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孕期母亲接触邻苯二甲酸盐和双酚A对孕周的影响。

Effects of maternal exposure to phthalates and bisphenol A during pregnancy on gestational age.

作者信息

Weinberger Barry, Vetrano Anna M, Archer Faith E, Marcella Stephen W, Buckley Brian, Wartenberg Daniel, Robson Mark G, Klim Jammie, Azhar Sana, Cavin Sarah, Wang Lu, Rich David Q

机构信息

Robert Wood Johnson Medical School .

出版信息

J Matern Fetal Neonatal Med. 2014 Mar;27(4):323-7. doi: 10.3109/14767058.2013.815718. Epub 2013 Jul 18.

Abstract

OBJECTIVE

Phthalates and bisphenol A (BPA) are ubiquitous environmental toxicants, present in high concentrations in numerous consumer products. We hypothesized that maternal exposure to phthalates and BPA in pregnancy is associated with shortened gestation.

METHODS

Urinary phthalate and BPA metabolites from 72 pregnant women were measured at the last obstetric clinic visit prior to delivery. Using linear regression models, we estimated the change in gestational age associated with each interquartile range (IQR) increase in phthalate and BPA metabolite concentration.

RESULTS

IQR increases in urinary mono(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP) and BPA concentrations were associated with 4.2 and 1.1 d decreases in gestation, respectively. When stratified by gender, these alterations were found only in male infants.

CONCLUSIONS

We conclude that MEHHP and BPA (free + glucuronide) are associated with reductions in gestation, with effects observed only in males. Our findings are consistent with the idea that these agents induce gender-specific alterations in signaling via PPAR-γ transcription factor, androgen precursors and/or inflammatory mediators during the initiation of labor.

摘要

目的

邻苯二甲酸盐和双酚A(BPA)是普遍存在的环境毒物,在众多消费品中浓度很高。我们假设孕期母亲接触邻苯二甲酸盐和BPA与妊娠期缩短有关。

方法

在分娩前最后一次产科门诊就诊时,测量了72名孕妇的尿中邻苯二甲酸盐和BPA代谢物。使用线性回归模型,我们估计了邻苯二甲酸盐和BPA代谢物浓度每增加一个四分位数间距(IQR)时,孕周的变化。

结果

尿中单(2-乙基-5-羟基己基)邻苯二甲酸酯(MEHHP)和BPA浓度每增加一个IQR,妊娠期分别缩短4.2天和1.1天。按性别分层时,这些变化仅在男婴中发现。

结论

我们得出结论,MEHHP和BPA(游离+葡萄糖醛酸结合物)与妊娠期缩短有关,且仅在男性中观察到这种影响。我们的研究结果与以下观点一致,即在分娩开始时,这些物质通过过氧化物酶体增殖物激活受体γ转录因子、雄激素前体和/或炎症介质诱导性别特异性的信号改变。

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