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1.
Commun Biol ; 7(1): 421, 2024 Apr 06.
Artigo em Inglês | MEDLINE | ID: mdl-38582813

RESUMO

Moderate noise exposure induces cochlear synaptopathy, the loss of afferent ribbon synapses between cochlear hair cells and spiral ganglion neurons, which is associated with functional hearing decline. Prior studies have demonstrated noise-induced changes in the distribution and number of synaptic components, but the dynamic changes that occur after noise exposure have not been directly visualized. Here, we describe a live imaging model using RIBEYE-tagRFP to enable direct observation of pre-synaptic ribbons in mature hearing mouse cochleae after synaptopathic noise exposure. Ribbon number does not change, but noise induces an increase in ribbon volume as well as movement suggesting unanchoring from synaptic tethers. A subgroup of basal ribbons displays concerted motion towards the cochlear nucleus with subsequent migration back to the cell membrane after noise cessation. Understanding the immediate dynamics of synaptic damage after noise exposure may facilitate identification of specific target pathways to treat cochlear synaptopathy.


Assuntos
Perda Auditiva Provocada por Ruído , Animais , Camundongos , Perda Auditiva Provocada por Ruído/etiologia , Perda Auditiva Provocada por Ruído/metabolismo , Cóclea , Audição , Ruído/efeitos adversos , Sinapses/fisiologia
2.
Sci Rep ; 14(1): 7058, 2024 03 25.
Artigo em Inglês | MEDLINE | ID: mdl-38528033

RESUMO

In the present study, an attempt has been made to assess the impact of vehicular noise upon the 3-wheeler tempo drivers and to know whether there is any relationship between hearing loss and cumulative noise exposure. For this purpose, 3-wheeler tempo drivers (Exposed group) and non-commercial light motor vehicle car drivers (Unexposed group) were chosen as study subjects. Three traffic routes were selected to assess the noise level during waiting and running time in the exposed and unexposed groups. Among all three routes, the highest mean noise level (Leq) was observed on the Chowk to Dubagga route for waiting and en-route noise measurement. It was measured as 84.13 dB(A) and 86.36 dB(A) for waiting and en-route periods of 7.68 ± 3.46 and 31.05 ± 6.6 min, respectively. Cumulative noise exposure was found to be significantly different (p < 0.001) in all age groups of exposed and unexposed drivers. Audiometric tests have been performed over both exposed and unexposed groups. The regression analysis has been done keeping hearing loss among tempo drivers as the dependent variable and age (years) and Energy (Pa2 Hrs) as the independent variable using three different criteria of hearing loss definitions, i.e., World Health Organization, National Institute for Occupational Safety and Health (NIOSH), Occupational Safety and Health Administration criteria. Among these three criteria, the NIOSH criterion of hearing loss best explained the independent variables. It could explain the total variation in dependent variable by independent variable quite well, i.e., 68.1%. The finding showed a linear relationship between cumulative noise exposures (Pa2 Hrs) and the exposed group's hearing loss (dB), i.e., hearing loss increases with increasing noise dose. Based on the findings, two model equations were developed to identify the safe and unsafe noise levels with exposure time.


Assuntos
Surdez , Perda Auditiva Provocada por Ruído , Ruído Ocupacional , Doenças Profissionais , Exposição Ocupacional , Humanos , Perda Auditiva Provocada por Ruído/diagnóstico , Perda Auditiva Provocada por Ruído/epidemiologia , Perda Auditiva Provocada por Ruído/etiologia , Cidades , Ruído Ocupacional/efeitos adversos , Exposição Ocupacional/efeitos adversos , Exposição Ocupacional/análise , Análise de Regressão , Índia/epidemiologia
3.
Trends Hear ; 28: 23312165241240353, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-38545653

RESUMO

Exposure to intense low-frequency sounds, for example inside tanks and armoured vehicles, can lead to noise-induced hearing loss (NIHL) with a variable audiometric pattern, including low- and mid-frequency hearing loss. It is not known how well existing methods for diagnosing NIHL apply in such cases. Here, the audiograms of 68 military personnel (mostly veterans) who had been exposed to intense low-frequency noise (together with other types of noise) and who had low-frequency hearing loss (defined as a pure-tone average loss at 0.25, 0.5 and 1 kHz ≥20 dB) were used to assess the sensitivity of three diagnostic methods: the method of Coles, Lutman and Buffin, denoted CLB, which depends on the identification of a notch or bulge in the audiogram near 4 kHz, and two methods specifically intended for diagnosing NIHL sustained during military service, the rM-NIHL method, which depends on the identification of a notch or bulge in the audiogram near 4 kHz and/or a hearing loss at high frequencies greater than expected from age alone, and the MLP(18) method based on a multi-layer perceptron. The proportion of individuals receiving a positive diagnosis for either or both ears, which provides an approximate measure of sensitivity, was 0.40 for the CLB method, 0.79 for the rM-NIHL method and 1.0 for the MLP(18) method. It is concluded that the MLP(18) method is suitable for diagnosing NIHL sustained during military service whether or not the exposure includes intense low-frequency sounds.


