[A case-control study on the relationship between DNA methylation and occupational noise hearing loss].

Objective: To explore the relationship between DNA methylation and occupational noise-induced hearing loss. Methods: A case-control study was conducted. People with hearing loss induced by occupational noise were recruited as the case group and those with normal hearing but still exposed to occupational noise were recruited as the control group. A total of 60 participants were included, of which 30 participants were in the case group and 30 in the control group. The methylation level was detected by 850k genome-wide DNA methylation chip technology. The significance of differential methylated position (DMP) was tested by R-packet 'Champ'. The differential methylated region (DMR) was analyzed by using Champ's Bumphunter algorithm. Cluster profiler was used to analyze the gene list for GO and KEGG pathway enrichment. Results: There was significant difference between two groups in binaural high-frequency average hearing threshold (P<0.05), but there was no significant difference in age, smoking, drinking, hypertension, physical exercise and cumulative noise exposure. The results of DMP and DMR analysis showed that 713875 sites were detected in the case group and the control group, and 439 methylation sites with significant difference, accounting for 0.06%; 650 regions were detected, and 72 methylation regions with significant differences, accounting for 11.08%. Compared with the control group, the results of GO enrichment analysis showed that the case group had statistically significant differences in four pathways: axogenesis of projection neurons in the central nervous system, neuronal development in the central nervous system, axogenesis of neurons in the central nervous system and neuronal differentiation in the central nervous system. KEGG enrichment analysis showed that there were significant differences in sphingolipid metabolism, aldosterone synthesis and secretion, primary bile acid biosynthesis pathway between the case group and the control group. Conclusion: The occurrence of occupational noise-induced hearing loss may be related to the regulation of gene expression related to axogenesis of projection neurons in the central nervous system, development of neurons in the central nervous system, axogenesis of neurons in the central nervous system, differentiation of neurons in the central nervous system, sphingolipid metabolism, aldosterone synthesis and secretion, primary bile acid biosynthesis and gene methylation related to metabolism.

[Analysis on the effect of sound insulation reconstruction in operation room of steel rolling production line in a steel plant].

Objective: To investigate the effect of sound insulation improvement on the noise exposure of workers in the operation room of hot rolling line for wide and heavy plate. Methods: From September 2019 to September 2017, based on the occupational health Survey, the data of 25 fixed operation rooms and workers in operation rooms of a steel rolling production line were collected retrospectively, the noise exposure levels before and after the improvement of sound insulation were statistically analyzed. Results: The noise exposure value of the workers, the qualified rate of 0 Grade 8 hours equivalent noise (L(EX, 8 h)) ≤85 dB (A) and the qualified rate of the design limit value of the operation room were all higher than those before the modification, the difference was statistically significant (P<0.01) , after the renovation, the Class II and above noise hazards were eliminated, the equivalent continuous a sound level (L(Aeq, 8 h)) >75 dB (A) of the workers in the operation room was 8h, and the noise level in the operation room still did not meet the Ergonomics limit standard. Conclusion: The improvement of sound insulation can effectively improve the working environment of noise workplace operating room and reduce the workers'noise exposure level.

[Relationship research among CDH23 gene and the risk of noise-induced hearing loss].

