P212 Cortisol blood level in chronic noise exposed workers

We previously observed greater ozone-induced lung function decrements in obese than non-obese women. Animal models suggest that obesity enhances ozone-induced airway reactivity and inflammation. In a controlled exposure study, we compared the acute effect of randomized 0.4ppm ozone and air exposures (2 h with intermittent light exercise) in obese (N = 20) (30<BMI<40Kg/m2) vs. non-obese (N = 20) (BMI<25Kg/m2) non-smoking 18–35 year old women. We measured spirometry and bronchial reactivity to inhaled methacholine (3h post-exposure). Inflammation and obesity markers were assessed in the blood (pre, 4h post, and 20h post exposures) and induced-sputum (4h post-exposures and on 24h pre-exposure training day, no exercise): measures of C reactive protein (CRP) (blood only), leptin (blood only), adiponectin, interleukins IL-6, IL-1b, and IL-8, and tumor necrosis factor alpha, and sputum cell differential cell counts. The pre- to post-exposure decrease in forced vital capacity after ozone (adjusted for the change after air exposure) was significantly greater in the obese group (12.5+/-7.5 vs. 8.0+/-5.8%, p<0.05). Post ozone exposure, 6 obese and 6 non-obese subjects responded to methacholine at ≤ 10mg/ml (the maximum dose); the degree of hyperresponsiveness was similar for the two groups. Both BMI groups showed similar and significant ozone-induced increases in sputum neutrophils. Plasma IL-6 was increased by exercise (4 hr post air exposure vs. pre) only in the obese but returned to pre-air exposure levels at 20hr post-exposure. Plasma IL-6 was significantly increased at 4hr post ozone exposure in both groups and returned to pre-exposure levels by 20h post-exposure. These results confirm our previous findings of greater post-ozone spirometric decrements in obese young women. However, acute ozone-induced airway reactivity to methacholine and airway inflammation did not differ by obesity at the exposure and exercise levels used.

Voluntary wheel exercise ameliorates cognitive impairment, hippocampal neurodegeneration and microglial abnormalities preceded by demyelination in a male mouse model of noise-induced hearing loss

Objectives:Studies on the relationship between occupational noise exposure and extended high-frequency (EHF) hearing loss are limited. This study investigated the relationship between occupational noise exposure and EHF hearing loss in workers exposed to noise as measured by sound pressure level, exposure duration, and kurtosis to help provide a basis for early detection and prevention of hearing loss in noise-exposed workers.Design:A cross-sectional survey was conducted among 602 participants with 472 noise-exposed workers and 130 non-noise-exposed controls. General demographic characteristics, noise exposure data, and hearing thresholds at conventional frequencies (0.25 to 8 kHz) and EHF (9 to 16 kHz) were collected and analyzed. Linear mixed-effects model analyses between hearing thresholds of EHF and noise exposure indicators including the 8-h equivalent continuous A-weighted sound pressure level (LAeq,8h), cumulative noise exposure (CNE), and kurtosis-adjusted CNE (CNE-K) were conducted.Results:Among the 602 participants included in the analysis, 472 individuals (78.4%) were occupationally exposed to noise exposures ≥75 dBA. Significant differences (p < 0.05) were observed in sex, exposure duration, LAeq,8h, CNE, and CNE-K between the noise-exposed group and the nonexposed group. The mean hearing thresholds for all tested extended high frequencies ranging from 9 to 16 kHz were significantly higher in the noise-exposed group than in the nonexposed group (p < 0.05). The mean hearing thresholds of subjects in different groups of LAeq,8h exposures were generally stable with little variance in the conventional frequencies (0.25 to 8 kHz) but differed in the EHF range. Moreover, EHF hearing loss appeared to be most prominent in the subjects exposed to noise with 80 dBA < LAeq,8h ≤ 85 dBA. After the combination of the sound pressure level, exposure duration, and kurtosis by using the noise exposure indicators CNE and CNE-K, the subjects at the different noise exposures showed significant differences in hearing thresholds at EHF (p < 0.05). Linear mixed-effected model analyses showed that the CNE-K was the best to indicate noise-induced hearing loss among the three noise exposure indicators at EHF.Conclusions:The results indicate that the EHF hearing threshold testing is more sensitive to identifying early occupational noise-induced hearing loss than conventional audiometry. The CNE-K, an indicator combining noise energy, exposure duration, and kurtosis, is a more comprehensive and effective method for assessing the risk of EHF hearing loss due to occupational noise exposure.

