Prevalence of Noise-Induced Hearing Loss Related to the Mills in the Markets of the Municipality of Parakou in 2021

Introduction: Noise is the second leading cause of hearing loss in adults after presbycusis. The objective of this work was to study hearing loss induced by the noise of mills in the markets of Parakou. Methods: This was a descriptive and analytical cross-sectional study, conducted from February 3 to June 3, 2021 in the markets of Parakou. It concerned millers and sellers located within a 5 meter radius around the mills and among whom pure-tone audiometry was performed to detect a hearing loss. Subjects with no particular medical health history, under 55 years of age and having been working in these markets since more than 12 months, were included. Results: In this study, 103 subjects were selected, including 43 millers and 61 sellers. Their average age was 29 ± 13 years. The sex ratio was 0.49. The average length of service in the profession was 8 years with the extremes of 3 months and 47 years. They were exposed to noise on average 10 hours per day and 6 days a week. The average duration of weekly noise exposure was 23 h 28 min ± 13 h 32 min with the extremes of 5 h 00 min and 52 h 30 min. The average level of noise exposure was 90 dB with the extremes of 72 and 110 dB. 24 subjects reported symptoms related to noise such as headache, tinnitus, and hearing loss, with respective proportions of 22.33%, 20.39% and 06.80%. The prevalence of noise-related hearing loss was 26.21% (n = 27/103). Subjects with a notch at 4000 Hz and normal Average Hearing Loss (AHL) (20.39%) had a seven-time greater risk of developing noise-induced hearing loss (OR = 6.58;95% CI [2.54 - 18.8], p Conclusion: Hearing loss related to the noise of mills affected both millers and sellers near the mills in markets, hence the importance of regulating mills.

Saturated hydrogen saline protects against noise-induced hearing loss

Objective To study effects of saturated hydrogen saline in preventing noise-induced hearing loss. Methods Fifteen guinea pigs were randomly divided into 3 groups （5 each）, group one was for control, group two was treated with normal saline and group three was treated with saturated hydrogen saline, which was given intraperitoneally at 1 hour before noise exposure at 1 ml/100 g. One hundred rounds of impulse noise （ 157 dB SPL peak） were delivered as noise exposure. Immediately after exposure to impulse noise and on Days 1, 2, 4 and 8 following exposure, auditory brainstem response （ABR） thresholds were measured. Outer hair cell morphological changes and sueeinate dehydrogenase （SDH） activity were examined on Day 8 post-exposure. Results Immediately after noise exposure, ABR thresholds in saturated hydrogen saline treated animals were lower than the non-treated animals （P 〈 0.05 ）. Microscopy showed little SDH staining, cell swelling and irregular cell arrangement in the non-treated or normal saline treated animals. Whereas in the saturated hydrogen saline treated animals, there was deep SDH staining with significantly reduced cell loss and more regular cellular arrangement compared to the other two groups. The surviving cells counts was 45.17 ±12.15 for non-treated animals, 44.50 ±10.02 for normal saline treated animals and,116.50±2.38 for animals treated with saturated hydrogen saline. While the count was similar between non-treated and normal saline treated animals, it was significantly higher in saturated sions Intraperitoneal injection of saturated hydrogen saline damage. hydrogen saline treated animals （P 〈 0.05）. Concluappears to protect the cochlea against noise-induced damage.

The impact of hearing impairment and noise-induced hearing injury on quality of life in the active-duty military population:challenges to the study of this issue

The objectives of this review were to 1)summarize the available evidence on the impact of hearing loss on quality of life(QOL)among U.S.active-duty service members,2)describe the QOL instruments that have been used to quantify the impact of hearing loss on quality of life,3)examine national population-level secondary databases and report on their utility for studying the impact of hearing loss on QOL among active-duty service members,and 4)provide recommendations for future studies that seek to quantify the impact of hearing loss in this population.There is a lack of literature that addresses the intersection of hearing impairment,the military population,and quality of life measures.For audiological research,U.S.military personnel offer a unique research population,as they are exposed to noise levels and blast environments that are highly unusual in civilian work settings and can serve as a model population for studying the impact on QOL associated with these conditions.This review recommends conducting a study on the active-duty service member population using a measurement instrument suitable for determining decreases in QOL specifically due to hearing loss.