Objective: To explore the relationship among CDH23 gene variation and the risk of noise-induced hearing loss (NIHL) . Methods: The nested case-control study was performed and this study followed a cohort of 6297 noise-exposed workers in a steel factory of Henan province in China from January 1, 2006 to December 31, 2015. In July 2019, subjects whose average hearing threshold were more than 40 dB in high frequency were defined as the case group, and subjects whose average hearing threshold were less than 35 dB in high frequency and less than 25 dB in speech frequency were defined as the control group. A nested case-control study which included 572 subjects was carried out, in which subjects consisted of 286 cases and 286 controls. 18 single nucleotide polymorphisms (SNPs) in CDH23 were selected and genotyped, then we analyzed the association among SNPs in CDH23, haplotypes in CDH23 and NIHL risk. Logistic regression was performed to analyze the main effects of SNPs and the interactions between CNE and SNPs adjusting cumulative noise exposure (CNE) , smoking, drinking, physical exercise and hypertension. Moreover, the association between haplotypes in CDH23 and NIHL risk were also analyzed. We ananlyzed the relationship amongst different SNP groups and NIHL risk using the generalized multifactor dimensionality reduction (GMDR) method. Results: The results suggested that significant associations were observed for rs3802711, rs3752751, rs3752752, rs11592462, rs10762480, rs3747867 for NIHL overall and/or various CNE strata by adjusting CNE, smoking, drinking, physical exercise and blood pressure. For rs3802711, workers exposure to noise carrying the AA/GA genotype of rs3802711 increased risk of NIHL than those carrying GG genotype (OR=3.121; 95%CI:1.054-9.239, P=0.035) in overall; In the stratified analysis of CNE (>97 dB (A) ·year at rs3802711 locus, workers exposure to noise carrying GA genotype (OR=2.056; 95%CI:1.226~3.448, P=0.006) and GA+AA/GA genotype (OR=2.221; 95%CI:1.340~3.681, P=0.002) increased NIHL risk. For rs11592462, workers exposure to noise carrying the GG genotype of rs11592462 increased risk of NIHL than those carrying CC genotype in overall (OR=3.951; 95%CI:1.104-14.137, P=0.04) ; workers exposure to noise carrying the GG genotype of rs11592462 increased risk of NIHL than those carrying CG+CC genotype in overall (OR=4.06; 95%CI:1.145-14.391, P=0.03) . After adjusting CNE, smoking, drinking, physical exercise and blood pressure, the haplotypes of CDH23 rs1227049, rs10999947, rs3752752, rs3752751, rs10762480, rs3802711, rs11592462, rs10466026, rs4747194, rs4747195 were not associated with the risk of NIHL. GMDR analysis showed no association between SNP combination and NIHL risk after adjusting CNE, smoking, drinking, physical exercise and blood pressure. Conclusion: Gene polymorphisms in CDH23 might associate significantly with the risk of 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.

[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 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.

[Retrospective investigation on explosive hearing loss of injured persons in explosion accidents involving a steel enterprise].

Objective: Through the investigation of the injured persons in explosion accidents, the impact of wearing the ear protectors device (anti-noise earplugs) on the auditory organs and hearing loss of the injured person was understood, which could provide reference for the clinical diagnosis, treatment and prevention of the explosive hearing impairment. Methods: A retrospective survey was conducted on 39 directly injured persons who were injured in 23 explosion accidents involving a steel plant from 1990 to 2016 as the explosive hearing loss, taking the time of the patient＇s injury and 3-6 months after the injury as the time of investigation and evidence collection, and according to whether to wear the ear protectors device for group comparison and statistical analysis. Results: There was no significant difference between the two groups in hearing loss, tinnitus, earache, headache, some patients with dizziness and craniocerebral injury, regardless of whether the injured person wore anti-noise earplugs or not (P=0.444-1) , the shock (coma) patients in the non-protected group were more common (34.8%, 8/23) , and the difference was statistically significant (P=0.012) ; Although auricle injury was detected in both groups and there was no significant difference between the two groups (P=1) , but the external ear canal injury, tympanic membrane perforation were more common in the non-protected group, and there was no external ear canal and tympanic membrane perforation in the wearing earplug group, and the difference between the two groups was significant (P=0.000) . After 3-6 months, the rehabilitation of auditory system and other symptoms in patients showed that the hearing loss, tinnitus, earache, headache, dizziness and other symptoms all disappeared in patients wearing earplugs, while the above symptoms in the non-protected group were improved but more persisted, and the difference between the two groups was statistically significant (P=0.000-0.012) , and there was no significant difference in rehabilitation conditions such as craniocerebral injury between the two groups (P=1) ; There were patients with unhealed auricle injury in both groups in 3-6 months after the injury, and there was no significant difference between the two groups (P=1) , however, in the non-protected group, 69.57% (16/23) of the patients with external auditory canal injury were still unhealed and none of the patients with tympanic membrane perforation recovered, and the difference between the two groups was obvious (P=0.000~0.001) ; Pure tone air conduction examination showed that the hearing of the earplugs wearers was well recovered at the time of the explosion, while irreversible hearing impairment was common in the non-protective group, the difference was statistically significant (P=0.000) . Conclusion: Ear protector plays an important role in protecting the auditory organs and hearing of workers in explosion accident, and it is an effective protective measure to prevent and reduce the damage of external ear canal, perforation of tympanic membrane and explosive hearing loss caused by explosion accidents.

