Sound: Production, perception, hearing loss and treatment options.

Sound is an important communication tool for humans that contain information about the surrounding environment. It may signify a danger or a reward for an organism. In humans, the mechanism of sound production and perception is complex and sophisticated. Sound is produced by vibrating body in a medium that contains molecules in the surrounding space. The sound perception starts in the human foetus at around the third trimester where it plays a vital role in organising the foetal brain. This process continues after birth and can be exploited by various endogenous and exogenous factors. Many mechanisms that can modulate hearing process at different levels lead to subclinical or clinical presentation of hearing-related problems. It is important to contemplate the mechanisms underlying sound production, perception and pathogenesis of hearing loss. This will facilitate prescribing a relevant treatment option according to the cause and its underlying mechanism. The current narrative review was planned to focus on sound production, its perception, types of hearing loss and available treatment options vited in relevant literature searched by using Google Scholar and PubMed.

[Association between PON2 gene polymorphisms and susceptibility to noise-induced hearing loss].

Objective: To investigate the relationship between SNP and noise-induced hearing loss (NIHL) susceptibility in occupational noise exposure population in China. Methods: From 6297 for a certain steel works in contact with noise, contact length of 3 years or more and workplace noise exposure intensity of 80 dB (A) , ears or high frequency (3 000, 4 000, 6 000 Hz) average of hearing acuity 40 dB (HL) , or high frequency loss in both ears, on the basis of single whisper frequency (500, 1, 000, 2 000 Hz) average threshold of 26 dB (HL) or object as case group. A case-control study was designed with 1:1 matching. Subjects with the same gender, the same type of work, age ±5 years old, and working age ±2 years after noise exposure were selected as the control group. Subjects with any whisper frequency (500, 1, 000, 2, 000 Hz) whose hearing threshold in any frequency band was ≤25 dB (A) and whose average high-frequency hearing threshold in pure tone hearing test was <35 dB (A) were selected as the control group. Four sites of PON2 gene were genotyped by medium-and high-throughput SNP genotyping. Univariate logistic regression was used to analyze the relationship between single SNP polymorphism and NIHL. Results: A total of 286 case-control pairs were included. Smoking was statistically significant difference between cases and controls (P<0.001) . Conclusion: No statistical difference has been found between single SNP polymorphism and NIHL. At the level of greater than 92 dB of high noise exposure, rs7785846 (CT+TT) genotype is a risk factor for occupational noise deafness, and its OR is 2.74 (95%CI: 1.09-6.89) compared with wild homozygous type (CC) . Conclusion. The rs7785846 (CT+TT) genotype carriers of PON2 gene are more susceptible to hearing impairment when exposed to high noise intensity.

[Association between GPX1 gene polymorphisms and noise-induced hearing loss].

Objective: To identify association between genetic polymorphism in the Glutathione peroxidase 1 gene (GPX1) and noise-induced hearing loss (NIHL) . Methods: A nested case control study was conducted based on a cohort of noise-exposed subjects. 392 cases were selected from the steel factory in Henan Province, 392 matched control subjects for each case were designated on the basis of the matched criterion including same gender, age (±5years) and duration of exposure to noise (±2years) . Two single nucleotide polymorphisms (SNPs) of GPX1 were genotyped by SNPscanTM multiplex SNP genotyping kit. Hardy-Weinberg equilibrium (HWE) tests were performed using Pearson's χ(2) for each SNP among control group, effects of genotypes of GPX1 on NIHL were analyzed by logistic regression. Results: All two SNPs were in HWE. After adjustment for covariates including smoking status, rs1987628 polymorphism was statistically significantly associated with the NIHL risk under codominant and Dominant inheritance models; In the subjects carrying rs1987628 GA genotype had a higher NIHL risk than those carrying the GG genotype, the adjusted OR value was 1.803 (95%CI 1.215-2.676, P=0.003) . And meanwhile, rs1987628 GA+AA genotype had a higher NIHL risk than those carrying the GG genotype, the adjusted OR value was 1.762 (95%CI 1.197-2.593, P=0.004) . Conclusion: It was suggested that genetic polymorphism in the GPX1 gene might be the genetic susceptible factor for NIHL.