NOISE INDUCED HEARING LOSS IN CHINA:A POTENTIALLY COSTLY PUBLIC HEALTH LSSUE

Hearing loss and tinnitus are among the most common consequences of long term noise exposure and re-main an under-addressed heath issue in most developing nations including China. The rapid industrializa-tion and life style changes in China increase the concern over noise exposure and noise induced hearing loss (NIHL). Research on NIHL in China is limited. The current paper reviews studies published in English and Chinese language literatures regarding noise exposure and NIHL in China. Their implication on the Chi-nese population is discussed. The possible utility of a research model such as the Dangerous Decibels? as a means to increase understanding of the scope of NIHL among the Chinese population, to educate the gener-al public in China (especially the young) about NIHL and its prevention, and to study effects of language and cultural factors on international information dissemination and behavioral interventions is proposed.

The Effect of a High-Frequency-Hearing-Threshold Weighted Value on the Diagnosis of Occupational-Noise-Induced Deafness

Objective: In order to provide a theoretical basis for the revision of the current diagnostic criteria for occupational noise-induced deafness (ONID), we evaluated the degree of ONID by analyzing different high-frequency-hearing- threshold-weighted values (HFTWVs). Methods: A retrospective study was conducted to evaluate the diagnosis of patients with ONID from January 2016 to January 2017 in Guangdong province, China. Based on 3 hearing tests (each interval between the tests was greater than 3 days), the minimum threshold value of each frequency was obtained using the 2007 edition’s diagnostic criteria for ONID. The speech frequency and the HFTWVs were analyzed based on age, noise exposure, and diagnostic classi-fication using SPSS21.0. Results: 168 patients in total were involved in this study, 154 males and 14 females, and the average age was 41.18 ± 6.07. The diagnosis rate was increased by the weighted value of the high frequencies and was more than the mean value of the pure speech frequency (MVPSF). The diagnosis rate for the weighted 4 kHz frequency level increased by 13.69% (χ2 = 9.880, P = 0.002), the weighted 6 kHz level increased by 15.47% (χ2 = 9.985, P = 0.002), and the weighted 4 kHz + 6 kHz level increased by 15.47% (χ2 = 9.985, P = 0.002). The differences were all statistically significant. The diagnostic rate of the different thresholds showed no obvious difference between the genders. The age groups were divided into less than or equal to 40 years old (group A) and 40 - 50 years old (group B). There were several groups with a high frequency: high frequency weighted 4 kHz ( group A χ2 = 3.380, P = 0.050;group B χ2 = 4.054, P = 0.032), high frequency weighted 6 kHz (group A χ2 = 6.362, P = 0.012;group B χ2 = 4.054, P = 0.032), weighted 4 kHz + 6 kHz (group A χ2 = 6.362 P = 0.012;B χ2 = 4.054, P = 0.032) than those of MVPSF in the same group on ONID diagnosis rate. The differences between the groups were statistically significant. There was no significant difference between the age groups (χ2 = 2.265, P = 0.944). The better ear’s (the smaller hearing threshold weighted value) MVPSF and the weighted values for the different high frequencies were examined in light of the number of working years;the group that was exposed to noise for more than 10 years had significantly higher values than those of the average thresholds of each frequency band in the groups with 3 - 5 years of exposure (F = 2.271, P = 0.001) and 6 - 10 years of exposure (F = 1.563, P = 0.046). The differences were statistically significant. The different HFTWVs were higher than those of the MVPSF values, and the high frequency weighted 4 kHz + 6 kHz level showed the greatest difference, with an average increase of 2.83 dB. The diagnostic rate that included the weighted high frequency values was higher for the mild, moderate, and severe cases than those patients who were only screened with the pure frequency tests. The results of the comparisons of the diagnosis rates for mild ONID were as follows: the weighted 3 kHz high frequency level (χ2 = 3.117, P = 0.077) had no significant difference, but the weighted 4 kHz level (χ2 = 10.835, P = 0.001), 6 kHz level (χ2 = 9.985, P = 0.002), 3 kHz + 4 kHz level (χ2 = 6.315, P = 0.012), 3 kHz + 6 kHz level (χ2 = 6.315, P = 0.012), 4 kHz + 6 kHz level (χ2 = 9.985, P = 0.002), and 3 kHz + 4 kHz + 6 kHz level (χ2 = 7.667, P = 0.002) were significantly higher than the diagnosis rate of the mean value of the PSF. There was no significant difference between the 2 groups for the moderate and severe grades (P > 0.05). Conclusion: Different HFTWVs increase the diagnostic rate of ONID. The weighted 4 kHz, 6 kHz, and 4 kHz + 6 kHz high frequency values greatly affected the diagnostic results, and the weighted 4 kHz + 6 kHz high frequency hearing threshold value has the maximum the effect on the ONID diagnosis results.

