Department of Epidemiology, Brown University, Providence, RI, 02912, Box G-S121, United States.
Department of Biostatistics, School of Public Health, Brown University, Providence, RI, United States.
Environ Res. 2022 Nov;214(Pt 3):114021. doi: 10.1016/j.envres.2022.114021. Epub 2022 Aug 8.
Exposure to per- and polyfluoroalkyl substances (PFAS) - endocrine disrupting chemicals - may increase cardiometabolic risk. We evaluated whether adolescent lifestyle factors modified associations between gestational PFAS exposure and cardiometabolic risk using a prospective cohort study.
In 166 mother-child pairs (HOME Study), we measured concentrations of four PFAS in maternal serum collected during pregnancy. When children were age 12 years, we calculated cardiometabolic risk scores from visceral adiposity area, blood pressure, and fasting serum biomarkers. We assessed adolescent physical activity and Healthy Eating Index scores using the Physical Activity Questionnaire for Older Children (PAQ-C), actigraphy, and 24-h diet recalls. Using multivariable linear regression and weighted quantile sum regression, we examined whether physical activity or diet modified covariate-adjusted associations of PFAS and their mixture with cardiometabolic risk scores.
Physical activity modified associations between perfluorooctanoic acid (PFOA) and cardiometabolic risk scores. Each doubling of PFOA was associated with worse cardiometabolic risk scores among children with PAQ-C scores < median (β:1.4; 95% CI:0.5, 2.2, n = 82), but not among those with PAQ-C scores ≥ median (β: 0.2; 95% CI: 1.2, 0.7, n = 84) (interaction p-value = 0.01). Associations were most prominent for insulin resistance, leptin-adiponectin ratio, and visceral fat area. We observed results suggesting that physical activity modified the association of PFAS mixture with cardiometabolic risk scores, insulin resistance, and visceral fat area (interaction p-values = 0.17, 0.07, and 0.10, respectively); however, the 95% CIs of the interaction terms included the null value. We observed similar, but attenuated patterns for PFOA and actigraphy-based measures of physical activity. Diet did not modify any associations. Physical activity or diet did not modify associations for other PFAS.
Childhood physical activity modified associations of prenatal serum PFOA concentrations with children's cardiometabolic risk in this cohort, indicating that lifestyle interventions may ameliorate the adverse effects of PFOA exposure.
接触全氟和多氟烷基物质(PFAS)-内分泌干扰化学物质-可能会增加心血管代谢风险。我们评估了青少年生活方式因素是否改变了妊娠期间 PFAS 暴露与心血管代谢风险之间的关联,使用了一项前瞻性队列研究。
在 166 对母婴(HOME 研究)中,我们测量了母亲在怀孕期间采集的血清中四种 PFAS 的浓度。当孩子 12 岁时,我们从内脏脂肪面积、血压和空腹血清生物标志物计算了心血管代谢风险评分。我们使用儿童体力活动问卷(PAQ-C)、活动记录仪和 24 小时饮食回忆评估了青少年的体力活动和健康饮食指数评分。使用多变量线性回归和加权分位数总和回归,我们检查了体力活动或饮食是否改变了 PFAS 及其混合物与心血管代谢风险评分的协变量调整关联。
体力活动改变了全氟辛酸(PFOA)与心血管代谢风险评分之间的关联。在 PAQ-C 评分<中位数的儿童中,每增加一倍 PFOA 与心血管代谢风险评分恶化相关(β:1.4;95%置信区间:0.5,2.2,n=82),但在 PAQ-C 评分≥中位数的儿童中则不然(β:0.2;95%置信区间:1.2,0.7,n=84)(交互 p 值=0.01)。这些关联在胰岛素抵抗、瘦素-脂联素比值和内脏脂肪面积方面最为明显。我们观察到的结果表明,体力活动改变了 PFAS 混合物与心血管代谢风险评分、胰岛素抵抗和内脏脂肪面积的关联(交互 p 值分别为 0.17、0.07 和 0.10);然而,交互项的 95%置信区间包含了零值。我们观察到了类似的,但减弱的模式,适用于 PFOA 和基于活动记录仪的体力活动测量。饮食没有改变任何关联。体力活动或饮食并没有改变其他 PFAS 的关联。
在该队列中,儿童期的体力活动改变了妊娠期间血清 PFOA 浓度与儿童心血管代谢风险之间的关联,表明生活方式干预可能会减轻 PFOA 暴露的不良影响。