Associations of prenatal exposure to perfluoroalkyl substances with preterm birth: A family-based birth cohort study

Associations of prenatal exposure to perfluoroalkyl substances with preterm birth: A family-based birth cohort study
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产前接触全氟烷基物质与早产的关联:基于家庭的出生队列研究

DOI:
10.1016/j.envres.2022.113803
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发表时间:
2022
影响因子:
8.3
通讯作者:
Guang-Hui Dong
Guang-Hui Dong
中科院分区:
环境科学与生态学2区
文献类型:
--
作者:
Yunjiang Yu;Xiao-Di Qin;Michael S Bloom;Chu Chu;Xin Dai;Qin-Qin Li;Zan-Xiong Chen;Min-Li Kong;Yan-Qi Xie;Wen-Jie Meng;Bo-Yi Yang;Li-Wen Hu;Xiao-Wen Zeng;Xiao-Miao Zhao;Yang Zhou;Guang-Hui Dong

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研究调查了母亲暴露于PFAS和早产之间的关联,但父亲和整个家庭暴露于PFAS混合物对早产的影响仍然未知。为了解决这一知识差距,在2016年至2018年期间,在中国沿海地区共选择了355名早产儿和481名对照儿童进行基于家庭的出生队列研究。对母亲、父亲和新生儿血清中的7种PFAS(全氟丁酸(PFBA)、全氟己酸(PFHxA)、全氟己磺酸(PFHxS)、全氟辛酸(PFOA)、全氟辛烷磺酸(PFOS)、全氟壬酸(PFNA)和全氟癸酸(PFDA))进行了定量分析。早产定义为小于37个完整孕周的活产。采用贝叶斯核机器回归(BKMR)模型对PFAS混合物的联合效应进行了检验。潜在类别分析用于确定家庭水平的PFAS暴露概况。多元线性回归分析显示,早产的几率与母亲PFBA较高有关(OR = 1.16,95%CI:1.09,1.25),PFOA(比值比= 1.51,95%CI:1.27,1.80),全氟辛烷磺酸(OR = 2.07,95%CI:1.70,2.52)和PFNA(OR = 1.36,95%CI:1.01,1.83),新生儿PFBA(OR = 1.16,95%CI:1.05,1.29),PFHxA(OR = 1.46,95%CI:1.32,1.62),PFHxS(OR = 1.15,95%CI:1.05,1.26)和PFNA(OR = 1.30,95%CI:1.09,1.56)。个体父亲PFAS暴露与早产之间的关联被逆转。在家庭水平上,较高的PFAS混合物浓度与早产几率较高相关。特别是,较高的PFNA和PFDA暴露与较高的早产风险相关(OR = 2.55,95%CI:1.45,4.50)。PFAS与早产的关联被家庭一级的海鲜消费所改变。我们的研究结果表明,较高的家庭水平的PFNA和PFDA暴露与更大的早产风险相关,尽管个体父亲,母亲和新生儿PFAS暴露的结果是矛盾的。如果在其他沿海地区复制,这些研究结果强调了需要关注家庭三联体,并在评估PFAS暴露的生殖毒性时考虑海鲜消费。
Studies have investigated associations between maternal exposure to PFAS and preterm birth, but the impact of paternal and overall family exposure to PFAS mixtures on preterm birth remains unknown. To address this knowledge gap, a total of 355 preterm births and 481 controls were selected for a family-based birth cohort study in a coastal area of China, between 2016 and 2018. Seven PFAS, including perfluorobutanoic acid (PFBA), perfluorohexanoic acid (PFHxA), perfluorohexanesulfonic acid (PFHxS), perfluorooctanoic acid (PFOA), perfluorooctanesulfonic acid (PFOS), perfluorononanoic acid (PFNA) and perfluorodecanoic acid (PFDA), were quantified in maternal, paternal and neonatal sera. Preterm birth was defined as live delivery at <37 completed gestational weeks. Bayesian kernel machine regression (BKMR) model was used to inspect the combined effect of family PFAS mixtures. Latent class analysis was used to identify family-level PFAS exposure profiles. Multiple linear regression analysis showed higher odds of preterm birth in association with higher maternal PFBA (OR = 1.16, 95%CI:1.09, 1.25), PFOA (OR = 1.51, 95%CI:1.27, 1.80), PFOS (OR = 2.07, 95%CI:1.70, 2.52) and PFNA (OR = 1.36, 95%CI: 1.01, 1.83), and neonatal PFBA (OR = 1.16, 95%CI:1.05,1.29), PFHxA (OR = 1.46, 95%CI:1.32, 1.62), PFHxS (OR = 1.15, 95%CI:1.05, 1.26) and PFNA (OR = 1.30, 95%CI:1.09,1.56). The associations were reversed between individual paternal PFAS exposures and preterm birth. At the family level, higher PFAS mixture concentration was associated with higher odds of preterm birth. In particular, higher PFNA and PFDA exposure was associated with greater preterm birth risk (OR = 2.55, 95%CI:1.45, 4.50). The PFAS-preterm association was modified by family-level seafood consumption. Our results suggest that higher family-level PFNA and PFDA exposure was associated with greater preterm birth risk, although the results for individual paternal, maternal and neonatal PFAS exposures were contradictory. If replicated in other coastal areas, these findings highlight a need to focus on the family triad and to consider seafood consumption when assessing the reproductive toxicity of PFAS exposure.