Assuntos
Surdez , Perda Auditiva Provocada por Ruído , Ruído Ocupacional , Humanos , Perda Auditiva Provocada por Ruído/diagnóstico , Perda Auditiva Provocada por Ruído/epidemiologia , Perda Auditiva Provocada por Ruído/etiologia , Audiometria/métodos , Testes Auditivos
4.
Hear Res ; 445: 108996, 2024 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-38547565

RESUMO

Acute noise-induced loss of synapses between inner hair cells (IHCs) and auditory nerve fibers (ANFs) has been documented in several strains of mice, but the extent of post-exposure recovery reportedly varies dramatically. If such inter-strain heterogeneity is real, it could be exploited to probe molecular pathways mediating neural remodeling in the adult cochlea. Here, we compared synaptopathy repair in CBA/CaJ vs. C57BL/6J, which are at opposite ends of the reported recovery spectrum. We evaluated C57BL/6J mice 0 h, 24 h, 2 wks or 8 wks after exposure for 2 h to octave-band noise (8-16 kHz) at either 90, 94 or 98 dB SPL, to compare with analogous post-exposure results in CBA/CaJ at 98 or 101 dB. We counted pre- and post-synaptic puncta in immunostained cochleas, using machine learning to classify paired (GluA2 and CtBP2) vs. orphan (CtBP2 only) puncta, and batch-processing to quantify immunostaining intensity. At 98 dB, both strains show ongoing loss of ribbons and synapses between 0 and 24 h, followed by partial recovery, however the extent and degree of these changes were greater in C57BL/6J. Much of the synaptic recovery is due to transient reduction in GluA2 intensity in synaptopathic regions. In contrast, CtBP2 intensity showed only transient increases (at 2 wks). Neurofilament staining revealed transient extension of ANF terminals in C57BL/6J, but not in CBA/CaJ, peaking at 24 h and reverting by 2 wks. Thus, although interstrain differences in synapse recovery are dominated by reversible changes in GluA2 receptor levels, the neurite extension seen in C57BL/6J suggests a qualitative difference in regenerative capacity.


Assuntos
Perda Auditiva Provocada por Ruído , Camundongos , Animais , Perda Auditiva Provocada por Ruído/etiologia , Perda Auditiva Provocada por Ruído/metabolismo , Camundongos Endogâmicos C57BL , Limiar Auditivo/fisiologia , Potenciais Evocados Auditivos do Tronco Encefálico/fisiologia , Camundongos Endogâmicos CBA , Cóclea/metabolismo , Sinapses/metabolismo
5.
Int Tinnitus J ; 27(2): 119-125, 2024 Mar 21.
Artigo em Inglês | MEDLINE | ID: mdl-38507624

RESUMO

BACKGROUND: Noise-Induced Hearing Loss (NIHL) is a prevalent occupational hazard among healthcare professionals, including medical students. Despite its detrimental effects, the awareness and utilization of hearing protection measures among medical students in Saudi Arabia remain understudied. OBJECTIVE: Is to determine the level of awareness and understanding of NIHL among medical students in Saudi Arabia, as well as their knowledge and usage of hearing protection measures and to identify potential barriers and facilitators for hearing protection utilization. METHODS: A mixed-methods approach was employed, involving a questionnaire survey and semi-structured interviews. The survey collected data on demographics, knowledge of NIHL, and hearing protection practices among medical students. Subsequently, a semi-structured interview was conducted to obtain in-depth insights into the students' experiences, attitudes, and beliefs regarding NIHL and the use of hearing protection. RESULTS: The level about NIHL was 59.32%. Better access to information is associated with increased odds of awareness (odds ratio=3.07, p=0.012). Having relatives with hearing loss increases the odds of awareness (odds ratio =2.49, p=0.034). Individuals with hearing loss or impairment have higher odds of awareness (odds ratio =2.27, p=0.046). Ear Pain, temporary hearing loss, tinnitus, or ringing in the ear: These factors are not significantly associated with awareness of noise-induced hearing loss (p>0.05). Using hearing aids is strongly associated with increased odds of awareness (odds ratio =3.94, p=0.006).The quantitative analysis provided statistical information on the prevalence rates and factors influencing hearing protection usage, while the qualitative analysis uncover nuanced perspectives and experiences. CONCLUSION: This research will contribute to the understanding of NIHL and hearing protection practices among medical students in Saudi Arabia. Improving hearing protection awareness and practices among medical students can ultimately reduce the incidence of NIHL and promote a healthier work environment within the healthcare sector.