[Association between GSTP1 gene polymorphisms and susceptibility to noise-induced hearing loss].

Objective: To investigate the association between the single nucleotide polymorphisms (SNPS) at rs1695 and rs6591256 in glutathione S-transferase P1 (GSTP1) gene and susceptibility to noise-induced hearing loss in Chinese Han workers exposed to noise. Methods: Using the 1: 1 nested case-control study and taking 6297 workers exposed to noise in a steel plant in Henan province as the cohort study population in July 2019, we screened those who have been exposed to noise for ≥3 years and whose binaural high frequency (3000, 4000, 6000 Hz) average hearing threshold is ≥40 dB (A) into the case group. The control group was selected according to the matching criteria of the same sex, same type of work, and the age difference was not more than 5 years old, and the working age difference was not more than 2 years. 276 subjects were selected into the case group and the control group respectively. The medium and high throughout single nucleotide polymorphism typing technology (SNPscanTM technology) was used to detect the polymorphism of three nucleotide sites of GSR gene, and conditional logistic regression was used to analyze the relationship between single nucleotide polymorphism (SNP) and NIHL, and the relationship between different polymorphic sites and the risk of NIHL after adjusting covariates. After stratification with different cumulative noise exposure (CNE) , Conditional logistic regression analysis was used to analysis the risk of NIHL at different loci. Results: The mean and standard deviation of age of the selected subjects was (40.28±8.00) , the mean and standard deviation of noise-exposed working years was (18.7±8.92) years. The range of noise exposure levels and comulative noise exposure were 80.05-93.35dB (A) and 86.83-107.92 dB (A) ·year, respectively. Compared with the control group, there were no statistically significant differences in age, noise-exposured working years, intensity of noise exposure, CNE, gender, drinking, hypertension prevalence and noise exposure level in the hearing loss group (P>0.05) , while there were statistically difference in smoking, binaural high-frequency average hearing threshold and binaural speech frequency (P<0.05) . After adjusting for smoking, drinking, hypertension and other factors, in the co-dominant model, compared with GGgenotype, the risk of NIHL was higher in rs1002149 GT genotype and rs2251780 GA genotype (OR=1.558, 95%CI: 1.028-2.361; OR=1.550, 95%CI: 1.020-2.355, P<0.05) ; compared with TT/GT genotype, the rs1002149 TT genotype has a higher risk of developing NIHL (OR=1.494, 95%CI: 1.002-2.228, P<0.05) , while rs3779647 genotype had no relationship with the risk of NIHL (P>0.05) . In the equivalent sound level (L(Aeq)) of noise >85 dB (A) stratification, compared with GG genotype, carrying rs1002149 GT genotype and rs2251780 GT genotype has higher risk of nihl (OR=1.801, 95%CI: 1.093-2.967; OR=1.720, 95%CI: 1.050-2.817, P<0.05) . Haplotype analysis of two sites, rs1002149 and rs2251780, was not found to be related to NIIHL susceptibility. Conclusion: The allele G of rs1695 and rs6591256 may be risk factors of NIHL.

[Prediction of KCNQ4gene polymorphism varies with CNE or noise exposure duration on the Risk of NIHL-Cox model analysis based on cohort study].

Objective: The purpose of this study was to explore the association between gene in the potassium recycling pathway 4 (KCNQ4) polymorphisms and the susceptibility to noise-induced hearing loss (NIHL) , and analysis the effect of cumulative noise exposure (CNE) and noise exposure duration on this association. Methods: A nested case-control study with 1∶1 matched was used based on the cohort of noise exposure in a steel factory. A total of 286 cases were selected as the group of hearing loss and 286 controls were chosen according to the matching standards of same gender, same type of work, age difference ≤ 5 years, noise exposure duration ≤ 2 years. The single nucleotide polymorphisms (SNPs) of rs4660468, rs4660470, rs34287852 in KCNQ4 were genotyped by SNPscan(TM) method. The codominant, dominant and recessive models were established to study KCNQ4 polymorphisms and the susceptibility to NIHL by single-factor conditional logistic regression analysis. The COX regression analysis was used to analyze the risk of developing NIHL in individuals with different genotypes along with the extending of noise exposure duration or CNE. Results: In the case of CNE≤96 dB (A) ·year, the risk of developing NIHL in individuals with TA genotype of rs4660470 was 2.197 times than individuals with TT genotypes (95%CI: 1.032~4.677) , and those with TA+AA and TT genotypes (HR=2.467, 95%CI: 1.025~5.934) With the increase of noise exposure duration, in rs4660470, individuals with TA genotype had a higher risk of suffering NIHL than those with TT genotype (HR=1.461, 95%CI: 1.061~2.011) , individuals with TA and/or AA genotype had a earlier risk of suffering NIHL than those with TT genotype. Conclusion: The mutant allele A of rs4660470 in KCNQ4 may be a risk factor for developing NIHL, CNE≤100 dB (A) ·year or the increase of noise exposure duration may further increase the risk of NIHL.

