Mandakh Yumjirmaa, Oudin Anna, Erlandsson Lena, Isaxon Christina, Hansson Stefan R, Broberg Karin, Malmqvist Ebba
Environment Society and Health, Division of Occupational and Environmental Medicine, Department of Laboratory Medicine, Lund University, Lund, Sweden.
Section of Sustainable Health, Department of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden.
Front Toxicol. 2021 May 26;3:659407. doi: 10.3389/ftox.2021.659407. eCollection 2021.
Studies have shown that ambient air pollution is linked to preeclampsia (PE), possibly via generation of oxidative stress in the placenta. Telomere length and mitochondrial DNA copy number (mtDNAcn) are sensitive to oxidative stress damage. To study the association between prenatal exposure to ambient nitrogen oxides (NO, a marker for traffic-related air pollution), and PE, as well as potential mediation effects by placental telomere length and mtDNAcn. This is a cross-sectional study of 42 preeclamptic and 95 arbitrarily selected normotensive pregnant women with gestational ambient NO exposure assessment in southern Scania, Sweden. Hourly concentrations of NO were estimated at the residential addresses by a Gaussian-plume dispersion model with 100 × 100 m spatial resolutions and aggregated into trimester-specific mean concentrations. Placental relative mtDNAcn and telomere length were measured using qPCR. Linear and logistic regression models were used to investigate associations, adjusted for perinatal and seasonal characteristics. Exposure was categorized into low and high exposures by median cut-offs during first [11.9 μg/m; interquartile range (IQR) 7.9, 17.9], second (11.6 μg/m; IQR: 7.1, 21.1), third trimesters (11.9 μg/m; IQR: 7.7, 19.5) and entire pregnancy (12.0 μg/m; IQR: 7.6, 20.1). Increased risk of PE was found for high prenatal NO exposure during the first trimester (OR 4.0; 95% CI: 1.4, 11.1; = 0.008), and entire pregnancy (OR 3.7; 95% CI: 1.3, 10.4; = 0.012). High exposed group during the first trimester had lower placental relative mtDNAcn compared with low exposed group (-0.20; 95% CI: -0.36, -0.04; = 0.01). Changes in relative mtDNAcn did not mediate the association between prenatal NO exposure and PE. No statistically significant association was found between placental relative telomere length, prenatal NO exposure and PE. In this region with relatively low levels of air pollution, ambient NO exposure during the first trimester was associated with reduced placental relative mtDNAcn and an increased risk of PE. However, we did not find any evidence that mtDNAcn or TL mediated the association between air pollution and PE. Future research should further investigate the role of mtDNAcn for pregnancy complications in relation to exposure to ambient air pollution during pregnancy.
研究表明，环境空气污染可能通过在胎盘中产生氧化应激与先兆子痫（PE）相关联。端粒长度和线粒体DNA拷贝数（mtDNAcn）对氧化应激损伤敏感。本研究旨在探讨孕期暴露于环境氮氧化物（NO，交通相关空气污染的标志物）与PE之间的关联，以及胎盘端粒长度和mtDNAcn的潜在中介作用。这是一项横断面研究，纳入了瑞典斯坎尼亚南部42例先兆子痫孕妇和95例随机选取的血压正常孕妇，对其孕期环境NO暴露进行评估。通过空间分辨率为100×100米的高斯烟羽扩散模型估算其居住地址每小时的NO浓度，并汇总为各孕期的平均浓度。采用qPCR测量胎盘相对mtDNAcn和端粒长度。使用线性和逻辑回归模型进行关联分析，并对围产期和季节特征进行了校正。根据中位数将暴露分为低暴露和高暴露组，第一孕期（11.9μg/m；四分位数间距（IQR）7.9，17.9）、第二孕期（11.6μg/m；IQR：7.1，21.1）、第三孕期（11.9μg/m；IQR：7.7，19.5）和整个孕期（12.0μg/m；IQR：7.6，20.1）。发现第一孕期（OR = 4.0；95%CI：1.4，11.1；P = 0.008）和整个孕期（OR = 3.7；95%CI：1.3，10.4；P = 0.012）高孕期NO暴露会增加PE风险。第一孕期高暴露组胎盘相对mtDNAcn低于低暴露组（-0.20；95%CI：-0.36，-0.04；P = 0.01）。相对mtDNAcn的变化并未介导孕期NO暴露与PE之间的关联。未发现胎盘相对端粒长度、孕期NO暴露与PE之间存在统计学显著关联。在该空气污染水平相对较低的地区，第一孕期环境NO暴露与胎盘相对mtDNAcn降低及PE风险增加相关。然而，我们未发现任何证据表明mtDNAcn或TL介导了空气污染与PE之间的关联。未来研究应进一步探讨mtDNAcn在孕期暴露于环境空气污染相关妊娠并发症中的作用。