Assuntos
Surdez , Perda Auditiva Provocada por Ruído , Ruído Ocupacional , Estudantes de Medicina , Zumbido , Humanos , Perda Auditiva Provocada por Ruído/epidemiologia , Perda Auditiva Provocada por Ruído/etiologia , Perda Auditiva Provocada por Ruído/prevenção & controle , Arábia Saudita/epidemiologia , Zumbido/etiologia , Audição , Ruído Ocupacional/efeitos adversos , Ruído Ocupacional/prevenção & controle
6.
J Acoust Soc Am ; 155(2): 867-878, 2024 02 01.
Artigo em Inglês | MEDLINE | ID: mdl-38310604

RESUMO

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.


Assuntos
Perda Auditiva Provocada por Ruído , Percepção da Fala , Humanos , Pessoa de Meia-Idade , Masculino , Feminino , Animais , Camundongos , Vocalização Animal , Ruído/efeitos adversos , Perda Auditiva Provocada por Ruído/etiologia , Teste do Limiar de Recepção da Fala , Limiar Auditivo
7.
J Acoust Soc Am ; 155(2): 1368-1378, 2024 02 01.
Artigo em Inglês | MEDLINE | ID: mdl-38364041

RESUMO

Chronic exposure to loud sound leads to noise-induced hearing loss. This is especially common in collegiate-level musicians. Existing methods for estimating exposure typically do not consider genre- or instrument-specific variability in soundscape/spectral characteristics. We measured sound exposure levels (SELs) across instruments, bands, and genres at a university music school. We found (1) considerable variability in SELs across instruments and bands, (2) that Jazz musicians are consistently exposed to the highest sound levels, and (3) that spectral features of music differ between instrument type and genre, and based on room size. These findings highlight the need for tailored guidelines that moderate the implementation of hearing conservation initiatives for collegiate musicians.


Assuntos
Perda Auditiva Provocada por Ruído , Música , Humanos , Perda Auditiva Provocada por Ruído/etiologia , Perda Auditiva Provocada por Ruído/prevenção & controle , Som , Estudantes , Acústica
8.
J Vet Med Sci ; 86(4): 381-388, 2024 Apr 01.
Artigo em Inglês | MEDLINE | ID: mdl-38369331

RESUMO

Sensorineural hearing loss (SNHL) induced by noise has increased in recent years due to personal headphone use and noisy urban environments. The study shows a novel model of gradually progressive SNHL induced by repeated exposure to moderate noise (8-kHz octave band noise, 90-dB sound pressure level) for 1 hr exposure per day in BALB/cCr mice. The results showed that the repeated exposure led to gradually progressive SNHL, which was dependent on the number of exposures, and resulted in permanent hearing loss after 5 exposures. Repeated exposure to noise causes a loss of synapses between the inner hair cells and the peripheral terminals of the auditory nerve fibers. Additionally, there is a reduction in the expression levels of c-fos and Arc, both of which are indicators of cochlear nerve responses to noise exposure. Oral administration of resveratrol (RSV, 50 mg/kg/day) during the noise exposure period significantly prevented the noise exposure-induced synapse loss and SNHL. Furthermore, the study found that RSV treatment prevented the noise-induced increase in the gene expression levels of the proinflammatory cytokine interleukin-1ß in the cochlea. These results demonstrated the potential usefulness of RSV in preventing noise-induced SNHL in the animal model established as gradually progressive SNHL.


Assuntos
Perda Auditiva Provocada por Ruído , Perda Auditiva Neurossensorial , Doenças dos Roedores , Camundongos , Animais , Resveratrol/uso terapêutico , Ruído/efeitos adversos , Perda Auditiva Neurossensorial/prevenção & controle , Perda Auditiva Neurossensorial/complicações , Perda Auditiva Neurossensorial/veterinária , Perda Auditiva Provocada por Ruído/prevenção & controle , Perda Auditiva Provocada por Ruído/etiologia , Perda Auditiva Provocada por Ruído/veterinária , Cóclea
9.
Int Arch Occup Environ Health ; 97(4): 365-375, 2024 May.
Artigo em Inglês | MEDLINE | ID: mdl-38421415

