Jiao J, Gu G Z, Chen G S, Li Y H, Zhang H L, Yang Q Y, Xu X R, Zhou W H, Wu H, He L H, Zheng Y X, Yu S F
Department of Occupational Health, Henan Provincial Institute for Occupational Health, Zhengzhou 450052, China.
Zhonghua Yu Fang Yi Xue Za Zhi. 2017 Jan 6;51(1):34-40. doi: 10.3760/cma.j.issn.0253-9624.2017.01.008.
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). 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 (=286) and the control group (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. 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) [ (95% ) were 0.18 (0.04- 0.82) and 0.19 (0.04- 0.88), respectively]. 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.
探讨线粒体12 S rRNA基因变异、tRNA基因变异及细胞色素氧化酶Ⅱ基因点突变与噪声性听力损失（NIHL）风险之间的关系。对中国河南省一家钢铁厂的7445名噪声暴露工人进行了一项巢式病例对照研究，研究时间从2006年1月1日至2015年12月31日。高频平均听力阈值大于40 dB(A)的受试者被定义为病例组，高频平均听力阈值小于35 dB(A)且言语频率平均听力阈值小于25 dB(A)的受试者被定义为对照组。根据性别、年龄、工作类别和噪声暴露时间，将受试者纳入病例组（n = 286）和对照组（286），并进行1∶1病例对照研究。我们使用SNPscan高通量基因分型技术对招募受试者的线粒体12 S rRNA基因、线粒体tRNA基因和线粒体细胞色素氧化酶Ⅱ基因中的8个单核苷酸多态性进行基因分型。使用条件逻辑回归分析以及亚组数据，分析了多态性位点与NIHL之间经协变量调整后的关系。招募受试者的平均年龄为（40.3±8.1）岁，噪声暴露工龄为（18.6±8.9）年。噪声暴露水平范围和累积噪声暴露（CNE）分别为80.1 - 93.4 dB(A)和86.8 - 107.9 dB(A)·年。对于CNE水平<98 dB(A)·年的噪声暴露工人，吸烟者发生NIHL的风险比非吸烟者增加了1.88（1.16 - 3.05）；对于CNE水平≥98 dB(A)·年的噪声暴露工人，吸烟者发生NIHL的风险比非吸烟者增加了2.53（1.49 - 4.30）。对于CNE水平<98 dB(A)·年的噪声暴露工人，经吸烟和CNE调整后的单因素分析和多因素分析结果表明，携带GG基因型（G827A）的噪声暴露工人发生NIHL的风险低于携带AA基因型（G827A）的噪声暴露NIHL工人[（95%）分别为0.18（0.04 - 0.82）和0.19（0.04 - 0.88）]。在本研究中，吸烟增加了NIHL的风险。对于CNE<98 dB(A)·年的工人，发现线粒体基因变异G827A与NIHL风险显著相关。