[Clinicopathological analysis of 12 cases of children synovial sarcoma].

Objective: To investigate histopathological characteristics, and differential diagnoses of childhood synovial sarcoma. Methods: HE staining, immunohistochemical staining and fusion gene detection by FISH were performed in 12 cases of synovial sarcoma in childhood at Beijing Children's Hospital from 2016 to 2018. Results: There were 6 cases of biphasic type, 1 case of monophasic epithelial type, 3 cases of monophasic spindle cell type and 2 cases of poorly differentiated synovial sarcomas. EMA, CKpan, bcl-2, CD99, TLE1 and CD34 immunostain positivities were observed in 10/12, 9/12, 12/12, 10/12, 10/12 and 0/12 cases respectively. Unique INI1 immunohistochemical staining was observed in 9/12 cases. SS18-SSX gene fusion was detected in 8 of 11 cases by FISH. Conclusions: Synovial sarcoma is rare in children. Histological morphology combined with immunohistochemistry and FISH SS18-SSX fusion gene detection are important for the diagnosis and differential diagnosis of synovial sarcoma in children.

[Association between variations in protocadherin 15 gene and occupational noise-induced hearing loss].

Objective: The aim of this study was to investigate whether genetic variability in the protocadherin 15 (PCDH15) gene may correspond with increased susceptibility to noise-induced hearing loss (NIHL) in a Chinese population. Methods: A nested case-control study was performed that followed a cohort of 7 445 noise-exposed workers in a steel factory of Henan province in China from January 1, 2006 to December 31, 2015. In this study, 394 cases who had an average hearing threshold of more than 40 dB (A) in high frequency were defined as the case group, and 721 controls who had an average hearing threshold of less than 35 dB (A) in high frequency and less than 25 dB (A) in speech frequency were defined as the control group. A questionnaire was completed by participants and a physical test was also conducted. SNP genotyping was performed using the SNPscanTM Kit. Multivariate unconditional logistic regression additive models were used to analyze the genotypes in different groups, and the association with NIHL. Unconditional logistic regression models were used to assess the associations between the genotypes and NIHL. Results: The average age of study participants was (40.5±8.3) years and the median number of noise-exposed working years M (P25, P75) was 21.1 (9.1, 27.3). The range of noise exposed levels and the levels of cumulative noise exposure (CNE) were 80.1- 98.8 dB(A) and 86.6- 111.2 dB(A), respectively. Only the distribution of the genotypes (TT/CC/CT) of rs11004085 in the PCDH15 gene showed a significant difference between the case and control groups (P=0.049). In the case group, the distribution was 370 (93.9%), 24 (6.1%) and 0; in the control group, the distribution was 694 (96.3%), 23 (3.2%) and 1 (0.1% ). After smoking, drinking, hypertension, height and CNE adjustment, compared with the TT genotype individuals with the CC/CT genotype had a 1.90-fold increased risk of NIHL (95% CI: 1.06- 3.40). After stratified these data by the noise exposure level or CNE when the noise exposure level was>85 dB (A), compared with cases with the AA genotype of rs10825113, individuals with the GA/GG genotype had a 2.63-fold increased risk of NIHL (95% CI: 1.12- 6.14). When the CNE was ≤ 98 dB(A), compared with cases with the TT genotype of rs11004085, individuals with the CC/CT genotype had a 2.96-fold increased risk of NIHL (95% CI: 1.33- 6.56). However, these differences were not significant after Bonferroni correction had been applied. Conclusions: The results confirmed that genetic variation within the PCDH15 gene may affect the susceptibility to NIHL.

[A cohort study on occupational noise induced hearing loss in workers at an iron and steel plant].