RESUMO

BACKGROUND: High-frequency hearing loss (HFHL) stands as a prevalent occupational morbidity globally, with numerous associated risk factors, some of which are modifiable. In the context of a comprehensive hearing conservation program, the initial steps involve early screening and identification of workers with these modifiable risk factors, aiming to reduce the prevalence of hearing loss. Our objective was to estimate the prevalence of HFHL and determine its predictors among mine workers. METHODS: We conducted a cross-sectional study among 226 mine workers in ten open-cast mines in Gujarat state, the western part of India, in November 2020. We collected data on socio-demography, addiction, occupation history and comorbidities, along with anthropometric, blood pressure, and blood sugar measurements. Audiometric evaluations using a portable diagnostic audiometer were employed to assess HFHL, defined as a hearing threshold exceeding 25 decibels (dB) at high frequencies (3000, 4000, 6000, and 8000 Hz). A generalized linear model (GLM) with a binomial family was performed to determine the predictors significantly predicting HFHL after adjusting for confounding variables. RESULTS: The prevalence of HFHL was 35% (95% CI: 29-42%) in our study setting. Office workers demonstrated a prevalence of 19%, whereas other job categories displayed a higher prevalence of 42%, resulting in a significant prevalence difference of 23% and a prevalence ratio of 2.2. The GLM analysis revealed that variables, such as noise exposure during work [adjusted prevalence ratio (aPR) 2.3 (95% CI: 1.2-4.7, p = 0.018)] and noise exposure duration [aPR 1.1 (95% CI: 1.0-1.1, p = 0.042)], were significant predictors of HFHL. CONCLUSIONS: In our study setting, mine workers exhibited a high prevalence of HFHL, with exposure to workplace noise and duration being modifiable predictors. Because HFHL advances slowly and is generally undetected by the individual, we recommend periodic testing using audiometry to identify it among mine workers and, if possible, shifting them from mining activities to office. Furthermore, we advocate for the implementation of a comprehensive hearing conservation program to the extent possible.


Assuntos
Perda Auditiva Provocada por Ruído , Mineradores , Ruído Ocupacional , Doenças Profissionais , Exposição Ocupacional , Humanos , Perda Auditiva de Alta Frequência/complicações , Perda Auditiva de Alta Frequência/epidemiologia , Estudos Transversais , Prevalência , Perda Auditiva Provocada por Ruído/diagnóstico , Perda Auditiva Provocada por Ruído/epidemiologia , Perda Auditiva Provocada por Ruído/etiologia , Índia/epidemiologia , Doenças Profissionais/etiologia , Audição , Ruído Ocupacional/efeitos adversos , Exposição Ocupacional/efeitos adversos
10.
ACS Nano ; 18(8): 6298-6313, 2024 Feb 27.
Artigo em Inglês | MEDLINE | ID: mdl-38345574

RESUMO

Noise-induced hearing loss (NIHL) often accompanies cochlear synaptopathy, which can be potentially reversed to restore hearing. However, there has been little success in achieving complete recovery of sensorineural deafness using nearly noninvasive middle ear drug delivery before. Here, we present a study demonstrating the efficacy of a middle ear delivery system employing brain-derived neurotrophic factor (BDNF)-poly-(dl-lactic acid-co-glycolic acid) (PLGA)-loaded hydrogel in reversing synaptopathy and restoring hearing function in a mouse model with NIHL. The mouse model achieved using the single noise exposure (NE, 115 dBL, 4 h) exhibited an average 20 dBL elevation of hearing thresholds with intact cochlear hair cells but a loss of ribbon synapses as the primary cause of hearing impairment. We developed a BDNF-PLGA-loaded thermosensitive hydrogel, which was administered via a single controllable injection into the tympanic cavity of noise-exposed mice, allowing its presence in the middle ear for a duration of 2 weeks. This intervention resulted in complete restoration of NIHL at frequencies of click, 4, 8, 16, and 32 kHz. Moreover, the cochlear ribbon synapses exhibited significant recovery, whereas other cochlear components (hair cells and auditory nerves) remained unchanged. Additionally, the cochlea of NE treated mice revealed activation of tropomyosin receptor kinase B (TRKB) signaling upon exposure to BDNF. These findings demonstrate a controllable and minimally invasive therapeutic approach that utilizes a BDNF-PLGA-loaded hydrogel to restore NIHL by specifically repairing cochlear synaptopathy. This tailored middle ear delivery system holds great promise for achieving ideal clinical outcomes in the treatment of NIHL and cochlear synaptopathy.


Assuntos
Surdez , Glicolatos , Perda Auditiva Provocada por Ruído , Animais , Camundongos , Fator Neurotrófico Derivado do Encéfalo/uso terapêutico , 60707 , Hidrogéis , Estimulação Acústica/efeitos adversos , Limiar Auditivo , Potenciais Evocados Auditivos do Tronco Encefálico/fisiologia , Perda Auditiva Provocada por Ruído/etiologia , Surdez/complicações , Orelha Média
11.
Hear Res ; 443: 108967, 2024 Mar 01.
Artigo em Inglês | MEDLINE | ID: mdl-38335624

RESUMO

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.