Noise Induced Hearing Loss in Children:Preventing the Silent Epidemic

Noise-induced hearing loss and related tinnitus are often unrecognized problems, especially in non-occupational settings. Research indicates that increasing numbers of children and adolescents have or are acquiring noise induced hearing losses. Noise induced hearing loss can almost completely be prevented with simple precautionary measures. Educational programs rarely exist outside of those mandated in occupational settings. Health Communication theory can be applied to hearing health for developing effective loss prevention programs. Dangerous Decibels is one example of an effective multi-disciplinary effort to develop and disseminated prevention strategies.

Hidden Hearing Loss: Causes, Current Knowledge, and Future Directions

Introduction: Hidden hearing loss (HHL) is a type of auditory disorder that affects the auditory neural processing and hearing sensitivity in subjects with normal hearing thresholds. Unlike central auditory processing disorders, HHL happens when the cochlea (the peripheral auditory organ) is affected. There are several known risk factors to HHL which includes noise exposure, ototoxic drugs, and peripheral neuropathies, and age. Recent studies have shed light on this type of hearing loss, its etiology, prevalence, and how it can affect the auditory acuity in humans. Methods: This paper covers the current research regarding HHL, its causes, the different mechanisms involved in this disorder, and the diagnosis and potential treatments related to it. We will delve deeply into different researches concerning HHL. 4 articles from 285 were selected focusing on normal hearing individuals with bad speech intelligibility were discussed in this paper. In addition, articles discussing the effects of noise exposure on hearing impaired individuals were not considered as this study solely aims to focus on normal hearing sensitivity individuals with HHL, resulting in 4 articles from 285. Results: Numerous literatures over the decades have suggested that HHL is due to the degeneration of cochlear ribbon synapses, or hair cells synapses without hair cell damage. Their association with HHL was noted several times through this study, whether we were studying the effect of noise exposure, of age, or of ototoxicity. In all cases, no significant hair cell damage was observed, and normal thresholds were recovered. However, a decline in the amplitude of Auditory Brainstem Response (ABR) peak I from auditory nerve (AN) responses in noise exposed subjects and a decline in compound action potential (CAP) was measured when certain drugs were applied to the round window of Guinea pigs. Conclusion: Most studies, have proven that cochlear synaptophysin is the major contributor to noise induced, age, and ototoxic related HHL. There are several audiometric tests that were used to help identify HHL including Puretone audiometry in background noise, ABR, CAP, Distortion Product Otoacoustic Emission (DPOAE).

Genetic Effects on Sensorineural Hearing Loss and Evidence-based Treatment for Sensorineural Hearing Loss

In this article,the mechanism of inheritance behind inherited hearing loss and genetic susceptibilityin noise-induced hearing loss are reviewed.Conventional treatments for sensorineural hearing loss(SNHL),i.e.hearing aid and cochlear implant,are effective for some cases,but not without limitations.For example,they provide little benefit for patients of profound SNHL or neural hearing loss,especially when the hearing loss is in poor dynamic range and with low frequency resolution.We emphasize the most recent evidence-based treatment in this field,which includes gene therapy and allotransplantation of stem cells.Their promising results have shown that they might be options of treatment for profound SNHL and neural hearing loss.Although some treatments are still at the experimental stage,it is helpful to be aware of the novel therapies and endeavour to explore the feasibility of their clinical application.

