脂谱受噪声和遗传变异的影响。然而,对职业噪声和遗传变异与年龄相关的血脂变化的关联知之甚少,动脉粥样硬化性心血管疾病的发生和发展的一个重要事件。我们旨在评估基于应激激素生物合成的基因中血脂变化率与职业噪声和遗传变异的关联。该队列成立于2012年和2013年,并一直跟进到2017年。共有952名参与者被纳入最终分析,所有参与者被分为两组,暴露组和对照组,根据工作区域中暴露的噪音水平。对基于应激激素生物合成的基因中的单核苷酸多态性(SNP)进行了基因分型。从2012年到2017年进行了五次体检,并重复五次血脂测量。血脂的估计年度变化(EAC)计算为任何2次相邻检查之间的血脂水平差异除以时间间隔(年)。使用具有可交换相关结构的重复测量分析的广义估计方程来评估暴露于噪声(与作为对照相比)和上述SNP对血脂EAC的影响。我们发现,参与者在暴露于噪声时经历了与年龄相关的高密度脂蛋白胆固醇(HDL-C)水平的加速下降(β=-0.38,95%置信区间(CI),-0.66至-0.10,P=0.007),调整工作持续时间后,性别,吸烟,酒精消费,和包年。这种趋势仅在COMT-rs165815TT基因型的参与者中发现(β=-1.19,95%CI,-1.80至-0.58,P<0.001),但不是在那些CC或CT基因型。在多次调整后,噪声暴露和rs165815的相互作用是微不足道的(P相互作用=0.010)。与DDC-rs11978267AA基因型携带者相比,携带rs11978267GG基因型的参与者甘油三酯(TG)的EAC降低(β=-5.06,95%CI,-9.07~-1.05,P=0.013).携带DBH-rs4740203CC基因型的参与者总胆固醇(TC)的EAC升高(β=1.19,95%CI,0.06至2.33,P=0.039)。然而,经过多次校正后,这些结果无统计学意义.这些结果表明,职业噪声暴露与HDL-C水平的年龄相关加速下降有关,COMT-rs165815基因型似乎改变了噪声暴露对职业人群HDL-C变化的影响。
Lipid profiles are influenced by both noise and genetic variants. However, little is known about the associations of occupational noise and genetic variants with age-related changes in blood lipids, a crucial event in the initiation and evolution of atherosclerotic cardiovascular diseases. We aimed to evaluate the associations of blood lipid change rates with occupational noise and genetic variants in stress hormone biosynthesis-based genes. This cohort was established in 2012 and 2013 and was followed up until 2017. A total of 952 participants were included in the final analysis and all of them were categorized to two groups, the exposed group and control group, according to the exposed noise levels in their working area. Single nucleotide polymorphisms (SNPs) in stress hormone biosynthesis-based genes were genotyped. Five physical examinations were conducted from 2012 to 2017 and lipid measurements were repeated five times. The estimated annual changes (EACs) of blood lipid were calculated as the difference in blood lipid levels between any 2 adjacent examinations divided by their time interval (year). The generalized estimating equations for repeated measures analyses with exchangeable correlation structures were used to evaluate the influence of exposing to noise (versus being a control) and the SNPs mentioned above on the EACs of blood lipids. We found that the participants experienced accelerated age-related decline in high-density lipoprotein cholesterol (HDL-C) levels as they were exposed to noise (β = -0.38, 95% confidence interval (CI), -0.66 to -0.10, P = 0.007), after adjusting for work duration, gender, smoking, alcohol consumption, and pack-years. This trend was only found in participants with COMT-rs165815 TT genotype (β = -1.19, 95% CI, -1.80 to -0.58, P < 0.001), but not in those with the CC or CT genotypes. The interaction of noise exposure and rs165815 was marginally significant (Pinteraction = 0.010) after multiple adjustments. Compared with DDC-rs11978267 AA genotype carriers, participants carrying rs11978267 GG genotype had decreased EAC of triglycerides (TG) (β = -5.06, 95% CI, -9.07 to -1.05, P = 0.013). Participants carrying DBH-rs4740203 CC genotype had increased EAC of total cholesterol (TC) (β = 1.19, 95% CI, 0.06 to 2.33, P = 0.039). However, these findings were not statistically significant after multiple adjustments. These results indicated that Occupational noise exposure was associated with accelerated age-related decreases in HDL-C levels, and the COMT-rs165815 genotype appeared to modify the effect of noise exposure on HDL-C changes among the occupational population.