Assuntos
Perda Auditiva Provocada por Ruído , Animais , Humanos , Perda Auditiva Provocada por Ruído/diagnóstico , Perda Auditiva Provocada por Ruído/etiologia , Ruído , Limiar Auditivo/fisiologia , 60707 , Percepção Auditiva , Cóclea , Sinapses , Potenciais Evocados Auditivos do Tronco Encefálico/fisiologia
12.
J Speech Lang Hear Res ; 67(2): 688-710, 2024 Feb 12.
Artigo em Inglês | MEDLINE | ID: mdl-38324255

RESUMO

PURPOSE: There is an increasing concern regarding hazardous recreational noise exposure among adolescents and young adults. Daily exposure to loud sound levels over a long period of time can increase the risk of noise-induced hearing loss. The full extent of the impact of recreational noise on hearing is not yet fully understood. The purpose of this review was to synthesize research that investigated hearing function in relation to recreational noise exposure in adolescents and young adults. METHOD: A systematic literature search of five databases covering the years 2000-2023 was performed. The articles included investigated audiological measurements of hearing function in relation to recreational noise exposure. RESULTS: Four hundred sixty records were identified, of which 20 met the inclusion criteria and were included in the results. This review showed that although some recreational noise activities can be potentially harmful, there is an unclear relationship between exposure and outcome. Some findings indicated hearing threshold shifts or reduced otoacoustic emission amplitudes after recreational noise exposure, but most changes were short term and in the extended high-frequency range. CONCLUSIONS: There seemed to be inconsistencies regarding the utilization of methods of measuring exposure and outcome between studies. This might be one reason for the differing results in studies on the reported impact on hearing function from recreational noise exposure. To draw more certain conclusions about long-term effects, there is a need for longitudinal research that utilizes sound level measurements to assess low and high degrees of recreational noise exposure in relation to hearing function. SUPPLEMENTAL MATERIAL: https://doi.org/10.23641/asha.25114193.


Assuntos
Perda Auditiva Provocada por Ruído , Audição , Humanos , Adolescente , Adulto Jovem , Ruído/efeitos adversos , Perda Auditiva Provocada por Ruído/epidemiologia , Perda Auditiva Provocada por Ruído/etiologia , Emissões Otoacústicas Espontâneas , Testes Auditivos
13.
S Afr J Commun Disord ; 71(1): e1-e12, 2024 Jan 17.
Artigo em Inglês | MEDLINE | ID: mdl-38299534

RESUMO

BACKGROUND:  Negative attitudes and beliefs are major contributing factors to the rising numbers of noise-induced hearing loss (NIHL) cases in coal mines both locally and internationally. International literature confirms limited knowledge surrounding employees' attitudes and beliefs regarding NIHL and hearing protection devices (HPDs), hence the need for the study. OBJECTIVES:  To ascertain the attitudes and beliefs about NIHL and HPD use among employees at a large scale underground coal mine in Mpumalanga. METHOD:  A descriptive and exploratory cross-sectional study was conducted using a self-administered questionnaire, developed by the National Institute for Occupational Safety and Health (NIOSH) on Beliefs about Hearing Protection and Hearing Loss (BHPHL). Participants (n = 241) included employees from a coal mine in Mpumalanga, South Africa. RESULTS:  Out of 241 completed surveys, this study found that 84% were aware of when to replace earmuffs; 95% believed wearing HPDs could prevent hearing loss in noisy environments; 83% felt their hearing was impacted by loud noise. Additionally, 86% mentioned discomfort from earmuff pressure; 95% emphasised HPD importance; and 95% used HPDs around loud sounds. Moreover, 98% knew how to properly wear earplugs, while lower education levels were linked to higher susceptibility to NIHL. CONCLUSION:  The study identified positive attitudes towards NIHL and HPD use, but existing NIHL cases must be acknowledged. Organisations can use the findings to develop tailored hearing conservation programmes (HCP), including education, involving employees in protection decisions and promoting diligent HPD usage.Contribution: This study contributes to the limited literature on noise perceptions, NIHL, and HPD use in mining, emphasising the impact attitude has on HPD use and assessing the effect of miners NIHL knowledge on compliance. The findings, unique to coal mining, hold significance for enhancing hearing conservation and reducing NIHL.


Assuntos
Perda Auditiva Provocada por Ruído , Doenças Profissionais , Humanos , Perda Auditiva Provocada por Ruído/etiologia , Perda Auditiva Provocada por Ruído/prevenção & controle , África do Sul , Estudos Transversais , Audição , Carvão Mineral , Doenças Profissionais/etiologia , Doenças Profissionais/prevenção & controle
14.
BMC Public Health ; 24(1): 541, 2024 Feb 21.
Artigo em Inglês | MEDLINE | ID: mdl-38383328

