal processing presumably by increasing the excitability of auditory brainstem neurons.

Alterations to cognitive abilities and functional networks in rats post broad-band intense noise exposure.

This study aimed to investigate the alterations of cognition and functional connectivity post noise, and find the progress and neural substrates of noise induced hearing loss (NIHL)-associated cognitive impairment. We exposed rats to 122dB broad-band noise for 2h to induce hearing loss and the auditory function was assessed by measuring auditory brainstem response thresholds. Morris water maze test and resting state MRI were computed at 0day, 1, 3, 6months post noise to reveal cognitive ability and neural substrate. The interregional connections in the auditory network and default mode network, as well as the connections using the auditory cortex and cingulate cortex as seeds were also examined addtionally. The deficit in spatial learning/memory was only observed at 6months after noise exposure. The internal connections in the auditory network and default mode network were enhanced at 0day and decreased at 6months post noise. The connectivity using the auditory cortex and cingulate cortex as seeds generally followed the rule of "enhancement-normal-decrease-widely decrease". A new model accounting for arousal, dementia, motor control of NIHL in is proposed. Our study highlights the fundamental flexibility of neural systems, and may also point toward novel therapeutic strategies for treating sensory disorders.

Unexpected Consequences of Noise-Induced Hearing Loss: Impaired Hippocampal Neurogenesis, Memory, and Stress.

Noise-induced hearing loss (NIHL), caused by direct damage to the cochlea, reduces the flow of auditory information to the central nervous system, depriving higher order structures, such as the hippocampus with vital sensory information needed to carry out complex, higher order functions. Although the hippocampus lies outside the classical auditory pathway, it nevertheless receives acoustic information that influence its activity. Here we review recent results that illustrate how NIHL and other types of cochlear hearing loss disrupt hippocampal function. The hippocampus, which continues to generate new neurons (neurogenesis) in adulthood, plays an important role in spatial navigation, memory, and emotion. The hippocampus, which contains place cells that respond when a subject enters a specific location in the environment, integrates information from multiple sensory systems, including the auditory system, to develop cognitive spatial maps to aid in navigation. Acute exposure to intense noise disrupts the place-specific firing patterns of hippocampal neurons, “spatially disorienting” the cells for days. More traumatic sound exposures that result in permanent NIHL chronically suppresses cell proliferation and neurogenesis in the hippocampus; these structural changes are associated with long-term spatial memory deficits. Hippocampal neurons, which contain numerous glucocorticoid hormone receptors, are part of a complex feedback network connected to the hypothalamic-pituitary (HPA) axis. Chronic exposure to intense intermittent noise results in prolonged stress which can cause a persistent increase in corticosterone, a rodent stress hormone known to suppress neurogenesis. In contrast, a single intense noise exposure sufficient to cause permanent hearing loss produces only a transient increase in corticosterone hormone. Although basal corticosterone levels return to normal after the noise exposure, glucocorticoid receptors (GRs) in the hippocampus remain chronically elevated. Thus, NIHL disrupts negative feedback from the hippocampus to the HPA axis which regulates the release of corticosterone. Preclinical studies suggest that the noise-induced changes in hippocampal place cells, neurogenesis, spatial memory, and glucocorticoid receptors may be ameliorated by therapeutic interventions that reduce oxidative stress and inflammation. These experimental results may provide new insights on why hearing loss is a risk factor for cognitive decline and suggest methods for preventing this decline.

Occluded insertion loss from intracochlear pressure measurements during acoustic shock wave exposure

Auditory injuries are a common result of high intensity noise exposure, and hearing protective devices (HPDs) can mitigate this injury. Current evaluation methods use manikins to measure ear canal SPLs, but neglect alternate sound conduction pathways. We have previously reported intracochlear pressures in cadaveric human specimens to high-level impulse noise, revealing a substantial bone conducted component. Here, we estimate insertion loss during HPD use from intracochlear pressures in those same specimens. Cadaveric specimens were exposed to shock waves with peak overpressures of 7–83 kPa. Fiber optic pressure sensors were placed in the external, middle, and inner ears and responses measured with ears unoccluded and with four HPDs. Spectral insertion loss was calculated for each exposure level in the frequency domain. Insertion losses calculated from EAC pressures were comparable across levels, consistent with results from acoustic manikins. In contrast, insertion loss calculated from intracochlear pressures were generally lower in magnitude, but increased with the exposure level, likely due to substantial contributions of secondary transmission pathways. Unfortunately, variability in intracochlear pressures limit insertion loss estimate utility. As a proof of concept, we show that averaging multiple exposures increased signal-to-noise considerably, similar noise reduction strategies should be utilized in future studies.

NRF2/HO-1 pathway activation by ATF3 in a noise-induced hearing loss murine model

BackgroundExcessive oxidative stress of the inner ear as a result of high, intense noise exposure is regarded as a major mechanism underlying the development of noise-induced hearing loss (NIHL). The present study was designed to explore the effect and mechanism of activated transcription factor 3 (ATF3) in reduction/oxidation homeostasis of NIHL. MethodIn vitro and in vivo assays were performed to investigate the functional role of ATF3 in the inner ear. Mice hearing was measured using auditory brainstem response. ATF3 short hairpin RNA (shRNA) was transfected into House Ear Institute-Organ of Corti 1 (HEI-OC1) cells to decrease ATF3 expression. Western blotting and quantitative real-time polymerase chain reaction (RT-qPCR) were performed to quantify ATF3, NRF2, HO-1 and NQO1 expression. Glutathione (GSH) assay was performed to detect intracellular GSH levels. ATF3 immunofluorescence analysis was carried out in cochlear cryosectioned samples and HEI-OC1 cells to localize ATF3 expression. Cell counting kit 8 assay and flow cytometry were performed to analyze cell viability. ResultATF3 was upregulated in noise-exposed cochleae and HEI-OC1 cells treated with H2O2. NRF2 is a key factor regulated by ATF3. NRF2, HO-1, NQO1, and GSH expression was significantly downregulated in shATF3 HEI-OC1 cells. ATF3 silencing promoted reactive oxygen species accumulation and increased apoptosis and necrosis with H2O2 stimulus. ConclusionATF3 functions as an antioxidative factor by activating the NRF2/HO-1 pathway.

