Department of Occupational and Environmental Health Sciences, School of Public Health, Peking University, Beijing, China.
Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA; Exposure, Epidemiology and Risk Program, Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Environ Int. 2020 Aug;141:105761. doi: 10.1016/j.envint.2020.105761. Epub 2020 May 7.
Ambient particulate matter (PM) has been associated with mitochondrial damage and dysfunction caused by excessive oxidative stress, but the associations between long-term PM exposure and leukocyte mitochondrial DNA copy number (mtDNAcn), a biomarker of mitochondrial dysfunction due to oxidative stress, are less studied.
To investigate the associations between short-, intermediate- and long-term exposure (1-, 3- and 12-months) to different size fractions of PM (PM, PM and PM) and leukocyte mtDNAcn in a cross-sectional study.
The associations between each of the PM exposure metrics with z scores of log-transformed mtDNAcn were examined using generalized linear regression models in 2758 female participants from the Nurses' Health Study (NHS). Monthly exposures to PM were estimated from spatio-temporal prediction models matched to each participants' address history. Potential effect modification by selected covariates was examined using multiplicative interaction terms and subgroup analyses.
In single-size fraction models, increases in all size fractions of PM were associated with decreases in mtDNAcn, although only models with longer averages of PM reached statistical significance. For example, an interquartile range (IQR) increase in 12-month average ambient PM (5.5 μg/m) was associated with a 0.07 [95% confidence interval (95% CI): -0.13, -0.01; p-value = 0.02] decrease in mtDNAcn z score in both basic- and multivariable-adjusted models. Associations for PM were stronger after controlling for PM in two size-fraction models.
Our study suggests that long-term exposure to ambient PM is associated with decreased mtDNAcn in healthy women.
环境颗粒物（PM）与过度氧化应激引起的线粒体损伤和功能障碍有关，但长期 PM 暴露与白细胞线粒体 DNA 拷贝数（mtDNAcn）之间的关联，即氧化应激引起的线粒体功能障碍的生物标志物，研究较少。
在一项横断面研究中，调查短期、中期和长期（1 个月、3 个月和 12 个月）暴露于不同粒径的 PM（PM、PM 和 PM）与白细胞 mtDNAcn 之间的关系。
在护士健康研究（NHS）中，对 2758 名女性参与者，使用广义线性回归模型，研究了每个 PM 暴露指标与白细胞 mtDNAcn 的对数变换 Z 分数之间的关系。每月 PM 暴露量是根据与每个参与者的地址历史相匹配的时空预测模型来估计的。通过乘法交互项和亚组分析来检查选定协变量的潜在效应修饰作用。
在单一分寸模型中，所有 PM 粒径的增加都与 mtDNAcn 的减少有关，尽管只有更长平均时间的 PM 模型才具有统计学意义。例如，12 个月平均环境 PM（5.5μg/m）的四分位间距（IQR）增加与基本调整和多变量调整模型中 mtDNAcn Z 分数分别降低 0.07（95%置信区间[95%CI]：-0.13，-0.01；p 值=0.02）相关。在两个单尺寸模型中，控制 PM 后，PM 与 PM 之间的关联更强。
我们的研究表明，长期暴露于环境 PM 与健康女性的 mtDNAcn 减少有关。