The anatomic determinants of conductive hearing loss secondary to tympanic membrane perforation

Objectives: Recent studies have introduced middle ear volume(MEV) as a novel determinant of perforation-induced conductive hearing loss(CHL) in a mechanism driven by trans-tympanic membrane pressure differences. The primary aims of this preliminary report are to: 1) correlate CHL with perforation size; 2) describe the relationship between CHL and MEV; and 3) compare CHL across a range of cholesteatoma involvement.Design: A retrospective pilot study was performed in 31 subjects with audiometry indicative of conductive hearing loss, temporal bone CT scans,and no prior middle ear surgery. Perforation size and MEV were analyzed with respect to CHL in a cohort of 10 perforated ears with no cholesteatoma. CHLs were compared in 3 groups defined by extent of cholesteatoma involvement.Results: Ears with large and small perforations showed mean ABG values of 32.0 ± 15.7 dB and 16.0 ± 16.4 dB, respectively. A direct relationship was observed between MEV and CHL for ears with large perforations across all frequencies, whereas this relationship for small perforations was frequency-dependent. Finally, a statistically significant increase in CHL was found across ears with increasing cholesteatoma involvement at 1000 Hz(X^2(2) = 9.786, p = 0.008),2000 Hz(x^2(2) = 8.455, p = 0.015),and 4000 Hz(x^2(2)= 8.253, p = 0.016).Conclusions: These pilot data suggest that greater perforation-induced conductive hearing losses may be associated with larger perforation sizes and cholesteatoma. The correlation between MEV and CHL may require additional study.

EFFECTS OF MODERATE NOISE EXPOSURE ON HEARING FUNCTION IN C57BL/6J MICE

Objective To study characteristics of hearing loss after exposure to moderate noise exposure in C57BL/6J mice. Methods Male C57BL/6J mice with normal hearing at age of 5-6 weeks were chosen for this study. The mice were randomly sclccted to be studied immediately after exposure （Group P0）, or 1 day （Group P1）, 3 days （Group P3）, 7 day （Group P7） or 14 days （P14） after exposure. Their before exposure condition served as the normal control. All mice were exposed to a broad-band white noise at 100 dB SPL for 2 hours, ABR thresholds were used to estimate hearing status at each time point. Results ABR threshold elevation was seen at every tested frequency at P0 （P〈0.01）. Elevation at high-frequencies （16 kHz and 32 kHz） was greater than at lower frequencies （4 kHz and 8 kHz, P〈0.05）. From P1 to P14, ABR thresholds continuously improved, and there was no significant difference between P14 and before exposure （P〉0.05）. Conclusion There is a frequency specific re- sponse to 100 dB SPL broad-band white noise in C57BL/6J mice, with the high-frequency being more susceptible. Hearing loss induced by moderate noise exposure appears reversible in C57BL/6J mice.

Impact of noise on hearing in the military

Hearing plays a vital role in the performance of a soldier and is important for speech processing. Noise-induced hearing loss is a significant impairment in the military and can affect combat performance. Military personnel are constantly exposed to high levels of noise and it is not surprising that noise induced hearing loss and tinnitus remain the second most prevalent service-connected disabilities. Unfortunately, unlike civilian personnel, military personnel have little option but to remain in noisy environments in order to complete specific tasks and missions. Use of hearing protection devices and follow-up audiological tests have become the mainstay of prevention of noise-induced hearing loss. This review focuses on sources of noise within the military, pathophysiology and management of patients with noise induced hearing loss.

Assessment of Hearing Status by Pure Tone Audiogram—An Institutional Study

Aim: To assess the hearing status of the study subjects in terms of degree and type of hearing loss, and establish the burden of this disability in the society. Materials and methods: This is a prospective study conducted in patients who attend our OPD. After an otorhinolaryngeal examination, all the patients were subjected to pure tone audiometry using MAICA-MA52 audiometer. Results: Our study comprises 1012 males (64%) and 563 females (36%). Out of this, about 15% have conductive deafness and 42% have sensorineural hearing loss. About 29% suffer from mild hearing loss, 26% moderate and 11% severe hearing loss. The alarming information is that about 5% have total hearing loss of Sudden Sensorineural type (SSNHL). Conclusion: Pure tone audiometry is cost effective and easy to perform. Early diagnosis and timely intervention will reduce the morbidity of deafness in our country. Hence it is necessary to identify and treat sudden sensorineural hearing loss and noise induced hearing loss at an early stage.

