环境污染物已成为危害人类健康的重要因素之一。新型环境污染物十溴联苯醚（BDE-209）和双酚A（BPA）均可通过母体吸收造成胎儿宫内暴露。动物实验及流行病学调查表明BDE-209及BPA均具有神经发育毒性，影响子代的学习与记忆能力，但具体的分子机制不清。已有研究提示BDE-209及BPA可以降低细胞的DNA甲基化程度。我们推测"BDE-209及BPA暴露通过降低DNA甲基化水平进而引起印记基因表达及基因组稳定性改变"是BDE-209、BPA神经发育毒性的新机制之一。我们拟应用人胚胎干细胞神经分化模型，利用免疫荧光染色、流式分析、亚硫酸盐测序、arrayCGH等技术检测BDE-209、BPA暴露后分化得到的神经上皮祖细胞的DNA甲基化水平、印记基因表达及DMR区甲基化状态、DNA拷贝数变异等状态从而证实我们的推测，进一步理解环境污染物的神经发育毒性机制。

Fetal in uterus can be exposed by decabromodiphenyl ether (BDE-209) and bisphenol A (BPA) which are new environmental pollutants by maternal absorption. Animal experiments and epidemiological investigation showed that BDE-209 and BPA have neurodevelopmental toxicity which can affect offspring learning and memory and abilities, but the specific molecular mechanism is unclear. Several studies suggested that BDE-209 and BPA can decrease DNA methylation level. We speculate that "the DNA hypomethylation caused by BDE-209 and BPA exposure lead to imprinting gene expression change and genome unstability "is the new mechanism of BDE-209 and BPA neurodevelopmental toxicity. We intend to use human embryonic stem cell neural differentiation model using immunofluorescence staining, flow analysis, bisulfite sequencing, arrayCGH to detect the DNA methylation, imprinting gene expression and DNA copy number variation of neural progenitor cells to confirm our speculation.