Sudden or chronic exposure to sound alters the functioning of cochlea. This results in temporary or permanent alteration of functioning of cochlear cells. Alteration of functioning of outer hair cells (OHC) of cochlea following exposure to noise can be assessed by measurement of transient otoacoustic emissions (TEOAE). Such a measurement is of great clinical importance in early detection of the damage to the OHC. In this study we aim to study effect of noise on outer hair cell function by studying the changes in TEOAE's amplitude following exposure to short term broad band noise in healthy volunteers. Twenty volunteers' ten males and ten females participated in the study. They underwent pure tone and impedance audiometry to rule out ear pathology. Then pre-exposure TEOAE's were recorded. After that they were exposed to broad band noise for two minutes. After gap of five minutes again TEOAE's were recorded. Pre and post exposure amplitude of TEOAE's was analysed statistically.s There was statistically significant difference between pre exposure and post-exposure amplitude of TEOAE's. Pre and post exposure values for A & B amplitudes showed p-value of 0.0001 whereas values for A-B amplitude showed p-value of 0.0001. Measurement of TEOAE's can detect early changes in the functioning of outer hair cells which cannot be picked by routine pure tone audiometry. Thus they can be used in assessing early changes in cochlear function following exposure to noise in individuals exposed to sudden noise or working in noisy environments. Thus preventive methods to reduce the noise induced hearing loss in such individuals can be implemented.

Basic and applied aspects of noise-induced hearing loss: R.J. Salvi, D. Henderson, R.P. Hamernik and V. Colletti (Eds.) (Plenum, New York, 1986, 666 p., U.S. $97.50)