Investigation on gunner's hearing organ damage:ear drum inspection and acoustic impedance measurement

The ear drums of 279 long-range gunners and 156 short-range gunners who hadparticipated in a battle for 4 months were inspected and 442 ears were subjected to acousticimpedance measurement.The results showed that retraction was the main change of the ear drums,then,opacity and atrophy.The average static compliance was 1.06,tympanograms were 75.6% oftype A and 21.1% of AD.No obvious difference in acoustic reflex threshold at different frequencieswas found between the 2 sorts of gunners.But the short-range cannon gunners suffered a more seri-ous high frequency hearing loss.

Prophylactic effect of Ca^(2+)-deficient artificial perilymph perfusion on noise-induced hearing loss

Objective To investigate the prophylactic effect of low calcium concentration perilymph on noise-induced hearing loss. Methods Forty guinea pigs with normal hearing weighing 250-350 g were assigned to five groups (8 in each group): (1) Ca2+-deficient perilymph perfusion (CDP) for 2 h; (2) white noise (120 dB SPL) exposure (WNE) only for 1 h, (3) combination of calcium-deficient perilymph perfusion and white noise (120 dB SPL) exposure (WNE+CDP); (4) normal artificial perilymph (NAP) perfusion for 2 h; and (5) white noise exposure + normal artificial perilymph perfusion (WNE+NAP) for 2 h. Compound action potentials (CAP) evoked by click was recorded from round window every 15 min. The cochleae from 5 animals in each group were examined with scanning electron microscope. Results The CAP for group 1 experienced a threshold shift (TS) of 15-26 dB, while group 2 yielded a 46-59 dB TS and group 3 a 37-45 dB TS; no threshold shift occurred in group 4. The CAP TS in group 5 was 33-64 dB. The CAP TS of group 3 was less than that of group 2. After one hour of noise exposure, the CAP TS of group 3 were 45.92±2.90 dB and 59.30±3.95dB in group 2. There were significant differences (P<0.05) between groups 3 and 2. The CAP TS of group 3 was less than that of group 5 at the points of 1, 1.5 and 2 h after noise exposure. There was a significant difference between groups 3 and 5 (P<0.01). Stereocilia of 89 OHC3 were in disarray in five cochleae after noise exposure in group 2. The cuticular plates of 8 OHC2,3 sank and the stereocilia became fused in only one animal cochlea after noise exposure in group 3 combined with low calcium perilymph perfusion. Conclusions Low calcium concentration appears to participate in preventing noise-induced hearing loss and the rising of calcium concentrations in inner hair cells after noise exposure, which may have been due to the opening of calcium channels in inner hair cells during noise exposure. The mechanism of the prophylactic effect might be caused by a lower calcium concentration in inner hair cells in the cochlea attenuating the influence of noise exposure on hearing loss; calcium deficient perilymph perfusion prevented calcium accumulation in inner hair cells of the cochlea. The motility of the OHCs might be partially inhibited by low calcium concentration that reduced noise-induced hearing loss in turn.