[Association between GSTP1 gave polymorphisms and susceptibility to noise-induced hearing loss].

Objective: To investigate the association between the single nucleotide polymorphisms (SNPS) at rs1695 and rs6591256 in glutathione S-transferase P1 (GSTP1) gene and susceptibility to noise-induced hearing loss in Chinese Han workers exposed to noise. Methods: A 1: 2 matched nested case-control study was performed, which based on the cohort of 6297 workers exposed to noise in an iron and steel plant in Henan, China, who were followed up from January 1, 2006 to December 31, 2015. According to the criteria of binaural average high-frequency hearing threshold ≥40 dB, a total of 292 workers were enrolled as hearing loss group; after the adjustment for sex, type of work, age (difference≤5 years) , and working years of noise exposure (difference≤2 years) , according to the criteria of binaural average high-frequency hearing threshold <35 dB, and the speech frequency hearing threshold of any ear at any frequency band ≤25 dB, a total of 584 workers were enrolled as control group. The single nucleotide polymorphisms (SNPs) of rs1695 and rs6591256 in GSTP1 were genotyped by high throughput SNP genotyping assay. Hardy-Weinberg equilibrium of control group was checked. The association between the SNPs at the two loci and susceptibility to NIHL was analyzed. Results: The L(Aeq, 8 h) range of workers exposed to noise was 80.2-98.8 dB (A) . The risk of NIHL in individuals with allele G of rs1695 was 1.291 times of those with allele A (95%CI: 1.042-1.598, P<0.05) . The risk of NIHL in individuals with allele G of rs6591256 was 1.390 times of those with allele A (95%CI: 1.119-1.728, P<0.05) . The risk of NIHL in individuals with AG and GG genotypes of rs6591256 was 1.437 times of those with AA genotype (95%CI: 1.057-1.952, P<0.05) . With the increase of noise exposure duration, individuals with AG and GG genotypes of rs6591256 had a higher risk of NIHL than those with AA genotype (HR=1.273, 95%CI: 1.002-1.616, P<0.05) . Conclusion: The allele G of rs1695 and rs6591256 may be risk factors of NIHL.

[Correlation between FOXO3 gene polymorphisms and susceptibility to occupational noise-induced deafness].

Objective: To investigate the association between the single nucleotide polymorphisms of rs12212067 in FOXO3 gene and the susceptibility to occupational noise-induced deafness in a Chinese Han population. Methods: A total of 1 066 cases of noise exposure workers from a large chemical fiber factory in Jiangsu Province were selected as the study subjects. All subjects' basic data and field exposure data were collected through questionnaires and occupational health surveys. The subjects were divided into case group (531 persons, double ear high frequency average hearing threshold>25 dB) and control group (535 persons, double ear high frequency average hearing threshold≤25 dB) according to their results of pure tone hearing test .2ml fasting venous blood was collected for DNA extraction and genotyping was performed by TaqMan-PCR technique. Results: Genotyping results suggested that the GT+GG genotype is a risk factor for occupational noise-induced deafness, with an adjusted OR 95% confidence interval of 2.044 (1.51-2.78) . After the noise exposure intensity was stratified, the adjusted OR values and the 95% confidence intervals of noise intensity ≤85, 85-92 and>92 dB respectively 2.43 (1.52-3.90) , 2.17 (1.03-4.59) and 1.74 (1.07-2.83) . Conclusion: GT-GG genotype in rs12212067 of FOXO3 gene may be a risk factor for occupational noise-induced deafness.