In 2017, the Centers for Disease Control and Prevention (CDC) reported that almost 25% of American adults age 20-69 had noise-induced hearing loss (NIHL), with 53% of them reporting no significant noise exposure. 1 If we were in the movie business, our recent paper in Proceedings of Meetings on Acoustics2 might be called a prequel to the CDC report because it explains why so many Americans are losing hearing without occupational noise exposure: They are exposed to too much noise.Shutterstock/ivectorTable 1: Common Nonoccupational Noise Exposures.Occupational hearing loss has been known from stonemasons in the Middle Ages to factory workers in the industrial era, but nonoccupational noise exposure was not recognized as a problem until the 1960s. 3 Before World War II, noise exposure outside the workplace was rare. That changed in postwar America. Convenient electric appliances, home stereo systems boasting about their wattage outputs, the advent of rock and roll music, and the use of amplified sound at parties and life cycle celebrations such as weddings became common. By the end of the 20th century, personal audio systems (PAS), also called personal music players or personal listening devices, were common, with their use accelerating dramatically after PAS became available on MP3 players and then smartphones. Young people especially use PAS to listen to loud music and audio content for hours a day. Often, users must turn up the volume to overcome high ambient noise, especially while commuting. Flamme, et al., found that although people spend most of their time in relatively quiet environments when not at work, total noise exposure is dominated by a small number of high-level exposures. 4 Occupational and nonoccupational noise and auditory risk relationships are based on the time-weighted average (TWA) of regular and intermittent sound levels, commonly measured in A-weighted decibels (dBA), over a specified exposure duration, typically 8-h daily for occupational noise and 24-h for non-occupational noise. 5,6 In the United States, 85 dBA is the recommended occupational noise exposure limit, not a safe noise exposure level for the public. 6 In adult workers, the risk of hearing impairment is 1% at 80 dBA, 8% at 85 dBA, and 25% at 90 dB TWA. 5 Although other etiologies can’t be ruled out on the basis of an audiogram, NIHL typically first develops in the 3-6 kHz speech frequency range. Risk estimates don’t consider additional auditory impairments characteristic of noise damage, including tinnitus, hyperacusis or decreased sound tolerance, speech-in-noise performance deficits, impaired otoacoustic emissions, and extended high-frequency hearing loss. 7,8 CALCULATING SAFE NOISE LEVELS What is the safe noise level for the public? As calculated by the Environmental Protection Agency (EPA), the only evidence-based safe noise exposure level to prevent NIHL is a 24-h daily average of 70 dBA, 6 and even that may be too high. One thing is known for sure: The oft-cited 85 dB threshold is not the sound pressure level at which hearing loss begins. The auditory injury threshold is only 75-78 dBA regardless of listening time. 4 Auditory systems process total sound intensity instantaneously in real-time, not as a TWA. Nonoccupational noise sources are ubiquitous, and most Americans are now exposed to sufficient noise in everyday life to cause NIHL. Flamme, et al., 4 found that 70% of research subjects in Grand Rapids, MI, exceeded the EPA safe noise level. Neitzel, et al., reported that 90% of New York City transit users and 87% of nonusers exceeded the EPA 70 dB safe daily noise limit, 9 as did about 88% of subjects in Sweden, 84% of people studied in Spain, and 85% in China. 10 Smith, et al., analyzing data collected by the Apple Hearing Study, found average daily noise exposure in the United States to be 73 dBA before COVID-19-related lockdowns began in March 2020. 11 These noise exposures, not ear infections, ototoxic drugs, or aging alone, are most likely the cause of the high prevalence of hearing loss reported in industrialized countries. In our paper, we summarized published sound levels from six categories of nonoccupational noise sources common in everyday life. All research was done meeting ethical requirements, using standard equipment (e.g., OSHA Type II noise dosimeters), following accepted audiometric protocols (e.g., ISO 8253-1:2010), with study designs appropriate to the specific question being investigated. Each study cited used different methods in different populations in different settings, but even allowing for variations in instrumentation, possible errors in calibration, observer error, and lack of standardization of measurement, the sound levels were generally consistent among reports from different authors and with our own unpublished measurements. The consistency of the numbers provides great confidence in the generalizability of this research. As shown in Table 1, common nonoccupational noise exposures range from 70 dBA on average at the low end to as much as 111 dBA. The cumulative daily noise dose from all these activities is clearly sufficient to cause NIHL. NIHL is entirely preventable but once acquired is permanent and irreversible. Hearing loss is an invisible disability with major social, health, and economic consequences for individuals and society, costing the global economy $980 billion annually. 12 Early hearing loss is associated with lower educational attainment and decreased lifetime income. Untreated hearing loss in older adults is correlated with increased hospital use and greater total health care costs. Among the elderly, hearing loss is strongly correlated with social isolation, depression, dementia, falls, and accidents, all in turn associated with increased mortality. ROLE OF HEARING CARE PROFESSIONALS Audiologists and physicians, particularly otolaryngologists, have a responsibility to educate the public about nonoccupational noise risk from daily average exposures >70 dBA. Especially in this era of concern about the accuracy of public health -advice, it is no longer acceptable for audiologists to post inaccurate information on their practice websites or to make inaccurate statements in media reports. Misleading statements such as, “Sounds at 85 dBA can lead to hearing loss if you listen to them for more than 8 hours at a time” are still available on the American Speech-Language Hearing Association website, but the National Institute on Deafness and Other Communication Disorders recently removed the factually incorrect statement, “Know which noises can cause damage (those at or above 85 dBA),” from its webpage about NIHL. An 85-dBA noise exposure that doesn’t prevent hearing loss in working adults is far too high for a child’s delicate ears that have to last an entire lifetime. Society should no longer accept common nonoccupational noise exposures. Prevention of NIHL is both better and less expensive than the long-term health care and socioeconomic costs of hearing loss. Smoking was once seen as something normal, a harmless habit. Cigarette smoke was everywhere—in buses, trains, airplanes, offices, even hospitals, and doctors’ waiting rooms. Then science showed that smoking caused cancer, that secondhand smoke was a Class A carcinogen with no safe lower level of exposure, and the air became smoke free. Similarly, excessive noise is now just part of everyday life. We hope that awareness of the dangers of noise will lead to a quieter world. Depending on the source, required noise control includes mandatory noise emission limits and venue noise policies, including hearing protection requirements. Editor’s note: This article is adapted from Fink, D., Mayes, J. Too loud: non-occupational noise exposure is causing hearing loss. Proc. Mtgs. Acoust. 43, 004002 (2021) https://doi.org/10.1121/2.0001436, with the permission of the Acoustical Society of America.