The Effectiveness of Hearing Protection Devices: A Systematic Review and Meta-Analysis.

To prevent intensive noise exposure in advance and be safely controlled during such exposure, hearing protection devices (HPDs) have been widely used by workers. The present study evaluates the effectiveness of these HPDs, partitioned into three different outcomes, such as sound attenuation, sound localization, and speech perception. Seven electronic journal databases were used to search for published articles from 2000 to 2021. Based on inclusion criteria, 20 articles were chosen and then analyzed. For a systematic review and meta-analysis, standardized mean differences (SMDs) and effect size were calculated using a random-effect model. The funnel plot and Egger’s regression analysis were conducted to assess the risk of bias. From the overall results of the included 20 articles, we found that the HPD function performed significantly well for their users (SMDs: 0.457, 95% confidence interval (CI): 0.034–0.881, p < 0.05). Specifically, a subgroup analysis showed a meaningful difference in sound attenuation (SMDs: 1.080, 95% CI: 0.167–1.993, p < 0.05) when to wear and not to wear HPDs, but indicated no significance between the groups for sound localization (SMDs: 0.177, 95% CI: 0.540–0.894, p = 0.628) and speech perception (SMDs: 0.366, 95% CI: −0.100–1.086, p = 0.103). The HPDs work well for their originally designated purposes without interfering to find the location of the sound sources and for talking between the workers. Taking into account various factors, such as the characteristics of the users, selection of appropriate types, and fitting methods for wearing in different circumstances, seems to be necessary for a reliable systematic analysis in terms of offering the most useful information to the workers.

A Computer simulation of noise of construction machinery operating in parallel

Prolonged, repeated or very intense noise exposure can damage human health. To reduce any dangerous effects of noise on human health, policies and restrictions are enshrined in national law and legislative regulations. In the Czech Republic, this issue is subject to the Ministry of Health. In other states it can be the Ministry of Health or more often the Ministry of the Environment. The protection of human health against noise and vibration is enshrined in Act No. 258/2000 Coll., on Protection of Public Health, specifically in şş 30-34 of this Act. Other restrictions are described in Act No. 309/2006 Coll., which regulates other requirements for safety and health protection at work in labour relations and on ensuring safety and health protection in activities or the provision of services outside of labour relations. Furthermore, hygienic limits for workplaces, protected indoor areas of buildings and protected outdoor areas are set in the new Regulation of the Government of the Czech Republic, No. 272/2011 Coll. as amended. This Regulation also sets limits for construction noise. They set limitations in so-called outdoor protected areas and the so-called outdoor protected areas of buildings. The hygienic limit of the equivalent sound pressure level A for noise from construction activities is set here by adding a correction of 5dB or 15dB according to the type of protected space to the basic value of the equivalent sound pressure level A 50dB. This limit must be adhered to. For buildings nearby, the term „protected facades“ is used, i.e. „protected façades“ include the nearest buildings that are inhabited and their occupants could be exposed to noise for a long period of time. We can measure the intensity of noise in these places if we have a "sound level meter". Predicting the intensity of noise and its longevity for future construction is more challenging. The computational evaluation of the noise load of the outdoor area of the monitored territory is based on the recommended theoretical acoustic relations for the transmission of sound from stationary noise sources according to ČSN ISO 9613/1-2. One of the possibilities of calculating the intensity of noise is the application of software programmes used for determining traffic noise, which, in contrast to construction noise, is handled very carefully and predicted in detail during the construction of transport infrastructure. Because here are the values and methodologies for the calculation of noise indicators set correctly and in detail, it is possible to use them also, provided that we work well with the background and input data. The calculation indicators are the values of the equivalent sound pressure level falling in front of the façade, on which we determine various measuring points. If the noise sources and acoustically significant elements are entered correctly, we obtain both correct values and also the possibility of displaying a map of the area with colour isophone bands, which expresses the level of noise in the construction site and its surroundings.

Auditory Brainstem Responses Predict Behavioral Deficits in Rats with Varying Levels of Noise-Induced Hearing Loss

Intense noise exposure is a leading cause of hearing loss, which results in degraded speech sound discrimination ability, particularly in noisy environments. The development of an animal model of speech discrimination deficits due to noise induced hearing loss (NIHL) would enable testing of potential therapies to improve speech sound processing. Rats can accurately detect and discriminate human speech sounds in the presence of quiet and background noise. Further, it is known that profound hearing loss results in functional deafness in rats. In this study, we generated rats with a range of impairments which model the large range of hearing impairments observed in patients with NIHL. One month after noise exposure, we stratified rats into three distinct deficit groups based on their auditory brainstem response (ABR) thresholds. These groups exhibited markedly different behavioral outcomes across a range of tasks. Rats with moderate hearing loss (30 dB shifts in ABR threshold) were not impaired in speech sound detection or discrimination. Rats with severe hearing loss (55 dB shifts) were impaired at discriminating speech sounds in the presence of background noise. Rats with profound hearing loss (70 dB shifts) were unable to detect and discriminate speech sounds above chance level performance. Across groups, ABR threshold accurately predicted behavioral performance on all tasks. This model of long-term impaired speech discrimination in noise, demonstrated by the severe group, mimics the most common clinical presentation of NIHL and represents a useful tool for developing and improving interventions to target restoration of hearing.