[Speech audiometry in expert assessment of hearing impairment]. / Sprachaudiometrie in der Begutachtung des Hörvermögens.

In the assessment process of hearing impairment the medical expert has to verify its causality and to quantify its severity as hearing loss in percentage. Based on the determined hearing loss in percentage, the degree of impairment/disability or, in the case of work-related noise-induced hearing loss, the reduction in earning capacity is estimated. In Germany the guideline for the expert assessment of work-related noise-induced hearing loss is the Königstein Guideline. Currently, the 5th edition from 2012 is used. Here, the hearing loss quantification depends mainly on the results of speech audiometry. Based on the Freiburg speech test, the hearing loss in percentage is determined using approved tables. For patients with a mild hearing loss, typically characterized by a high-frequency hearing loss, tone audiometry results are consulted additionally. Speech-in-noise tests are available and are frequently used to measure the benefit of hearing systems. They allow for the detection of these patients' hearing impairment, which generally occurs in noisy environments. The first suggestions for a table to determine hearing loss in noise in percent are available. In experimental studies it was shown that tests in quiet, other than the Freiburg speech test, can be used and the same tables can be applied. In this article the current use of speech audiometry for expert assessment is presented, and options of using further developed speech test material are discussed.

Effect of smoking on hearing loss in refractory's factory male worker with occupational noise exposure in Iran.

OBJECTIVE: To assess the effect of smoking on hearing loss in factory workers with occupational noise exposure. METHODS: This cross-sectional study was conducted at Birjand University of Medical Sciences, Birjand, Iran, from May to July 2013, and comprised smoking and non-smoking factory male workers. All of them were exposed to occupational noise level more than 85 decibels for at least 10 years. All participants underwent audiometric testing. SPSS 15 was used for data analysis.. RESULTS: Of the 150 participants, 55(36.7%) were smokers and 95(63.3%) were non-smokers. The mean age of the participants was 43.26±7.81 years while the mean working experience was 15.51±3.87 years. Furthermore, 18(32.7%) of the smokers and 8(8.4%) of the non-smokers suffered tinnitus (p=0.07). The mean noise intensity in the working place of the individuals was 89±2.63 A-weighted decibels. At a frequency of 500 Hz, the mean hearing loss was 4.8±5.7 decibels among smokers and 3.3±4.6 decibels among non-smokers in the left ear (p=0.52), whereas it was 4.8±5.1 decibels and 3.00±4.5 decibels in the right ear (p=0.15). The difference between the smokers and the non-smokers was significant in both ears at 1000Hz, 2000Hz, 4000Hz and 8000Hz (p<0.05 each). CONCLUSIONS: Smoking had an additive role in hearing loss among workers who were in close contact with excessive noise exposure.

The use of personal hearing protection in hostile territory and the effect of health promotion activity: advice falling upon deaf ears.

INTRODUCTION: Noise-induced hearing loss is a significant cause of morbidity among serving soldiers despite provision of a range of personal hearing protection (PHP) and education and training. It appears that soldiers are choosing to forego PHP. This audit aimed to evaluate the effect of health promotion activity on the use of hearing protection in hostile territory. METHOD: 46 dismounted infantry soldiers operating out of a forward operating base in Afghanistan during Op HERRICK 17 were directly observed in order to determine the rate of wearing PHP before and after health promotion activity. RESULTS: In the initial phase, 39% of soldiers (range 16-74%) wore PHP in at least one ear, but following health promotion activity the rate fell to 12% (range 9-14%). CONCLUSIONS: The reduction in the wearing of PHP appears to have been because the perceived diminished threat of enemy contact was outweighed by any benefit of health promotion activity. Reasons for poor compliance were not investigated, but it appears that behavioural factors, and specifically, leadership at the smallest unit level, are important. These should be investigated and considered in the development of future PHP.