Personal Audio Systems Unsafe At Any Sound

Introdução: A perda auditiva induzida por ruído consiste atualmente em uma das maiores causas de perdas auditivas neurossensoriais. Objetivo: O objetivo desse trabalho foi estudar os limiares de audibilidade e as emissões otoacústicas por produto de distorção, pré e pós-exposição a níveis elevados de ruído branco (100 dB NPS por 10 minutos), em função das variáveis lado da orelha e sexo, buscando informações para estabelecer a eficácia de ambos para detectar pequenas mudanças temporárias no limiar. Forma de estudo: prospectivo clínico randomizado. Material e método: Foram avaliados quarenta indivíduos otologicamente normais, sendo 20 do sexo masculino e 20 do sexo feminino, com idade variando de 18 a 36 anos. Ambos os testes, audiometria tonal e emissões otoacústicas por produto de distorção, foram realizadas de forma prévia e posterior à exposição ao ruído branco. Resultados: Os resultados mostraram que a audiometria tonal liminar é sensível para evidenciar mudanças temporárias nos limiares de audibilidade após exposição ao ruído branco nas freqüências de 2, 3, 4 KHz, independentemente, do lado da orelha e sexo, e que as emissões otoacústicas evidenciaram mudanças temporárias na sensibilidade auditiva após exposição ao ruído através da redução de suas amplitudes, nas freqüências de 2588 e 3614 Hz para o sexo feminino e nas freqüências de 932, 1304, 2588, 5128 Hz para o sexo masculino. Conclusão: Concluímos que tanto a audiometria tonal quanto as emissões otoacústicas evidenciaram sensibilidade para detectar mudanças temporárias significantes nos limiares de audibilidade e amplitudes, respectivamente, após a exposição ao ruído, variando de acordo com as freqüências estudadas.

Previous animal studies have shown that stromal cell-derived factor-1 (SDF-1)/CXC chemokine receptor-4 (CXCR4) signaling pathway plays an important role in the targeted migration of bone marrow-derived mesenchymal stem cells (BMSCs) to the injured area. In the present study, we aimed to investigate the potential role of chemotactic SDF-1/CXCR4 signaling pathway in the homing of transplanted BMSCs to the injured cochlea after noise-induced hearing loss (NIHL) in a rat model. White noise exposure (110 dB) paradigm was used for hearing loss induction in male rats for 6 hours in 5 days. Distortion-product otoacoustic emission (DPOAE) responses were recorded before the experiment and post noise exposure. Hoechst 33342-labeled BMSCs and CXCR4 antagonist (AMD3100)-treated BMSCs were injected into the rat cochlea through the round window. SDF-1 protein expression in the cochlear tissue was assayed using western blot assay. The number of labeled BMSCs reaching the endolymph was determined after 24 hours. SDF-1 was significantly increased in the cochlear tissue of rats in the noise exposure group than in the control group. The number of Hoechst 33342-labeled BMSCs reaching the endolymph of the cochlea was significantly smaller in the AMD3100-treated BMSCs group than in the normal BMSCs group. Our present findings suggest that the SDF-1/CXCR4 signaling pathway has a critical role in BMSCs migration to the injured cochlea in a rat model of noise-induced hearing loss.

Background: Noise is defined as sound intensity that is unwanted and can pose risks to health and safety at work, such as the risk of hypertension and noise-induced hearing loss. This study aims to analyze the effect of occupational noise on the risk of hypertension and noise induced hearing loss in industrial workers.Subjects and Method: A systematic review and meta-analysis was carried out using the PRISMA guidelines and the PICO model. Population: industrial workers. Intervention: occupational noise exposure ≥85 dB. Comparison: occupational noise exposure &lt;85 dB. Outcome: hypertension and noise induced hearing loss. Articles are collected from PubMed, Science Direct, and Google Schoolar. The keywords used “occupational noise and hypertension” OR “occupational noise and hearing loss” AND “occupational noise” OR “hypertension” AND “hearing loss” AND “cross sectional study”. A total of 13 articles met the inclusion criteria, namely primary full text paper, cross-sectional study design, with a relationship size adjusted Odds Ratio (aOR), labor research subjects, interventions in the form of exposure to noise ≥85 dB and outcomes in the form of hypertension and noise induced hearing loss for meta-analyses were then assessed using RevMan 5.3.Results: Meta-analysis included 13 cross sectional studies from China, Brazil, Ethiopia, Jordan, South Africa, Thailand, Kuwait, and Pakistan. Occupational noise ≥85 dB significantly increased the risk of hypertension (aOR= 2.07; 95% CI= 1.31 to 3.26; p= 0.002) and hearing loss (aOR= 1.97; 95% CI= 1.36 to 2.85; p= 0.003) than occupational noise &lt;85 dB.Conclusion: Occupational noise ≥85 dB increases the risk of hypertension and hearing loss in industrial workers. Keywords: occupational noise, hypertension, hearing loss, workers Correspondence:Ila Izzatus Salamah. Masters Program in Public Health, Universitas Sebelas Maret. Jl. Ir. Sutami 36A, Surakarta 57126, Central Java, Indonesia. Email: ilaizzatus31@gmail.com. Mobile: +62858868132490.