Objective: To analyze the incidence rate of occupational noise-induced hearing loss in noise-exposed workers in an iron and steel plant from 2006 to 2015. Methods: Using a cohort study method, workers exposed to occupational noise from Jan 1, 2006 to Dec 12, 2015 were followed up and the pure tone hearing test was conducted. In total, 6 297 subjects completed two or more physical checks and the pure tone hearing test and were included in the analysis. The noise exposure level at the workplace and the equivalent continuous A-weighted sound pressure level for workers was monitored and the cumulative noise exposure dose was evaluated. The subjects were divided into low, middle and high exposure groups according to the noise exposure level, and the equivalent continuous A-weighted sound pressure level for 8 hours for each group was 80.6-85.0, 85.1-90.0 and 90.1-103.4 dB (A), respectively. While the RR and 95% CI were derived from unconditional logistic regression models. In logistic regression analysis, confounding factors such as age, gender, smoking habit, drinking habit, high temperature exposure and chemical hazards exposure level were controlled. Results: During the follow-up period, 392 cases of occupational noise-induced hearing loss were diagnosed among the 6 297 subjects, with an incidence rate of 6.23%; 318 cases of high-frequency hearing loss were diagnosed, with an incidence rate of 5.05%; and 74 cases of occupational noise-induced deafness were diagnosed, with an incidence rate of 1.18% . The incidence rates of hearing loss among the high, medium and low exposure groups were 9.22% (158/1 737), 6.49% (204/3 142) and 2.08% (30/1 442), respectively; the rates of high-frequency hearing loss were 7.41% (127/1 737), 5.25% (165/3 142) and 1.80% (26/1 442), respectively; and the rates of occupational noise-induced deafness were 1.81% (31/1 737), 1.24% (39/3 142) and 0.28% (4/1 442), respectively. For the groups corresponding to cumulative noise exposure doses of ≤84.99, 85.00- 87.99, 88.00- 90.99, 91.00- 93.99, 94.00- 96.99, 97.00- 100.99, 101.00- 102.99 and ≥103.00 dB (A) · year, the incidence rates of hearing loss were 0 (0/185), 1.22% (2/164), 2.52% (17/674), 3.83% (35/913), 5.80% (106/1 827), 6.02% (67/1 113), 9.20% (95/1 003) and 18.04% (70/388), respectively. Compared with the low exposure group, the RR of hearing loss, high-frequency hearing loss and occupational noise-induced deafness for the high exposure group were 4.78 (95% CI: 3.22- 7.11), 4.36 (95% CI: 2.84- 6.69) and 6.63 (95% CI: 2.33- 18.82), respectively; and for the medium exposure group were 3.27 (95% CI: 2.22-4.82), 3.02 (95% CI: 1.99-4.59) and 4.52 (95% CI: 1.61-12.67), respectively. Conclusion: The incidence rate of hearing loss for workers exposed to noise in an iron and steel plant was related to the cumulative noise exposure dose, gender, age, educational level, smoking habits, drinking habits and exposure to high temperature.

[Association between eye absent homolog 4 gene polymorphisms and occupational noise-induced hearing loss].

Objective: To identify the association between genetic polymorphisms in the eye absent homolog 4 (EYA4) gene and noise-induced hearing loss (NIHL). Method: A nested case control study was conducted based on a cohort of noise-exposed subjects. In total, 292 cases were selected from a steel factory from 6 297 subjects during Jan 1, 2006 to Dec 12, 2015,who had an average hearing threshold of more than 40 dB(A); 584 matched control subjects for each case were designated on the basis of matched criteria including same gender, age (±5 years) and duration of exposure to noise (±2 years). What's more, the control group had an average hearing threshold of less than 35 dB(A) in high frequency and less than 25 dB(A) in speech frequency. Four single nucleotide polymorphisms (SNPs) of the EYA4 gene were genotyped using a SNPscanTM multiplex SNP genotyping kit. Hardy-Weinberg equilibrium tests were performed using a χ2 test for goodness-of-fit for each SNP among the control group, and the effects of genotypes of the EYA4 gene on NIHL were analyzed by logistic regression. The haplotypes were established and their frequencies in the two groups were assessed using Haploview 4.2 and Phase 2.1 software, and interactive effects between haplotypes and cumulative noise exposure were analyzed. Results: The average age of the subjects was (40.1±8.4) years and the average number of noise-exposed working years was 20.3 (8.4, 27.3) years. The range of noise exposure levels and the cumulative noise exposure were 80.2- 98.8 dB (A) and 86.6- 111.2 dB(A) · year, respectively. After adjustment for covariates including height, blood pressure, drinking status and smoking status, in the noise intensity>85 dB (A) group, subjects carrying the rs3813346 TT genotype had a higher NIHL risk than those carrying the GG genotype, and the adjusted OR (95% CI) value was 2.12 (1.21- 3.69). In the cumulative noise exposure>98 dB (A) · year group, compared with haplotype TGC, haplotype CGT showed a protective effect in the development of NIHL, with an adjusted OR (95% CI) value of 0.60 (0.37-0.97), however, the significance of intercation between EY4 gene of noise was lost after Bonferroni correction. Conclusion: Genetic polymorphism in the EYA4 gene may be a genetic susceptibility factor for NIHL.