Hearing health and noise exposure in population between 18 to 64 years old in Bogotá, Colombia, 2014-2018 / Salud auditiva y exposición a ruido ambiental en población de 18 a 64 años de Bogotá, Colombia, entre el 2014 y el 2018.

Introduction: Hearing health is a public health concern that affects the quality of life and can be disturbed by noise exposure, generating auditory and extra-auditory symptoms. Objective. To identify the hearing health status in adults living in Bogotá and its association with environmental noise exposure and individual and otological factors. Objective: To identify the hearing health status in adults living in Bogotá and its association with environmental noise exposure and individual and otological factors. Materials and methods: We conducted a cross-sectional study using a database with 10,311 records from 2014 to 2018, consigned in a structured survey of noise perception and hearing screening. We performed a descriptive, bivariate, and binary logistic regression analysis. Results: Of the included participants, 35.4% presented hearing impairment. In the perception component, 13.0 % reported not hearing well; 28.8 % had extra-auditory symptoms, 53.3 % informed otological antecedents and 69.0 % presented discomfort due to extramural noise. In the logistic regression, the variables with the highest association for hearing impairment were living in noisy areas (OR = 1.50) (95% CI: 1.34-1.69), being male (OR = 1.85) (95% CI: 1.64-2.09), increasing age (for each year of life, the risk of hearing impairment increased 6%), and having history of extra-auditory symptoms (OR = 1.86) (95% CI: 1.66-2.08). Conclusions: Hearing impairment is multi-causal in the studied population. The factors that promote its prevalence are increasing age, being male, smoking, ototoxic medications, living in areas with high noise exposure, and extra-auditory symptoms.

Introducción. La salud auditiva es un tema de interés en salud pública que afecta la calidad de vida y que puede afectarse por la exposición continua al ruido, un factor de riesgo que genera síntomas auditivos y extraauditivos. Objetivo. Identificar el estado de salud auditiva de adultos que viven en Bogotá, y su asociación con factores de exposición a ruido ambiental, individuales y otológicos. Materiales y métodos. Se realizó un estudio transversal mediante el análisis de una base de datos con 10.311 registros, obtenidos entre los años 2014 y 2018, producto de una encuesta estructurada de percepción de ruido y tamizaje auditivo. Se hizo un análisis descriptivo bivariado y una regresión logística binaria. Resultados. El 35,4 % de los participantes presentó disminución auditiva. En el componente de percepción: 13,0 % refirió no escuchar bien, 28,8 % informó síntomas extraauditivos, 53,3 % tenía antecedentes otológicos, y 69,0 % manifestó molestia por ruido extramural. En la regresión logística, las variables más asociadas con disminución auditiva fueron: de las ambientales, vivir en zonas de mayor ruido (OR = 1,50) (IC95%: 1,34-1,69); de las individuales, ser hombre (OR = 1,85) (IC95%: 1,64-2,09) y la edad (por cada año de vida, el riesgo de disminución auditiva aumentó 6 %); y de las otológicas, tener antecedente de síntomas otológicos (OR = 1,86) (IC95%: 1,66-2,08). Conclusiones. La disminución auditiva es multicausal en la población evaluada. Los factores que aumentan su prevalencia son incremento de la edad, ser hombre, tabaquismo, medicamentos ototóxicos, vivir en zonas de mayor exposición a ruido y presentar síntomas extraauditivos.

Comparative transcriptome profiling reveals RNA splicing alterations and biological function in patients exposed to occupational noise.

Genetic factors play an important role in susceptibility to noise-induced hearing loss (NIHL). Alternative splicing (AS) is an essential mechanism affecting gene expression associated with disease pathogenesis at the post-transcriptional level, but has rarely been studied in NIHL. To explore the role of AS in the development of NIHL, we performed a comprehensive analysis of RNA splicing alterations by comparing the RNA-seq data from blood samples from NIHL patients and subjects with normal hearing who were exposed to the same noise environment. A total of 356 differentially expressed genes, including 23 transcription factors, were identified between the two groups. Of particular note was the identification of 56 aberrant alternative splicing events generated by 41 differentially expressed genes between the two groups, with exon skipping events accounting for 54% of all the differentially alternative splicing (DAS) events. The results of functional enrichment analysis showed that these intersecting DAS genes and differentially expressed genes were significantly enriched in autophagy and mitochondria-related pathways. Together, our findings provide insights into the role of AS events in susceptibility and pathogenesis of NIHL.