RESUMO

INTRODUCTION: An increasing number of original studies suggested that occupational noise exposure might be associated with the risk of hypertension, but the results remain inconsistent and inconclusive. In addition, the attributable fraction (AF) of occupational noise exposure has not been well quantified. We aimed to conduct a large-scale occupational population-based study to comprehensively investigate the relationship between occupational noise exposure and blood pressure and different hypertension subtypes and to estimate the AF for hypertension burden attributable to occupational noise exposure. METHODS: A total of 715,135 workers aged 18-60 years were included in this study based on the Key Occupational Diseases Surveillance Project of Guangdong in 2020. Multiple linear regression was performed to explore the relationships of occupational noise exposure status, the combination of occupational noise exposure and binaural high frequency threshold on average (BHFTA) with systolic and diastolic blood pressure (SBP, DBP). Multivariable logistic regression was used to examine the relationshipassociation between occupational noise exposure status, occupational noise exposure combined with BHFTA and hypertension. Furthermore, the attributable risk (AR) was calculated to estimate the hypertension burden attributed to occupational exposure to noise. RESULTS: The prevalence of hypertension among occupational noise-exposed participants was 13·7%. SBP and DBP were both significantly associated with the occupational noise exposure status and classification of occupational noise exposure combined with BHFTA in the crude and adjusted models (all P < 0·0001). Compared with workers without occupational noise exposure, the risk of hypertension was 50% greater among those exposed to occupational noise in the adjusted model (95% CI 1·42-1·58). For participants of occupational noise exposed with BHFTA normal, and occupational noise exposed with BHFTA elevated, the corresponding risks of hypertension were 48% (1·41-1·56) and 56% (1·46-1·63) greater than those of occupational noise non-exposed with BHFTA normal, respectively. A similar association was found in isolated systolic hypertension (ISH) and prehypertension. Subgroup analysis by sex and age showed that the positive associations between occupational noise exposure and hypertension remained statistically significant across all subgroups (all P < 0.001). Significant interactions between occupational noise status, classification of occupational noise exposure combined with BHFTA, and age in relation to hypertension risk were identified (all P for interaction < 0.001). The associations of occupational noise status, classification of occupational noise exposure combined with BHFTA and hypertension were most pronounced in the 18-29 age groups. The AR% of occupational noise exposure for hypertension was 28·05% in the final adjusted model. CONCLUSIONS: Occupational noise exposure was positively associated with blood pressure levels and the prevalence of hypertension, ISH, and prehypertension in a large occupational population-based study. A significantly increased risk of hypertension was found even in individuals with normal BHFTA exposed to occupational noise, with a further elevated risk observed in those with elevated BHFTA. Our findings provide epidemiological evidence for key groups associated with occupational noise exposure and hypertension, and more than one-fourth of hypertension cases would have been prevented by avoiding occupational noise exposure.


Assuntos
Perda Auditiva Provocada por Ruído , Hipertensão , Ruído Ocupacional , Doenças Profissionais , Exposição Ocupacional , Pré-Hipertensão , Humanos , Ruído Ocupacional/efeitos adversos , Estudos Transversais , Hipertensão/epidemiologia , Hipertensão/etiologia , Exposição Ocupacional/efeitos adversos , Exposição Ocupacional/análise , Doenças Profissionais/epidemiologia , Perda Auditiva Provocada por Ruído/etiologia , China/epidemiologia
15.
Exp Brain Res ; 242(1): 257-265, 2024 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-38010535

RESUMO

The purpose of the study was to which investigate whether dexamethasone, which has anti-inflammatory and immune response suppression roles, could treat noise-induced hearing loss caused by damage to hair cells in the cochlea. The experiment used 8-week-old CBA mice exposed to white noise at an intensity of 110 dB SPL for 2 h, with hearing loss confirmed by the auditory brainstem response test. Dexamethasone was administered by intraperitoneal injection for 5 days, and the therapeutic effect was investigated for 3 weeks. The experimental groups were 3 mg/kg of dexamethasone (3 mpk) and 10 mg/kg of dexamethasone (10 mpk), and the control group was a saline-administered group. The results showed that compared to the control group, the hearing threshold value was recovered by 10 dB SPL compared to the saline group from the 14th day in the 3 mpk group. In the 10 mpk group, thresholds were recovered from the 7th day compared to the saline group. This difference was similar at 4 kHz, and in the case of the 10 mpk group, the threshold was recovered by 20 dB SPL compared to the saline group. The study also confirmed the restoration of nerve cell activity and showed a recovery effect of about 20 µV in the amplitude value change in the 10 mpk group. In conclusion, the study suggests that dexamethasone has a therapeutic effect for noise-induced hearing loss by increasing the activity of nerve cells and showing a recovery effect from hair cells damaged by noise.


Assuntos
Perda Auditiva Provocada por Ruído , Camundongos , Animais , Perda Auditiva Provocada por Ruído/tratamento farmacológico , Perda Auditiva Provocada por Ruído/etiologia , Limiar Auditivo/fisiologia , Camundongos Endogâmicos CBA , Cóclea , Modelos Animais de Doenças , Dexametasona/farmacologia , Dexametasona/uso terapêutico , Potenciais Evocados Auditivos do Tronco Encefálico/fisiologia
16.
Mil Med ; 189(3-4): e698-e704, 2024 Feb 27.
Artigo em Inglês | MEDLINE | ID: mdl-37651596

RESUMO

INTRODUCTION: 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. MATERIALS AND METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.