[Investigation into the relationship between mitochondrial 12 S rRNA gene, tRNA gene and cytochrome oxidase â ¡ gene variations and the risk of noise-induced hearing loss].

Objective: To explore the relationship between mitochondrial 12 S rRNA gene variation, tRNA gene variation and cytochrome oxidase Ⅱ gene point mutations and the risk of noise-induced hearing loss (NIHL). Methods: A nested case-control study was performed that followed a cohort of 7 445 noise-exposed workers in a steel factory in Henan province, China, from January 1, 2006 to December 31, 2015. Subjects whose average hearing threshold was more than 40 dB(A) in high frequency were defined as the case group, and subjects whose average hearing threshold was less than 35 dB(A) in high frequency and less than 25 dB (A) in speech frequency were defined as the control group. Subjects was recruited into the case group (n=286) and the control group (n=286) according to gender, age, job category and time of exposure to noise, and a 1∶1 case-control study was carried out. We genotyped eight single nucleotide polymorphisms in the mitochondrial 12 S rRNA gene, the mitochondrial tRNA gene and the mitochondrial cytochrome oxidase Ⅱ gene using SNPscan high-throughput genotyping technology from the recruited subjects. The relationship between polymorphic sites and NIHL, adjusted for covariates, was analyzed using conditional logistic regression analysis, as were the subgroup data. Results: The average age of the recruited subjects was (40.3±8.1) years and the length of service exposure to noise was (18.6±8.9) years. The range of noise exposed levels and cumulative noise exposure (CNE) was 80.1- 93.4 dB (A) and 86.8- 107.9 dB (A) · year, respectively. For workers exposed to noise at a CNE level<98 dB (A) · year, smokers showed an increased risk of NIHL of 1.88 (1.16-3.05) compared with non-smokers; for workers exposed to noise at a CNE level ≥98 dB(A) · year, smokers showed an increased risk of NIHL of 2.53 (1.49- 4.30) compared with non-smokers. For workers exposed to noise at a CNE level<98 dB (A) · year, the results of univariate analysis and multifactor analysis, adjusted by smoking and CNE, suggested that the risk of NIHL in workers exposed to noise carrying the GG genotype (G827A) was lower than that of NIHL workers exposed to noise carrying the AA genotype (G827A) [OR (95% CI) were 0.18 (0.04- 0.82) and 0.19 (0.04- 0.88), respectively]. Conclusion: Smoking increased the risk of NIHL in the present study. For workers subjected to a CNE<98 dB(A)·year, the mitochondrial genetic variant G827A was found to be significantly associated with the risk of NIHL.

[Association between grainyhead-like 2 gene polymorphisms and noise-induced hearing loss].

