From the Epidemiology Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD (C.J.N., A.W., M.O., P.M.).
Emmes Company, Rockville, MD (S.S.).
Hypertension. 2019 Aug;74(2):384-390. doi: 10.1161/HYPERTENSIONAHA.119.12731. Epub 2019 Jun 24.
Although ambient air pollution may increase hypertension risk through endothelial damage and oxidative stress, evidence is inconsistent regarding its effect on hypertension in pregnancy. Prior research has evaluated a limited scope of pollution species and often not differentiated preeclampsia, which may have a placental origin, from gestational hypertension. Among 49 607 women with at least 2 singleton deliveries in the Eunice Kennedy Shriver National Institute of Child Health and Human Development Consecutive Pregnancies Study (2002-2010), we estimated criteria pollutant and volatile organic compound levels during pregnancy using Community Multiscale Air Quality models and abstracted gestational hypertension and preeclampsia diagnoses from medical records. Generalized estimating equations accounted for repeat pregnancies and adjusted for ambient temperature and maternal age, race/ethnicity, body mass index, smoking, alcohol, parity, insurance, marital status, and asthma. Air pollution levels were low to moderate (eg, median 41.6 ppb [interquartile range, 38.9-43.7 ppb] for ozone and 35.1 ppb [28.9-40.3 ppb] for nitrogen oxides). Higher levels of most criteria pollutants during preconception and the first trimester were associated with lower preeclampsia risk, while higher second-trimester levels were associated with greater gestational hypertension risk. For example, an interquartile increase in first-trimester carbon monoxide was associated with a relative risk of 0.88 (95% CI, 0.81-0.95) for preeclampsia and second-trimester carbon monoxide a relative risk of 1.14 (95% CI, 1.07-1.22) for gestational hypertension. Volatile organic compounds, conversely, were not associated with gestational hypertension but consistently associated with higher preeclampsia risk. These findings further suggest air pollution may affect the development of hypertension in pregnancy, although differing causes of preeclampsia and gestational hypertension may alter these relationships.
虽然环境空气污染可能通过内皮损伤和氧化应激增加高血压风险，但关于其对妊娠高血压的影响，证据并不一致。先前的研究评估了有限范围的污染物质，并且通常没有区分可能起源于胎盘的子痫前期与妊娠高血压。在 Eunice Kennedy Shriver 国家儿童健康与人类发展研究所连续妊娠研究（2002-2010 年）中，有 49607 名至少有 2 次单胎分娩的女性，我们使用社区多尺度空气质量模型估计了怀孕期间的标准污染物和挥发性有机化合物水平，并从病历中提取了妊娠高血压和子痫前期的诊断。广义估计方程考虑了重复妊娠，并根据环境温度和母亲年龄、种族/民族、体重指数、吸烟、饮酒、产次、保险、婚姻状况和哮喘进行了调整。空气污染水平较低至中等（例如，臭氧的中位数为 41.6 ppb [四分位距，38.9-43.7 ppb]，氮氧化物为 35.1 ppb [28.9-40.3 ppb]）。在受孕前和孕早期，大多数标准污染物水平较高与子痫前期风险降低相关，而在孕中期，较高的污染物水平与妊娠高血压风险增加相关。例如，第一孕期一氧化碳的四分位间距增加与子痫前期的相对风险为 0.88（95%可信区间，0.81-0.95）相关，而第二孕期一氧化碳的相对风险为 1.14（95%可信区间，1.07-1.22）与妊娠高血压相关。相反，挥发性有机化合物与妊娠高血压无关，但与子痫前期风险增加一致相关。这些发现进一步表明，空气污染可能影响妊娠高血压的发展，尽管子痫前期和妊娠高血压的不同病因可能会改变这些关系。
