School of Public Health, Hangzhou Normal University, Hangzhou, China.
Wu Yun Shan Hospital of Hangzhou, Hangzhou, China.
Noise Health. 2023 Jul-Sep;25(118):143-157. doi: 10.4103/nah.nah_65_22.
To explore the association of lifestyles, caspase gene (CASP), and noise kurtosis with noise-induced hearing loss (NIHL).
Three hundred seven NIHL individuals and 307 matched controls from factories in Chinese factories participated in this case-control study. Age, sex, noise exposure, exfoliated oral mucosa cells, and lifestyles of participants were gathered by the authors. The single nucleotide polymorphisms (SNPs) were genotyped using the Kompetitive Allele Specific polymerase chain reaction (KASP) method.
The risk of NIHL was higher for people who worked in the complex noise environment than for people exposed to steady noise environment (adjusted: OR = 1.806, P = 0.002). Smoking and regular earphone use increased the risk of NIHL (adjusted: OR = 1.486, P = 0.038). The GG genotype of the recessive model and G allele in rs1049216, together with the TT genotype of the recessive model in rs6948 decreased the NIHL risk (adjusted: OR = 0.659, P = 0.017). Oppositely, the AA genotype of additive model in rs12415607 had a higher NIHL risk (adjusted: OR = 1.804, P = 0.024). In the additive models, there was a positive interaction between noise kurtosis and CASP3 polymorphisms (RERI = 1.294, P = 0.013; RERI = 1.198, P = 0.031).
Noise kurtosis, three SNPs (rs1049216, rs6948, and rs12415607), smoking and earphone use were found to be related to NIHL, and there was a positive interaction between noise kurtosis and CASP3. Results from this study can be used to prevent and detect NIHL and for genetic testing.
探讨生活方式、半胱氨酸蛋白酶基因(CASP)和噪声峰度与噪声性听力损失(NIHL)的关系。
本病例对照研究纳入了来自中国工厂的 307 名 NIHL 患者和 307 名匹配对照。作者收集了参与者的年龄、性别、噪声暴露、脱落口腔黏膜细胞和生活方式等信息。采用 Kompetitive Allele Specific polymerase chain reaction(KASP)方法对单核苷酸多态性(SNP)进行基因分型。
与接触稳定噪声环境的人群相比,工作于复杂噪声环境中的人群发生 NIHL 的风险更高(调整后:OR=1.806,P=0.002)。吸烟和经常使用耳机也会增加 NIHL 的发病风险(调整后:OR=1.486,P=0.038)。rs1049216 中的隐性模型 GG 基因型和 G 等位基因,以及 rs6948 中的隐性模型 TT 基因型降低了 NIHL 的发病风险(调整后:OR=0.659,P=0.017)。相反,rs12415607 中的加性模型 AA 基因型具有更高的 NIHL 发病风险(调整后:OR=1.804,P=0.024)。在加性模型中,噪声峰度和 CASP3 多态性之间存在正交互作用(RERI=1.294,P=0.013;RERI=1.198,P=0.031)。
噪声峰度、三个 SNP(rs1049216、rs6948 和 rs12415607)、吸烟和耳机使用与 NIHL 相关,噪声峰度和 CASP3 之间存在正交互作用。本研究结果可用于预防和检测 NIHL,并进行遗传检测。