Assuntos
Perda Auditiva Provocada por Ruído , Militares , Masculino , Humanos , Adulto Jovem , Adulto , Perda Auditiva Provocada por Ruído/epidemiologia , Perda Auditiva Provocada por Ruído/etiologia , Perda Auditiva Provocada por Ruído/diagnóstico , Estudos Retrospectivos , Qualidade de Vida , Corticosteroides
17.
Am J Otolaryngol ; 45(1): 104049, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-37738880

RESUMO

OBJECTIVE: Noise-induced hearing loss in the non-surgical ear during otologic/neurotologic surgery has not been well studied. The purpose of this study was to evaluate changes in hearing that may occur in the contralateral (i.e., non-surgical) ear after various otologic/neurotologic surgeries due to noise generated by drills. We hypothesized that otologic/neurotologic surgeries, longer in duration, would suggest longer drilling times and result in decreased hearing in the contralateral ear as evidenced by a change post-operative pure tone air conduction thresholds when compared to pre-operative thresholds. METHODS: A retrospective chart review at a tertiary referral center. Adult patients (18-75 years old) who underwent otologic/neurotologic surgeries from May 1, 2016 through May 1, 2021 were considered for inclusion. Surgeries included vestibular schwannoma resection (translabyrinthine, middle cranial fossa, or retrosigmoid approaches), endolymphatic sac/shunt and labyrinthectomy for Meniere's disease, and tympanomastoid surgery for middle ear pathology (e.g., cholesteatoma). Patient characteristics obtained through record review included age, sex, surgical procedure, pre-operative and post-operative audiometric thresholds and word recognition scores (WRS) for the contralateral ear, and duration of surgery. RESULTS: No significant differences were observed for change in audiometric thresholds in the contralateral ear for any surgery when considering individual frequencies. Additionally, no significant change in WRS was observed for any surgical approach. CONCLUSIONS: The risk of hearing loss in the non-surgical ear during various otologic/neurotologic surgeries appears to be minimal when measured via routine clinical tests.


Assuntos
Orelha Interna , Perda Auditiva Provocada por Ruído , Doença de Meniere , Adulto , Humanos , Adolescente , Adulto Jovem , Pessoa de Meia-Idade , Idoso , Perda Auditiva Provocada por Ruído/etiologia , Estudos Retrospectivos , Audiometria de Tons Puros , Orelha Interna/cirurgia
18.
Hear Res ; 441: 108927, 2024 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-38096707

RESUMO

Cochlear synaptopathy is a common pathology in humans associated with aging and potentially sound overexposure. Synaptopathy is widely expected to cause "hidden hearing loss," including difficulty perceiving speech in noise, but support for this hypothesis is controversial. Here in budgerigars (Melopsittacus undulatus), we evaluated the impact of long-term cochlear synaptopathy on behavioral discrimination of Gaussian noise (GN) and low-noise noise (LNN) signals processed to have a flatter envelope. Stimuli had center frequencies of 1-3kHz, 100-Hz bandwidth, and were presented at sensation levels (SLs) from 10 to 30dB. We reasoned that narrowband, low-SL stimuli of this type should minimize spread of excitation across auditory-nerve fibers, and hence might reveal synaptopathy-related defects if they exist. Cochlear synaptopathy was induced without hair-cell injury using kainic acid (KA). Behavioral threshold tracking experiments characterized the minimum stimulus duration above which animals could reliably discriminate between LNN and GN. Budgerigar thresholds for LNN-GN discrimination ranged from 40 to 60ms at 30dB SL, were similar across frequencies, and increased for lower SLs. Notably, animals with long-term 39-77% estimated synaptopathy performed similarly to controls, requiring on average a ∼7.5% shorter stimulus duration (-0.7±1.0dB; mean difference ±SE) for LNN-GN discrimination. Decision-variable correlation analyses of detailed behavioral response patterns showed that individual animals relied on envelope cues to discriminate LNN and GN, with lesser roles of FM and energy cues; no difference was found between KA-exposed and control groups. These results suggest that long-term cochlear synaptopathy does not impair discrimination of low-level signals with different envelope statistics.