Objective. A study was conducted to verify if there is an association between occupational noise exposure, noise-induced hearing loss and driving safety expanding on previous findings by Picard, et al. (2008) that the two factors did increase accident risk in the workplace. Methods. This study was made possible when driving records of all Quebec drivers were made available by the Société de l'assurance automobile du Québec (SAAQ is the state monopoly responsible for the provision of motor vehicle insurance and the compensation of victims of traffic accidents). These records were linked with personal records maintained by the Quebec National Institute of Public Health as part of its mission to prevent noise induced hearing loss in the workplace. Individualized information on occupational noise exposure and hearing sensitivity was available for 46,030 male workers employed in noisy industries who also held a valid driver's permit. The observation period is of five years duration, starting with the most recent audiometric examination. The associations between occupational noise exposure levels, hearing status, and personal driving record were examined by log-binomial regression on data adjusted for age and duration of exposure. Daily noise exposures and bilateral average hearing threshold levels at 3, 4, and 6 kHz were used as independent variables while the dependent variables were 1) the number of motor vehicle accidents experienced by participants during the study period and 2) participants' records of registered traffic violations of the highway safety code. The findings are reported as prevalence ratios (PRs) with their 95% confidence intervals (CIs). Attributable numbers of events were computed with the relevant PRs, lesser-noise, exposed workers and those with normal hearing levels making the group of reference. Results. Adjusting for age confirmed that experienced workers had fewer traffic accidents. The data show that occupational noise exposure and hearing loss have the same effect on driving safety record than that reported on the risk of accident in noisy industrial settings. Specifically, the risk of traffic accident (PR = 1.07 (CI 95% [1.01; 1.15]) is significantly associated with the daily occupational noise exposures ≥ 100 dBA. For participants having a bilateral average hearing loss ranging from 16 to 30 dB, the PR of traffic accident is 1.06 (CI 95% [1.01; 1.11]) and reaches 1.31 (CI 95% [1.2; 1.42]) when the hearing loss exceeds of 50 dB. A reduction in the number of speeding violations occurred among workers occupationally exposed to noise levels ≥ 90 dBA and those with noise-induced hearing loss ≥16 dB. By contrast, the same individuals had an increase in other violations of the Highway safety code. This suggests that noise-exposed workers might be less vigilant to other traffic hazards. Conclusion. Daily occupational noise exposures ≥ 100 dBA and noise-induced hearing losses—even when just barely noticeable—may interfere with the safe operation of motor vehicles.

The clinical application of click-evoked otoacoustic emissions (EOAE) in the assessment of noise-induced hearing loss (NIHL) was examined in a group of 72 ears with NIHL and 61 ears with normal hearing (NH). The characteristics of the EOAE in ears with NIHL significantly differed from the NH, according to all EOAE parameters tested in the present study. The mean overall EOAE level was lower and the mean EOAE nonlinearity threshold was worse in the NIHL group. In 95% of the NH ears the EOAE spectrum range was wide, while in 91.5% of the NIHL ears the range was narrow. Moreover, in 94% of the ears with NIHL, the frequency at which the hearing loss began (BHL) was at or above the frequency of the last peak in the EOAE spectrum (FLP). Furthermore, combination of EOAE spectral measures correctly discriminate on average 93.5% of ears with NH from NIHL (sensitivity) and 92% of ears with NIHL from NH (specificity). In contrast, the nonlinearity threshold and the overall level of EOAE yielded lower specificity of less than 33%. It was therefore concluded that EOAE spectrum may serve as a useful and objective tool in screening adults with suspected noise-induced high frequency hearing loss.