OBJECTIVE: To investigate association between genetic polymorphism in the grainyhead-like 2 gene (GRHL2) and noise-induced hearing loss (NIHL) in the Chinese population. METHODS: A matched case-control association study was employed, In which, 3 790 workers exposed to continuous and steady-state occupational noise in a steel factory participated. The questionnaires were adopted to collect individual features and audiometry tests performed. In the sstudy, 286 subjects were diagnosed as cases, Which were each designated on the basis of the matched criterion, and 286 paired samples were selected finally. Noise intensity was measured according to the standards given in 'Measurement of Noise in the Workplace'(Occupational Health Standard of the People's Republic of China, GBZ/T189.8-2007). Cumulative noise exposure (CNE) was calculated, according to monitoring data on A-weighed sound pressure level and employment time. Genomic DNA was obtained from peripheral blood samples using 2 mL DNA extraction Kit following the manufacturer's protocol. Five single nucleotide polymorphisms (SNPs) of GRHL2 were genotyped by multiplex SNP genotyping kit. The continuous variables and categorical variables were analyzed by t-test and chi-square test respectively. Multivariate Logistic regression was used to test the association between genetic frequency and disease status, with adjustments for the possible confounding variables. The haplotypes were established and their frequencies in the two groups were assessed by haploview and phase softwares. RESULTS: All the five SNPs (rs3735713, rs3824090, rs3735714, rs3735715 and rs611419) were in Hardy-Weinberg equilibrium (HWE) (P>0.05). The subjects carrying rs3735715 GG genotype had a higher NIHL risk than those carrying the GA genotype under the co-dominant model (OR=0.644, 95% CI: 0.442-0.939, P=0.022) after adjustment for height, blood pressure, drinking status and smoking status. After being stratified by CNE, in the CNE ≥ 98 dB (A) group, rs3735715 polymorphism was associated with the NIHL under the co-dominant model (OR=0.509, 95% CI: 0.281-0.923, P=0.026) after adjustment for height, blood pressure, drinking status and smoking status as well. However, no statistical significant difference was found in variant genotypes of the other SNPs between the case and control subjects. Four-locus (rs3735713, rs3824090, rs3735714 and rs3735715) haplotypes were constructed, and no risk or protective haplotypes was identified. CONCLUSION: It is suggested that GRHL2 polymorphisms may be associated with development of NIHL.

[Factors influencing electrocardiogram results in workers exposed to noise in steel-making and steel-rolling workshops of an iron and steel plant].

OBJECTIVE: To investigate the factors influencing the electrocardiogram results in the workers exposed to noise in steel-making and steel rolling workshops of an iron and steel plant. METHODS: From September to December, 2013, cluster sampling was used to select 3 150 workers exposed to noise in the steel-making and steel-rolling workshops of an iron and steel plant, and a questionnaire survey and physical examinations were performed. The number of valid workers was 2 915, consisting of 1 606 workers in the steel-rolling workshop and 1 309 in the steel-making workshop. The electrocardiogram results of the workers in steel-making and steel-rolling workshops were analyzed. RESULTS: The overall abnormal rate of electrocardiogram was 26.35%, and the workers in the steel-making workshop had a significantly higher abnormal rate of electrocardiogram than those in the steel-rolling workshop(32.24% vs 21.54%, P<0.05). Male workers had a significantly higher abnormal rate of electrocardiogram than female workers(27.59% vs 18.61%, P<0.05). The workers with a drinking habit had a significantly higher abnormal rate of electrocardiogram than those who did not drink(28.17% vs 23.75%, P<0.05). The workers exposed to high temperature had a significantly higher abnormal rate of electrocardiogram than those who were not exposed to high temperature(29.43% vs 20.14%, P<0.05). The abnormal rates of electrocardiogram in the workers with cumulative noise exposure levels of <90, 90~94, 95~99, 100~104, and 105~113 dB(A)·year were 21.21%, 21.76%, 26.50%, 27.27%, and 32.16%, respectively, with significant differences between any two groups(P<0.05). The multivariate logistic regression analysis showed that a cumulative noise exposure of 105-113 dB(A)·year(OR=1.36, 95% CI: 1.03~1.80), a drinking habit(OR=1.20, 95% CI: 1.01~1.43), and high temperature(OR=1.60, 95% CI: 1.32~1.92) were the risk factors for abnormal electrocardiogram results. CONCLUSION: High cumulative noise exposure, alcohol consumption, and high temperature may affect the abnormal rate of electrocardiogram in the workers exposed to noise in steel-making and steel-rolling workshops.

[Association between single nucleotide polymorphismsin human heat shock protein 70 gene and susceptibility to noise-induced hearing loss].

