Division of Epidemiology, Department of Environmental Health, University of Cincinnati College of Medicine, P.O. Box 670056, Cincinnati, OH 45267, USA.
Division of General and Community Pediatrics, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, University of Cincinnati College of Medicine, 3333 Burnet Avenue, MLC 7035, Cincinnati, OH 45229, USA.
Environ Int. 2018 Oct;119:212-219. doi: 10.1016/j.envint.2018.06.028. Epub 2018 Jul 4.
Toxicological studies highlight the potential neurotoxicity of perfluoroalkyl substances (PFAS) during fetal development. However, few epidemiological studies have examined the impact of childhood PFAS on neurodevelopment.
We employed data from 208 children in the Health Outcomes and Measures of the Environment Study, a birth cohort (Cincinnati, OH), to examine associations of six serum PFAS concentrations measured at 3 and 8 years with executive function assessed at 8 years using the validated parent-completed Behavior Rating Inventory of Executive Function survey. We used multiple informant models to identify susceptible windows of neurotoxicity to PFAS and executive function. We investigated trajectories of PFAS concentrations and whether sex modified these associations.
Each ln-increase in perfluorononanoate (PFNA) at 8 years was associated with a 3.4-point increase (95% CI 0.4, 6.3) in metacognition score, indicating poorer function. Children with PFNA above the median at 8 years had poorer global executive functioning compared to children with concentrations consistently below median levels (β = 6.5, 95% CI 0.2, 12.9). Higher concurrent PFNA was associated with poorer behavior regulation among males, while associations among females were null (p = 0.018). Children with higher concurrent perfluorooctanoate (PFOA) had increased odds of being at risk of having clinical impairments in metacognition (OR = 3.18, 95% CI 1.17, 8.60). There were no associations between perfluorooctane sulfonate and perfluorohexane sulfonate and executive function.
PFNA and PFOA at 8 years, but not 3 years, may be related to poorer executive function at 8 years. Results need to be confirmed in cohort studies with larger sample sizes.
毒理学研究强调了在胎儿发育过程中全氟烷基物质（PFAS）潜在的神经毒性。然而，很少有流行病学研究探讨儿童时期 PFAS 对神经发育的影响。
我们利用了环境健康结果和测量研究中 208 名儿童的数据，该研究是一个出生队列（俄亥俄州辛辛那提），以检验在 8 岁时测量的六种血清 PFAS 浓度与使用经过验证的父母完成的行为评定量表中评估的执行功能之间的关联。我们使用多信息模型来确定对 PFAS 和执行功能的神经毒性易感窗口。我们研究了 PFAS 浓度的轨迹，以及性别是否改变了这些关联。
在 8 岁时，每增加一个 ln-单位的全氟壬酸（PFNA），元认知评分就会增加 3.4 分（95%CI 0.4, 6.3），表明功能更差。8 岁时 PFNA 中位数以上的儿童与浓度始终低于中位数水平的儿童相比，整体执行功能更差（β=6.5，95%CI 0.2, 12.9）。在男性中，较高的 PFNA 与行为调节能力较差有关，而女性中则没有关联（p=0.018）。同时，较高的全氟辛酸（PFOA）浓度与元认知出现临床损伤的风险增加有关（OR=3.18，95%CI 1.17, 8.60）。在 8 岁时，没有发现全氟辛烷磺酸和全氟己烷磺酸与执行功能之间存在关联。
8 岁时的 PFNA 和 PFOA，但不是 3 岁时的，可能与 8 岁时的执行功能较差有关。结果需要在具有更大样本量的队列研究中进行验证。
