Department of Environmental Health Sciences, University of Michigan School of Public Health, Ann Arbor, MI, United States.
Division of Maternal-Fetal Medicine, Brigham and Women's Hospital, Boston, MA, United States; Harvard Medical School, Boston, MA, United States.
Environ Int. 2014 Sep;70:118-24. doi: 10.1016/j.envint.2014.05.016. Epub 2014 Jun 13.
Preterm birth is a significant public health problem, affecting over 1 in 10 live births and contributing largely to infant mortality and morbidity. Everyday exposure to environmental chemicals such as phthalates could contribute to prematurity, and may be modifiable. In the present study we examine variability in phthalate exposure across gestation and identify windows of susceptibility for the relationship with preterm birth.
Women were recruited early in pregnancy as part of a prospective, longitudinal birth cohort at the Brigham and Women's Hospital in Boston, Massachusetts. Urine samples were collected at up to 4 time points during gestation for phthalate measurement, and birth outcomes were recorded at delivery. From this population we selected all 130 cases of preterm birth, defined as delivery before 37 weeks of completed gestation, as well as 352 random controls.
Urinary phthalate metabolite levels were moderately variable over pregnancy, but levels measured at multiple time points were associated with increased odds of preterm birth. Adjusted odds ratios (aOR) for spontaneous preterm birth were strongest in association with phthalate metabolite concentrations measured at the beginning of the third trimester (aOR for summed di-2-ethylhexyl phthalate metabolites [∑DEHP]=1.33, 95% confidence interval [CI]=1.02, 1.73). Odds ratios for placental preterm birth, defined as delivery with presentation of preeclampsia or intrauterine growth restriction, were slightly elevated in the first trimester for DEHP metabolites (aOR for ∑DEHP=1.33, 95% CI=0.99, 1.78).
Pregnant women with exposure to phthalates both early and late in pregnancy are at an increased risk of delivering preterm, but mechanisms may differ based on etiology.
早产是一个重大的公共卫生问题，影响超过十分之一的活产儿，是婴儿死亡率和发病率的主要原因。日常接触邻苯二甲酸酯等环境化学物质可能会导致早产，而且这些因素可能是可以改变的。在本研究中，我们研究了妊娠期间邻苯二甲酸酯暴露的变异性，并确定了与早产相关的易感窗口期。
妇女在怀孕早期作为马萨诸塞州波士顿布莱根妇女医院前瞻性纵向出生队列的一部分被招募。在妊娠期间最多采集 4 次尿液样本进行邻苯二甲酸酯检测，并在分娩时记录出生结局。从该人群中，我们选择了所有 130 例早产病例，定义为妊娠 37 周前分娩，以及 352 例随机对照病例。
妊娠期间尿液邻苯二甲酸酯代谢物水平存在中度变异性，但多个时间点测量的水平与早产的几率增加相关。与妊娠早期相比，与第三孕期开始时测量的邻苯二甲酸酯代谢物浓度相关的自发性早产调整比值比（aOR）更强（二（2-乙基己基）邻苯二甲酸酯代谢物总和[∑DEHP]的 aOR=1.33，95%置信区间[CI]=1.02，1.73）。与子痫前期或宫内生长受限相关的胎盘早产的比值比在妊娠早期 DEHP 代谢物略有升高（∑DEHP 的 aOR=1.33，95%CI=0.99，1.78）。
在妊娠早期和晚期接触邻苯二甲酸酯的孕妇早产风险增加，但发病机制可能因病因而异。