[Research progress on antioxidant therapy and prevention in noise- induced hearing loss].

Noise- induced hearing loss usually refers to auditory impairment which is caused by long-term exposure to noise. The occupational noise problem is serious and urgently needs to be addressed, along with the lack of effective treatments. Recent studies have shown that the imbalance between oxidation and antioxidation is the source of the disease. To correct the redox reaction imbalance and to maintain an equilibrium of the redox reaction have always been the research focus of the prevention and treatment in noise induced hearing loss. This article reviews antioxidant therapy and prevention in noise induced hearing loss, including antioxidants, antioxidant enzymes and herbal medicine.

Acoustic shock: an update review.

BACKGROUND: This paper discusses the concept of acoustic shock based on a literature review and the results of our own research into cases seen in both clinical and medicolegal practice. With the demise of traditional 'metal bashing' and 'smoke stack' heavy industries, there has been a decline in the incidence of noise-induced hearing loss and tinnitus in this form of employment. However, with the increasing establishment of call centre work, the emergence of acoustic shock has been noted. Acoustic shock is recognised as a clinical entity distinct from noise-induced hearing loss and acoustic trauma. OBJECTIVE: This article discusses clinical implications, medicolegal considerations in light of a recent high-profile court case and proposed criteria for diagnosis.

[Noise-induced blood-labyrinth-barrier trauma of guinea pig and the protective effect of matrix metalloproteinase inhibitors].

Objective: The research is to study the expression and distribution of matrix metalloproteinase (MMPs)-2 and -9 in the guinea pig cochlea after noise exposure, and to explore the role of MMPs in the blood-labyrinth-barrier (BLB). In addition, the role of MMPs inhibitor doxycycline in noise-induced BLB trauma was studied as well, which provides the basis for further studies and prophylaxis of noise-induced hearing loss. Methods: A total of 45 healthy adult guinea pigs were randomly divided into the control group (15 received intraperitoneal injection of 0.9% saline for 4 consecutive days), the noise-exposure group (15 exposed by 120 dB SPL white noise for 4 h per day for continuous 2 d, intraperitoneal injection of normal saline for 4 consecutive days) and the noise-exposure + doxycycline group (15 exposed by 120 dB SPL white noise exposure for 4 h per day for 2 consecutive days, and intraperitoneal injection of doxycycline 50 mg/kg/d for 4 consecutive days), respectively. Immunofluorescence staining, western blot, and real-time quantitative PCR were used to analyze the distribution and differential expression of MMP-2 and -9 in the stria vascularis of guinea pigs in comparison with the normal control group, noise only group, and noise & doxycycline treatment group. Immunofluorescence staining was used to observe the changes in tight junction (TJ) protein ZO-1 in stria vascularis in three groups and to investigate the effect of acoustic injury on TJs. And ABR tests were utilized to detect the hearing function of guinea pigs in the three groups. Intravenous Evans blue was administrated intravenously as an indicator of vascular leakage among three groups to study the changes in BLB permeability in context of acoustic injury. SPSS 22.0 was used for statistical analysis. Results: There was no significant difference in hearing function between the noise-exposure group and the noise & doxycycline group two hours after noise exposure. After seven, 14 and 28 days noise exposure, the hearing recovery of the noise & doxycycline treatment group was significantly greater than that of the noise-exposure group (P<0.05) . Immunofluorescence staining showed that there was only a small amount of MMP-2 and -9 in the stria vascular in the normal control group, and ZO-1 showed dense linear expression. While, in the noise-explore group, MMP-2 and -9 in the stria vascular was significantly elevated (P<0.05), and the configuration of ZO-1 became loose and discontinuous. However, the MMP-2 and -9 in the noise & doxycycline treatment group were not significantly different from the normal control group (P>0.05), which were significantly less than that in the noise-exposure group, and just a little break of ZO-1 was observed, however, the overall structure remained dense. The leakage of Evans blue from stria vascular capillary in the noise-exposure group was significantly increased, and the difference between the other two groups did not show any statistical significance (P>0.05). Conclusions: The damage of tight junction structure induced by MMP-2 and -9 may play an important role in BLB destruction. In addition, doxycycline can inhibit MMPs secretion, thereby, to some extent, protecting the integrity of BLB from acoustic injury, and contributing to the long-term hearing recovery.