Assuntos
Perda Auditiva Provocada por Ruído , Melopsittacus , Humanos , Animais , Cóclea/patologia , Ácido Caínico/toxicidade , Estimulação Acústica/efeitos adversos , Limiar Auditivo/fisiologia , 60707 , Potenciais Evocados Auditivos do Tronco Encefálico/fisiologia , Perda Auditiva Provocada por Ruído/etiologia , Perda Auditiva Provocada por Ruído/patologia
19.
Hear Res ; 442: 108925, 2024 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-38141520

RESUMO

Otoacoustic emissions (OAEs) are a non-invasive metric of cochlear function. Studies of OAEs in musicians have yielded mixed results, ranging from evidence of diminished OAEs in musicians-suggesting noise-induced hearing loss-to no difference when compared to non-musicians, or even a trend for stronger OAEs in musicians. The goal of this study was to use a large sample of college students with normal hearing (n = 160) to compare OAE SNRs in musicians and non-musicians and to explore potential effects of training recency and noise exposure on OAEs in these cohorts. The musician cohort included both active musicians (who at the time of enrollment practiced at least weekly) and past musicians (who had at least 6 years of training). All participants completed a questionnaire about recent noise exposure (previous 12 months), and a subset of participants (71 musicians and 15 non-musicians) wore a personal noise dosimeter for one week to obtain a more nuanced and objective measure of exposure to assess how different exposure levels may affect OAEs before the emergence of a clinically significant hearing loss. OAEs were tested using both transient-evoked OAEs (TEOAEs) and distortion-product OAEs (DPOAEs). As predicted from the literature, musicians experienced significantly higher noise levels than non-musicians based on both subjective (self-reported) and objective measures. Yet we found stronger TEOAEs and DPOAEs in musicians compared to non-musicians in the ∼1-5 kHz range. Comparisons between past and active musicians suggest that enhanced cochlear function in young adult musicians does not require active, ongoing musical practice. Although there were no significant relations between OAEs and noise exposure as measured by dosimetry or questionnaire, active musicians had weaker DPOAEs than past musicians when the entire DPOAE frequency range was considered (up to ∼16 kHz), consistent with a subclinical noise-induced hearing loss that only becomes apparent when active musicians are contrasted with a cohort of individuals with comparable training but without the ongoing risks of noise exposure. Our findings suggest, therefore, that separate norms should be developed for musicians for earlier detection of incipient hearing loss. Potential explanations for enhanced cochlear function in musicians include pre-existing (inborn or demographic) differences, training-related enhancements of cochlear function (e.g., upregulation of prestin, stronger efferent feedback mechanisms), or a combination thereof. Further studies are needed to determine if OAE enhancements offer musicians protection against damage caused by noise exposure.


Assuntos
Surdez , Perda Auditiva Provocada por Ruído , Música , Humanos , Adulto Jovem , Perda Auditiva Provocada por Ruído/diagnóstico , Perda Auditiva Provocada por Ruído/etiologia , Emissões Otoacústicas Espontâneas/fisiologia , Ruído/efeitos adversos , Testes Auditivos , Cóclea/fisiologia , Limiar Auditivo/fisiologia
20.
Am J Ind Med ; 67(1): 10-17, 2024 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-37830428

RESUMO

OBJECTIVES: It has been suggested that noise exposure can accelerate hearing decline after the noise exposure has ceased. We aimed to assess long-term hearing decline in persons with and without prior occupational noise exposure. METHODS: We conducted a population-based longitudinal study in Norway using the Trøndelag Health Study (HUNT) from 1996 to 1998 (baseline) and from 2017 to 2019 (follow-up). The sample included 1648 participants with baseline age ≥55 years (42% men, mean age 60 years) and <5 years occupational noise exposure after baseline. We analyzed the association between occupational noise exposure before baseline and mean hearing decline between 1998 and 2018 (20-year decline) at each frequency, adjusted for age, sex, education, and impulse noise exposure before baseline. RESULTS: Occupational noise exposure before baseline (N = 603) was associated with baseline hearing loss, but not with later accelerated 20-year decline, at any frequency. Noise-exposed persons had less subsequent 20-year decline at 3 kHz than did nonexposed. Restricting the noise-exposed group to persons who also had a baseline Coles notch (hearing thresholds at 3, 4, or 6 kHz of 10 dB or more compared with thresholds at 1 or 2 kHz and 6 or 8 kHz; N = 211), the exposed group showed less 20-year decline at both 3 and 4 kHz, as well as less accelerated 20-year decline at 8 kHz, compared with the nonexposed. CONCLUSION: Our large long-term longitudinal study shows no increased risk of continuing hearing decline after occupational noise exposure has ceased. The finding supports a conclusion that ear damage stops when the noise exposure is ended.


Assuntos
Perda Auditiva Provocada por Ruído , Ruído Ocupacional , Doenças Profissionais , Exposição Ocupacional , Masculino , Humanos , Pessoa de Meia-Idade , Feminino , Estudos Longitudinais , Perda Auditiva Provocada por Ruído/epidemiologia , Perda Auditiva Provocada por Ruído/etiologia , Ruído Ocupacional/efeitos adversos , Audição , Exposição Ocupacional/efeitos adversos , Doenças Profissionais/epidemiologia , Doenças Profissionais/etiologia
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