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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.
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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.
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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.
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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.
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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 col-lect individual features and audiometry tests performed.In the sstudy,286 subjects were diagnosed as ca-ses,Which were each designated on the basis of the matched criterion,and 286 paired samples were se-lected 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 /T1 89.8 -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 polymor-phisms (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 re-gression 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 (rs373571 3, rs3824090,rs373571 4,rs373571 5 and rs61 1 41 9)were in Hardy-Weinberg equilibrium (HWE)(P >0.05).The subjects carrying rs373571 5 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 ad-justment for height,blood pressure,drinking status and smoking status.After being stratified by CNE,in the CNE ≥ 98 dB (A)group,rs373571 5 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 (rs373571 3,rs3824090,rs373571 4 and rs373571 5)haplotypes were constructed,and no risk or protec-tive haplotypes was identified.Conclusion:It is suggested that GRHL2 polymorphisms may be associated with development of NIHL.
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<p><b>OBJECTIVE</b>To investigate the prevalence and influence factors of hypertension among the workers exposed to noise in steel making and steel rolling workshop of an iron and steel plant.</p><p><b>METHODS</b>Using cluster sampling method, 3 150 workers exposed to noise participated in this study. According to do questionnaire survey and blood pressure measurement, 2 924 workers were tested, among which 1 313 workers were from steel making workshop and 1 611 workers were from steel rolling workshop. The relationships between different demographic characteristics, different habits, and different cumulative noise exposures of workers exposed to noise and hypertension were analyzed.</p><p><b>RESULTS</b>For the hypertension prevalence rate, the total prevalence rate was 27.43% (802/2 924), the male was higher than the female (29.88 % (753/2 520) vs 12.13% (49/404), χ² = 55.13, P < 0.001), married ones were higher than the unmarried (29.84% (718/2 406) vs 16.22% (84/518), χ² = 39.76, P < 0.001), the smoking subjects were higher than the no smoking (30.31% (438/1 445) vs 24.61% (364/1 479), χ² = 11.93, P = 0.001), drinking ones were higher than the no drinking (31.53% (541/1 716) vs 21.61% (261/1 208), χ² = 35.05, P < 0.001). The hypertension prevalence rates among the subjects with education background in junior high school and below, high school (secondary) and university and above were separately 44.96%(125/278), 29.95%(455/1 519) and 19.70%(222/1 127) (χ² = 81.65, P < 0.001), among cumulative exposure groups 77-89, 90-94, 95-99, 100-104 and 105-113 were separately 8.43% (14/166), 14.48% (53/366), 24.28% (297/1 223), 36.65% (335/914) and 40.39%(103/255) (χ² = 127.58, P < 0.001). Multivariate logistic regression analysis showed that workers who exposed to cumulative noise in 95-99, 100-104 and 105-113 dB(A) ·year had the higher risk of hypertension, the OR (95%CI) were 1.84 (95% CI: 1.35-2.51), 1.74 (95% CI: 1.24-2.45) and 1.68 (95% CI: 1.09-2.58). Drinking (OR = 1.60, 95% CI: 1.32-1.95) and BMI ≥ 24.0 kg/m² (OR = 1.26, 95% CI: 1.22-1.30) were the risk factors for hypertension as well.</p><p><b>CONCLUSION</b>Cumulative noise exposure, alcohol consumption and above normal BMI may affect the hypertension prevalence rate of the workers exposed to noise.</p>
Subject(s)
Animals , Female , Humans , Male , Alcohol Drinking , Demography , Hypertension , Iron , Noise , Occupational Exposure , Overweight , Prevalence , Risk Factors , Smoking , Steel , Surveys and QuestionnairesABSTRACT
<p><b>OBJECTIVE</b>To explore depressive symptoms and influencing factors in employees from 13 enterprises.</p><p><b>METHODS</b>A total of 6711 workers from 13 enterprises were investigated by cluster sampling, and data were collected anonymously between November 2008 and June 2009. Job satisfaction, occupational stressors, strains, coping strategy, and social support were measured using occupational stress instruments, job content questionnaire, and effort-reward imbalance questionnaire.</p><p><b>RESULTS</b>Median and P25~P75 values of depression score were 14 and 9~21, respectively. The depression score of male workers (16.31 ± 10.12) was significantly higher than that of female workers(14.50 ± 9.08) (Z=4.09, P<0.01). The depression score of managers was lowest (12.89 ± 8.70), and the front-line workers scored highest (16.02 ± 9.94), with a significant difference between the two groups (χ² =9.90, P<0.01). The depression score of shift workers (16.79 ± 9.974) was significantly higher than that of non-shift workers (14.81 ± 9.63) (Z=53.43, P<0.01). The depression scores of workers with weekly job times of ≤ 40 h, ~50 h, ~59 h, and ≥ 60 h were (14.70 ± 9.94), (15.76 ± 9.84), (15.46 ± 9.91), and (19.70 ± 10.67), respectively (χ² = 31.79, P <0.01). Correlation analysis revealed that depression score was negatively correlated with the scores of job control (r=-0.236, P <0.01), reward (r=-0.443, P<0.01), job satisfaction (r=-0.418, P<0.01), positive affectivity (r=-0.307, P <0.01), superior support (r=-0.287, P<0.01), colleague support (r=-0.235, P<0.01), and coping strategy (r=-0.208, P<0.01), but positively correlated with the scores of external effort (r=0.225, P<0.01), inherent effort (r=0.248, P<0.01), psychological demands (r = 0.246, P <0.01), physical demands (r=0.246, P<0.01), and negative affectivity (r=0.525, P<0.01). Multivariate logistic regression analysis revealed that the risk of depressive symptoms in workers with high negative affectivity was about four times as high as that in workers with low negative affectivity. The risks of depressive symptoms in workers with low reward, having disease in the past six months, and with high inherent effort were 1.62, 1.50, and 1.48 times, respectively, as high as those for their counterparts.</p><p><b>CONCLUSION</b>Occupational stress, individual factors, health status, and shift work affect the depressive symptoms of workers. Reducing negative affectivity and increasing rewards are main measures to relieve depressive symptoms.</p>