Cochlear Damage Caused by the Striking Noise of Titanium Head Golf Driver.

OBJECTIVES: To investigate how mouse cochleae are affected by the striking noise of titanium head golf driver. METHODS: Thirty-two BALB/c mice (20-22 g) with normal hearing were used. The impact acoustic stimulus generated by the striking of titanium golf driver head was centered around 4.5 kHz with 120.5 dB sound pressure level. The recorded impact noise was provided to mice in two ways with the same exposure time of 288 seconds: 1,440 repetitions and an impact duration of 0.2 seconds for 2 hours (repetitive noise) or serially connected impact noise for 288 seconds (continuous noise). Auditory brainstem responses were measured at baseline, day 7, and day 14 after exposure. The mice were then sacrificed for histology. RESULTS: Both groups showed statistically significant threshold shifts immediately after noise exposure. Mice in the continuous exposure group, except for those exposed to 32 kHz noise, recovered from threshold shifts 1-2 weeks after noise exposure. However, in the repetitive exposure group, threshold shifts remained for 2 weeks after exposure. The repetitive exposure group had greater hair cell damage than did the continuous exposure group. Structural changes in the stria vascularis were observed in the repetitive exposure group. CONCLUSION: Overexposure to impact noise caused by hitting of titanium head golf driver may be hazardous to the cochlea, and repetitive exposure may induce greater damage than continuous exposure.

The effect of earplug training on noise protection.

BACKGROUND: Noise-induced hearing loss is an occupational disease, and workplace noise exposure is a major hazard in Korea. Although hearing protectors effectively reduce a worker's exposure to noise, their success is compromised by the wearer's inability to fit the protectors correctly, and there are no proper training methods for using hearing protectors in small-scale industries. This study aims to evaluate the effect of earplug training on hearing protection using field microphone-in-real-ear (F-MIRE) and prevent noise-induced hearing loss. METHODS: The study population comprised 172 noise-exposed manufacturing workers who visited occupational health facilities in Daegu, South Korea, between July 2014 and September 2017. Personal attenuation ratings (PARs) were calculated with F-MIRE. Paired t-tests were used to compare the differences in PAR (dB) before and after training, and generalized estimating equations (GEEs) were used to compare the differences in PAR according to the number of trainings. RESULTS: Mean PARs increased after the first and second training, and the differences were statistically significant. Among the 30 participants who received all 4 trainings, PARs were significantly higher after each training than before the training. As the number of training increased, the differences in PARs significantly increased. When comparing pretraining PARs for each training session, we found statistically significant differences between the first and second training and between the second and third training, but not between the third and fourth training. CONCLUSION: In this study, the short- and long-term effects of earplug training were statistically significant. In particular, the PAR before and after the fourth training showed the greatest increase, and the PARs continued to increase during each training.

Comparison of oral steroid regimens for acute acoustic trauma caused by gunshot noise exposure.

BACKGROUND: There are no definite guidelines regarding the most adequate steroid regimens for acute acoustic trauma. OBJECTIVE: To elucidate the dose-dependent differing benefits of oral steroids on hearing improvement following acute acoustic trauma. METHODS: Twenty-nine patients treated with oral steroids following a diagnosis of unilateral acute acoustic trauma were retrospectively reviewed. Patients were sorted into two groups with an oral steroid regimen. Group 1 received a 14-day course of treatment: 60 mg prednisolone daily for 10 days, tapering off over days 11-14. Group 2 received prednisolone for a total of 10 days: 60 mg for 5 days, tapering down each day for the remainder. Multivariable linear regression analysis was performed to evaluate the factors associated with the hearing gain. RESULTS: In the multivariable regression (R2 = 0.51, p < 0.001), patients in group 1 showed more significant improvement in the degree of hearing gain compared to group 2 (p = 0.03). CONCLUSION: After comparing the differing benefits of oral steroids on hearing improvement by dosage, we recommend a high dose of prednisolone (60 mg per day) for 10 days, tapering over the remaining 4 days, for better hearing recovery following acute acoustic trauma.