BackgroundBoth environmental and genetic factors are attributable to the incidence of noise-induced hearing loss (NIHL). The purpose of this study was to examine the associations between genetic variations in the EYA4, GRHL2 and DFNA5 genes and the risk to noise-induced hearing loss (NIHL) in a Chinese population.MethodsA case–control study was conducted with 476 NIHL workers and 475 normal hearing workers matched with gender, years of noise exposure, and intensity of noise exposure. Twelve tag single-nucleotide polymorphisms (SNP) in the EYA4, GRHL2 and DFNA5 genes were genotyped using nanofluidic dynamic arrays on the Fluidigm platform. Multiple logistic regression was used to analyze the associations of genetic variations with NIHL adjusted by age, smoking/drinking status, and cumulative noise exposure and their interactions with noise exposure.ResultsThe SNPs of rs3777781and rs212769 in the EYA4 gene were significantly associated with NIHL risk. In rs3777781, comparing with the subjects carrying with TT types, the carriers with AT and AA genotypes had the decreased risk of NIHL (OR = 0.721, 95 % CI = 0.522 - 0.996). In rs212769, the AG and AA carriers had increased NIHL risk (OR = 1.430, 95 % CI = 1.014 - 2.016) compared with the subjects with GG genotype. Rs666026 in the associated GRHL2 gene and rs2521758 in the DFNA5 gene were marginally t associated with NIHL (P = 0.065 and 0.052, respectively). Rs2521758 and rs212769 had significantly interacted with noise exposure (P < 0.05).ConclusionsGenetic variations in the EYA4, GRHL2 and DFNA5 genes and their interactions with occupational noise exposure may play an important role in the incidence of NIHL.

Noise-induced hearing loss (NIHL) may result from occupational noise exposures and is considered as an 'Occupational Disease'; therefore, it is compensable. To verify the existence and severity of the work-related hearing loss, there is a need of an objective, reliable auditory measure in cases of arbitration of financial disputes to resolve any medicolegal aspects. The objective of the study was to compare between the ABR and ASSR for predicting the behavioural threshold in subjects with normal hearing or NIHL. The study included 82 subjects regularly exposed to high levels of occupational noise, with normal hearing and NIHL. ABR to clicks and to tone bursts were recorded followed by multiple-frequency ASSR. Physiological and behavioural thresholds were compared for specific frequencies (1000, 2000 Hz) and average of high-frequency range (2000 and 4000 Hz). In addition, Pearson correlations and the specificity and sensitivity of each measure were also calculated using receiver operating characteristic (ROC) curves. In the NIHL group, there was a significantly smaller difference between the behavioural threshold and click-ABR than the ASSR in high-frequency range. Pearson correlations were significantly higher for click-ABR. Analysis of specific frequencies yielded a smaller difference between behavioural and ASSR than tone-burst-ABR thresholds, with a slightly better correlation for ASSR than tone-burst-ABR. Higher sensitivity but lower specificity was suggested for ASSR than ABR. ASSR is associated with high-frequency specificity, shorter test sessions and good correlations with behavioural thresholds, making it a potentially better measure than ABR for predicting audiograms in subjects with NIHL. These findings have diagnostic implications, especially in cases of workers' compensation when subjects may be uncooperative.

A 41‐year‐old male firefighter arrived at a hospital emergency room 43 h post acute noise exposure (mechanical siren, 2.5 min total exposure time in an enclosed space) with complaints of tinnitus, decreased hearing, and vague balance problems. He was subsequently evaluated in an otolaryngology clinic and an audiology clinic. The presented complaints resolved during the next month. The subject did return for follow‐up. ENT findings were unremarkable at both visits. OSHA baseline audiometrics, audiometry at 47 h post noise insult, and audiometry at 30 days post noise exposure were reviewed. Extended high‐frequency audiometry (8 to 20 kHz) was obtained during the initial hospital audiometry (47 h post noise insult) and at the time of the follow‐up audiometry. Conventional audiometry and extended high‐frequency threshold data were explored and changes in threshold hearing acuity were examined for potential correlation with subjective complaints. Extended high‐tone andiometry did suggest a tenuous correlation with the presented complaints. Formal sound pressure readings during mechanical siren operation were taken at the site of noise exposure to delineate noise dosage. Implications of siren noise exposure on long‐term hearing sensitivity change were explored.