星形胶质细胞在噪声损伤后小鼠耳蜗核突触修复中的作用

目的·通过形态学分析和分子生物学技术,探究噪声引起的耳蜗核损伤的病理生理变化以及星形胶质细胞对损伤的调节功能。方法·将48只C57BL/6J雄性小鼠随机分成2组暴露在110 dB声压级(sound pressure level,SPL)的宽频噪声下,持续2 h。然后在噪声暴露后的第1、7、14、30和90日对小鼠进行听性脑干反应(auditory brainstem response,ABR)测试;并对耳蜗核组织进行免疫荧光染色观察耳蜗核神经元、听觉突触损伤情况以及星形胶质细胞激活程度;此外,通过蛋白质印迹法(Western blotting)进一步验证噪声对耳蜗核神经元与神经突触的损伤情况。结果·噪声暴露后,腹侧耳蜗核中丛细胞数量显著减少。Western blotting结果显示耳蜗核神经元中神经纤维严重丢失,表明噪声对耳蜗核神经元造成了严重的损害。囊泡谷氨酸转运蛋白1(vesicular glutamate transporter 1,Vglut1)标记的听觉神经突触明显丧失,其中在噪声暴露后的第14日丧失最为严重,随后在第90日呈缓慢恢复趋势。此外,在噪声暴露后,耳蜗核中星形胶质细胞呈现出明显的聚集和激活。通过胶质酸性纤维蛋白(glial fibrillary acidic protein,GFAP)染色,提示在噪声暴露之前,大多数星形胶质细胞分布在耳蜗核的周边、颗粒细胞区和听觉神经根周围,并且形态较小。然而,在噪声暴露后的第14日,腹侧耳蜗核中大量激活的星形胶质细胞积聚,并且它们都表现出在突触周围生长的模式。结论·噪声暴露导致耳蜗核神经突触损伤,星形胶质细胞可能参与其损伤和修复过程。这些研究结果将为进一步理解耳蜗核中声音信号分析、整合和神经可塑性的机制提供关键基础。

钙蛋白酶与内毛细胞带状突触噪声损伤的相关性研究

目的通过比较噪声暴露后基底膜不同区域内毛细胞(IHCs)带状突触损伤差异,探讨带状突触损伤易感性的相关因素。方法将28只C57BL/6J雄性小鼠随机分为噪声暴露组和对照组,每组14只。噪声暴露组小鼠给予强度103 dB SPL、频率2~20 kHz、持续2 h的宽带噪声暴露,对照组小鼠则饲养于安静环境中。噪声暴露前及噪声暴露后第一天进行ABR测试及毛细胞带状突触免疫荧光染色实验。使用全细胞膜片钳技术比较不同区域IHCs的钙离子流入。通过免疫荧光染色比较噪声暴露后的耳蜗基底膜顶回、中回、底回IHCs钙蛋白酶(Calpain)表达水平,并用蛋白质印迹实验验证钙蛋白酶对IHCs带状突触蛋白CtBP2的损伤作用。结果噪声暴露后一天,噪声暴露组在11.3、16.0、22.6、32.0 kHz的ABR阈值较对照组显著上升(均为P<0.001),中回、底回IHCs带状突触数量明显减少(P<0.05)。全细胞膜片钳实验结果表明耳蜗基底膜中回IHCs有较多的钙离子通道(P<0.01),但其单通道电流较小(P<0.01),顶回、中回IHCs钙离子通道开放率无显著差异(P>0.05)。噪声暴露后,耳蜗基底膜中回、底回IHCs的Calpain表达水平显著高于顶回(P<0.001),蛋白质印迹实验结果表明Calpain以钙离子依赖的方式降解带状突触蛋白CtBP2。结论钙蛋白酶是基底膜高频区内毛细胞带状突触噪声损伤易感的重要因素。

基于化学计量学和COX-2抑制活性筛选红树共生放线菌中防治药源性听力损失成分

目的利用代谢组学技术和药源性聋细胞模型寻找红树共生放线菌链霉菌属Streptomyces sp.(No.1624117)代谢产物中防治药源性听力损失成分。方法从菌株粗提物中筛选具有抗炎活性的极性分段样,采用超高效液相色谱-串联质谱法(UPLC-MS)对菌株粗提物和活性分段样的化学成分进行数据采集;通过主成分分析法(PCA)与正交偏最小二乘法-判别分析法(OPLS-DA)进行多元统计学分析,筛选差异成分;经过柱层析和高效液相色谱(HPLC)定点分离目标差异点,利用核磁和质谱鉴定结构;最后通过顺铂诱导的HEI-OC1细胞损伤模型考察化合物对耳蜗毛细胞的保护作用。结果代谢组学分析有38个差异代谢物,结合抗炎活性测定结果,分离纯化出6个化学成分并确定了结构。在顺铂诱导的HEI-OC1细胞损伤模型中,化合物1,2,3,4和6均显示出对耳蜗毛细胞具有保护作用。结论本研究建立了一种基于代谢组学技术挖掘放线菌代谢产物中防治药源性听力损失成分的方法,为寻找防治听力损失活性化合物提供了新途径。