Enfrentamento da subnotificação da perda auditiva induzida por ruído relacionada ao trabalho: a experiência de uma oficina educativa em planejamento e programação local em saúde do trabalhador / Addressing underreported occupational noise-induced hearing loss: the experience of an educational workshop on local occupational health planning and program

Resumo Introdução: a subnotificação da Perda Auditiva Induzida por Ruído (Pair) relacionada ao trabalho é um problema que contribui para a invisibilidade e falta de prioridade deste agravo nos programas de Saúde do Trabalhador (ST). Logo, ações de educação permanente voltadas ao planejamento estratégico-situacional podem contribuir para o enfrentamento desta realidade. Objetivo: apresentar e discutir a experiência de uma intervenção educativa com técnicos da ST de uma macrorregião de saúde do estado da Bahia, Brasil, sobre o uso do Planejamento e Programação Local em Saúde (PPLS) como ferramenta para ampliação da notificação da Pair relacionada ao trabalho Métodos: a intervenção consistiu em uma oficina estruturada em cinco etapas, as quais proporcionaram discussão sobre a Pair, conhecimento do PPLS, prática do PPLS, socialização dos resultados e avaliação do evento. Resultados: a prática do PPLS, a partir de um problema real, viabilizou o delineamento de ações concretas de enfrentamento da subnotificação da Pair a serem implementadas nos Centros de Referência em Saúde do Trabalhador (Cerest) e no estado como um todo. Conclusão: a experiência mostrou-se bem-sucedida ao fomentar a tomada de consciência e mobilização dos técnicos para enfrentamento da subnotificação da Pair, ao tempo que propiciou qualificação em PPLS dos participantes.

Abstract Introduction: underreported occupational noise-induced hearing loss (ONIHL) is an issue that increases the invisibility and lack of priority of this condition in occupational health (OH) programs. Hence, permanent education actions focused on strategic-situational planning may help address the situation. Objective: to present and discuss the experience of an educational intervention in OH technicians of a larger health region in the state of Bahia, Brazil, approaching the use of the Local Health Planning and Program (PPLS, in Portuguese) as a toll to increase reports of ONIHL. Methods: the intervention had a workshop structured into five stages, which approached ONIHL discussions, PPLS knowledge, PPLS practice, result socialization, and event evaluation. Results: real-problem PPLS practice made it possible to outline concrete actions to address underreported ONIHL, which can be implemented in Occupational Health Reference Centers (Cerest) and other settings statewide. Conclusion: the experience proved to be positive, raising technicians' awareness of underreported ONIHL and mobilizing them to address the underreporting of ONIHL, while also effectively training participants to use PPLS.

Blood Pressure of Jordanian Workers Chronically Exposed to Noise in Industrial Plants.

BACKGROUND: Occupational studies investigating the association between blood pressure and noise exposure are almost lacking in the Eastern Mediterranean Region countries. OBJECTIVE: To determine the association between occupational exposure to high level of noise and blood pressure among a group of workers in Jordan. METHODS: All workers who had been exposing to noise for at least 3 years in 3 plants in Madaba governorate in Jordan were included in this cross-sectional study. A structured questionnaire was used to collect data. The occupational noise level was measured with a portable calibrated sound meter. RESULTS: We studied 191 male workers, of whom 145 (75.9%) were exposed to a noise level higher than the permissible limit of 85 dBA. The mean systolic blood pressure (SBP) and diastolic blood pressure (DBP) and the prevalence of hypertension were significantly higher among those exposed to higher noise level. In multivariate analysis, workers exposed to high level of noise had a significantly higher odds of hypertension compared to those exposed to noise level lower than the permissible limit (OR 4.7, 95% CI 1.6 to 13.8). The odds of hypertension increased by 17% (95% CI 10% to 30%) for each dB increase in noise intensity. CONCLUSION: Exposure to high level of noise is associated with elevated blood pressure.