Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University Medical Center, New York, NY, USA.
Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University Medical Center, New York, NY, USA.
Environ Res. 2021 Jan;192:110341. doi: 10.1016/j.envres.2020.110341. Epub 2020 Oct 14.
Prenatal phthalate exposures may affect processes that underlie offspring cardiometabolic health, but findings from studies examining these associations are conflicting. We examined associations between biomarkers of phthalate exposures during pregnancy with child lipid and adipokine levels.
Data were from 463 mother-child pairs in the PROGRESS cohort of Mexico City. We quantified 15 phthalate metabolites in 2nd and 3rd trimester maternal urine samples and created an average pregnancy measure using the geometric mean. We evaluated the 15 metabolites as nine biomarkers, including four metabolite molar sums. We measured fasting serum triglycerides, non-HDL cholesterol, leptin, and adiponectin in children at the six-year follow-up visit (mean = 6.8 years). We estimated associations using linear regression, Bayesian kernel machine regression (BKMR), and weighted quantile sum (WQS) and assessed effect modification by sex.
In BKMR and WQS models, higher concentrations of the total mixture of phthalate biomarkers were associated with lower triglycerides (β = -3.7% [-6.5, -0.78] per 1 unit increase in WQS biomarker index) and non-HDL cholesterol (β = -2.0 [-3.7, -0.25] ng/ml per increase in WQS biomarker index). Associations between individual biomarkers and child outcomes were largely null. We observed some evidence of effect modification by child sex for mono-3-carboxypropyl phthalate (β = 19.4% [1.26, 40.7] per doubling of phthalate) and monobenzyl phthalate (β = -7.6% [-14.4, -0.23]) in girls for adiponectin.
Individual prenatal phthalate biomarkers were not associated with child lipid or adipokine levels. Contrary to our hypothesis, the total phthalate mixture was associated with lower child triglycerides and non-HDL cholesterol.
产前邻苯二甲酸酯暴露可能会影响后代心脏代谢健康的相关过程,但目前研究这些关联的结果存在冲突。我们研究了孕妇在怀孕期间接触邻苯二甲酸酯的生物标志物与儿童脂质和脂肪因子水平之间的关系。
本研究的数据来自墨西哥城 PROGRESS 队列的 463 对母婴。我们在孕妇的第 2 期和第 3 期尿液样本中定量检测了 15 种邻苯二甲酸酯代谢物,并使用几何平均值创建了一个平均妊娠指标。我们评估了 15 种代谢物,包括 4 种代谢物摩尔总和,作为 9 种生物标志物。在 6 岁的随访中(平均=6.8 岁),我们测量了儿童的空腹血清甘油三酯、非高密度脂蛋白胆固醇、瘦素和脂联素。我们使用线性回归、贝叶斯核机器回归(BKMR)和加权分位数总和(WQS)评估了关联,并评估了性别对效应修饰的影响。
在 BKMR 和 WQS 模型中,较高浓度的邻苯二甲酸酯生物标志物总混合物与较低的甘油三酯(β=-3.7%[-6.5,-0.78],每增加 1 个 WQS 生物标志物指数单位)和非高密度脂蛋白胆固醇(β=-2.0[-3.7,-0.25]ng/ml,每增加 1 个 WQS 生物标志物指数单位)相关。个别生物标志物与儿童结局之间的关联大多为零。我们观察到一些证据表明,邻苯二甲酸单 3-羧丙酯(β=19.4%[1.26,40.7],每翻倍)和邻苯二甲酸单苄酯(β=-7.6%[-14.4,-0.23])与女孩的脂联素之间存在性别效应修饰。
个体产前邻苯二甲酸酯生物标志物与儿童脂质或脂肪因子水平无关。与我们的假设相反,总邻苯二甲酸酯混合物与儿童甘油三酯和非高密度脂蛋白胆固醇水平较低有关。