航空机务人员噪声性听力损失的现状调查

目的探究噪声接触时长对听觉功能的影响,分析不同工龄航空机务人员的高频听力变化,明确噪声性听力损失的演变状况。方法依据工龄时间将187例男性航空机务人员分为0~5年(97例)、6~10年(43例)、>10年(47例)3组,进行纯音听力测试,分析各组单耳高频、双耳高频噪声性听力损失的发生率、高频平均听阈及听力损失演变情况。结果0~5年工龄组听力损失者26例,高频平均听阈为15.99±11.42 dB,单耳高频听力损失者12例,双耳高频听力损失者14例。6~10年工龄组听力损失者12例,高频平均听阈为15.90±10.89 dB,单耳高频听力损失者7例,双耳高频听力损失者5例。>10年工龄组听力损失者16例,高频平均听阈为20.56±12.61 dB,单耳高频听力损失者5例,双耳高频听力损失者11例。结论航空机务人员噪声性听力损失的发病率并未随工作时间延长而增加,高频气导平均听阈与工作时间呈显著相关性,发病多以单耳6 kHz开始,逐渐向其他高频扩展,随着噪声接触延长而发展为双耳噪声性聋且噪声性听力损失的程度逐渐加重。

公共交通噪声性听力损失研究进展

公共交通噪声是指交通工具运行时产生的妨害人们正常生活和工作的声音。分为机动车噪声、飞机噪声、火车噪声等。一般指机动车辆在城市内交通干线上行驶时产生的噪声。在飞速发展的时代,因公共交通造成的听力损失不容小觑。造成听力损失的公共交通来源广泛,如公交车、地铁等,听力损失的占比也有初步统计,目前探究的可能影响因素有工龄和身体的健康情况等,可能的机制有声波对内耳机械刺激以及氧化应激等。听力损失的防治也主要是通过管理和保护措施来控制噪声源、切断噪声传播途径和加强个人防护等。本文就近年来公共交通驾驶员噪声性听力损失的特点、机制、防治等进行综述。以期对公共交通驾驶员噪声性听力损失的深入研究及减少我国因公共交通造成的噪声性听力损失的发病率有提供参考。

银杏叶提取物注射液对噪音性听力损失的保护机制研究

目的研究银杏叶提取物注射液(EGB)调控磷脂酰肌醇3激酶(PI3K)/丝裂原活化蛋白激酶(MAPK)信号通路对噪音性听力损失(NIHL)的保护作用及机制。方法将SD大鼠随机分为对照组(Control组)、NIHL模型组(Model组)、低剂量EGB组(EGB-L组,0.7 mg·kg^(-1))、高剂量EGB组(EGB-H组,1.4 mg·kg^(-1))和高剂量EGB+PI3K激活剂740Y-P组(EGB-H+740Y-P组,1.4 mg·kg^(-1)EGB+0.02 mg·kg^(-1)740Y-P)。听觉脑干反应(ABR)评估各组大鼠的听力;HE染色观察大鼠耳蜗组织病理学与螺旋神经节细胞数量;RT-qPCR法测定大鼠耳蜗组织PI3K、MAPK mRNA表达;免疫印迹试验(Western Blot)法检测大鼠耳蜗组织PI3K/MAPK信号通路相关蛋白表达。CCK-8法测定耳蜗毛细胞增殖活性。结果与Control组相比,Model组大鼠在2、4、8 kHz处左、右耳的听力阈值、耳蜗组织PI3K、MAPK mRNA表达、耳蜗组织PI3K、MAPK、AKT磷酸化水平显著升高(P<0.05),耳蜗组织螺旋神经节细胞和毛细胞数量显著减少(P<0.05);与Model组相比,EGB-H组大鼠相关指标变化与上述相反(P<0.05)。PI3K激活剂740Y-P减弱EGB对大鼠NIHL保护作用。结论EGB可能通过下调PI3K/MAPK信号通路保护大鼠NIHL。