Prospective associations of mid-childhood plasma per- and polyfluoroalkyl substances and pubertal timing.

Prospective associations of mid-childhood plasma per- and polyfluoroalkyl substances and pubertal timing.
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DOI:
10.1016/j.envint.2021.106729
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发表时间:
2021-11
影响因子:
11.8
通讯作者:
Fleisch AF
Fleisch AF
中科院分区:
环境科学与生态学1区
文献类型:
--
作者:
Carwile JL;Seshasayee SM;Aris IM;Rifas-Shiman SL;Claus Henn B;Calafat AM;Sagiv SK;Oken E;Fleisch AF

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接触全氟烷基物质和多氟烷基物质 (PFAS) 可能会扰乱青春期时间。较高的 PFAS 血浆浓度与女孩的青春期时间较晚有关,但横断面研究结果可能可以用相反的因果关系来解释。评估儿童中期 PFAS 血浆浓度与男性和女性青少年青春期时间标志物之间的前瞻性关联。我们研究了波士顿地区前瞻性队列 Project Viva 中的 640 名儿童。我们研究了平均 7.9 (SD 0.8) 年 (2007-2010) 测量的 6 种 PFAS 血浆浓度与青春期时间标记的关联。父母在青春期早期报告了 5 项青春期发育评分(平均 13.1 (SD 0.8) 岁),并每年报告初潮年龄。我们利用身高的研究和临床测量来计算峰值身高速度的年龄。我们使用性别特异性线性和 Cox 比例风险回归来估计单一 PFAS 与结果的关联,并使用贝叶斯核机器回归 (BKMR) 来估计 PFAS 混合物与结果的关联。全氟辛烷磺酸 (PFOS) 的血浆浓度最高 [中位数 (IQR) 6.4(5.6) ng/mL],其次是全氟辛酸 (PFOA) [4.4(3.0) ng/mL]。在青春期早期,女孩的青春期发育比男孩提前[女孩的青春期发育得分平均值 (SD) 为 2.9 (0.7),男孩为 2.2(0.7);身高峰值速度平均年龄 (SD) 女孩为 11.2 岁 (1.0),男孩为 13.1 岁 (1.0)]。 PFAS 仅与女孩青春期时间较晚的标志相关。例如,PFOA的每增加一倍都与较低的青春期发育评分(-0.18单位;95% CI:-0.30,-0.06)和峰值身高速度年龄较大(0.23岁;95% CI:0.06,0.40)]相关。我们观察到 PFOS、全氟癸酸酯 (PFDA) 和 PFAS 混合物也存在类似的关联。 PFAS 血浆浓度与男孩初潮年龄或青春期时间标记无关。童年中期较高的 PFAS 血浆浓度与女孩青春期开始较晚有关。
Exposure to per- and polyfluoroalkyl substances (PFAS) may disrupt pubertal timing. Higher PFAS plasma concentrations have been associated with later pubertal timing in girls, but cross-sectional findings may be explained by reverse causation. To assess prospective associations between PFAS plasma concentrations in mid-childhood and markers of pubertal timing in male and female adolescents. We studied 640 children in Project Viva, a Boston-area prospective cohort. We examined associations of plasma concentrations of 6 PFAS measured at mean 7.9 (SD 0.8) years (2007–2010) with markers of pubertal timing. Parents reported a 5-item pubertal development score at early adolescence (mean 13.1 (SD 0.8) years) and reported age at menarche annually. We calculated age at peak height velocity using research and clinical measures of height. We used sex-specific linear and Cox proportional hazards regression to estimate associations of single PFAS with outcomes, and we used Bayesian Kernel Machine Regression (BKMR) to estimate associations of the PFAS mixture with outcomes. Plasma concentrations were highest for perfluorooctane sulfonate (PFOS) [median (IQR) 6.4(5.6) ng/mL], followed by perfluorooctanoate (PFOA) [4.4(3.0) ng/mL]. In early adolescence, girls were further along in puberty than boys [pubertal development score mean (SD) 2.9 (0.7) for girls and 2.2(0.7) for boys; age at peak height velocity mean (SD) 11.2y (1.0) for girls and 13.1y (1.0) for boys]. PFAS was associated with later markers of pubertal timing in girls only. For example, each doubling of PFOA was associated with lower pubertal development score (−0.18 units; 95% CI: −0.30, −0.06) and older age at peak height velocity (0.23 years; 95% CI: 0.06, 0.40)]. We observed similar associations for PFOS, perfluorodecanoate (PFDA), and the PFAS mixture. PFAS plasma concentrations were not associated with age at menarche or markers of pubertal timing in boys. Higher PFAS plasma concentrations in mid-childhood were associated with later onset of puberty in girls.