Objective: To investigate the association between the single nucleotide polymorphisms (SNPs) at rs1043618, rs2075800, and rs2763979 in human heat shock protein 70 (HSP70) gene and susceptibility to noise-induced hearing loss (NIHL) . Methods: A case-control study was performed, and 5 934 workers exposed to noise in an iron and steel plant in Henan, China, who underwent physical examination from 2006 to 2015, were enrolled as study subjects. According to the criteria of binaural average high - frequency (3000, 4000, and 6000 Hz) hearing threshold≥40 dB (HL) and monauralaverage speech-frequency (500, 1000, 2000 Hz) hearing threshold≥26 dB (HL) on the basis of binauralhigh frequency loss measured by pure tone audiometry, as well as the exclusion of NIHL, a total of 286 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) , 286 workers were enrolled as control group. A 2 ml blood genomic DNA extraction kit was used to perform DNA extraction for the peripheral blood samples, and a multiple SNP typing kit was used to determine the genotypes at the three loci in 572 samples. The association between the SNPs at the three loci and susceptibility to NIHL was analyzed. Results: In all workers, the equivalent sound level (L(Aeq)) of noise was 75.0~96.8 dB (A) . The hearing loss group had a significantly higher binauralhigh - frequencyhearing threshold than the control group (t=56.908, P<0.05) . With CC+TC genotype as control, TT genotype at rs2763979 in HSP70 gene was associated with the susceptibility to NIHL (OR=1.731, 95%CI 1.021-2.935) . In the group with cumulative noise exposure of 96 dB (A) ·year, TT genotype at rs2763979was associated with the susceptibility to NIHL (OR=5.694, 95%CI 1.256-25.817) . The rs1043618 and rs2075800 loci of HSP70 were not associated with the susceptibility to NIHL (both P>0.05) . After the adjustment for confounding factors including smoking and drinking, haplotype CCT was associated with the susceptibility to NIHL (OR=1.425, 95%CI 1.035-1.961) . Conclusion: TT genotype at rs2763979 of HSP70 gene and haplotype CCT are risk factors for NIHL.

[Association between serum magnesium ion level and risk of noise-induced hearing loss].

Objective: To investigate the association between serum magnesium ion level and risk of noise-induced hearing loss (NIHL) . Methods: Acohort study was performed for 7 445 workers exposed to noise in the steelmaking and steel rolling workshops of an iron and steel enterprise in Henan Province, China. The follow-up time was from January 1, 2006 to December 31, 2015. The workers with a binaural average high-frequency hearing threshold of ≥40 dB (HL) were enrolled as case group, and those with a binaural average high-frequency hearing threshold of <35 dB (HL) and a binaural average speech frequency of ≤25 dB (HL) were enrolled as control group. After being matched for age, working years of noise exposure, sex, and type of work at a ratio of 1∶1, 187 workers each were enrolled in the case group and the control group. Flame atomic absorption spectrometry was used to measure the serum magnesium ionlevel. Aconditional logistic regression analysis was performed to investigate the association of serum magnesium ion level, body mass index, cumulative noise exposure (CNE) , smoking, drinking, hypertension, and physical exercise with NIHL, as well as the association between serum magnesium ion level and risk of NIHL after the adjustment for covariants. Results: There was no significant difference in the serum magnesium ion level between the case group and the control group (24.63±7.92 mg/m(3) vs 24.91±7.33 mg/m(3), P>0.05) . Smoking (OR=1.687, 95%CI 1.090-2.613) was a risk factor for NIHL, and physical exercise (OR=0.509, 95%CI 0.325-0.796) reduced the risk of NIHL. In the workers with CNE>98 dB (A) ·year, the risk of NIHL in the workers with higher CNE was 1.305 times (95%CI 1.051-1.620) that in those with lower CNE. After the adjustment for CNE, smoking, and physical exercise, there was no significant difference in the influence of serum magnesium ion level on the risk of NIHL between the two groups (P>0.05) . Conclusion: Serum magnesium ion level may not be associated with NIHL. Increased CNE and smoking may increase the risk of NIHL and physical exercise may reduce the risk of NIHL.