BPA enhances fear memory and increases serotonin metabolites 5hydroxyindoleacetic acid levels and 5-HIAA/serotonin in the hippocampus, striatum and midbrain in juvenile female mice, and delays perinatal chloride shift by significantly decreasing potassium chloride co-transporter 2 mRNA expression in developing rat, mouse, and human cortical neurons. BPA also AbMole BioScience kinase inhibitors causes adverse effects on neuronal morphology and functions as to interrupting neuronal dendritic and synaptic development in cultures of fetal rat hypothalamus cells at 10 and 100 nM. BPA suppresses neurite extension by inhibiting phosphorylation of mitogen activated protein kinase in rat pheochromocytoma PC12 cells differentiated neuronal-like cells. Furthermore, perinatal exposure to BPA causes GABAergic disinhibition and dopaminergic enhancement that is related to abnormal cortical basolateral amygdala synaptic transmission and plasticity; this effect may be responsible for hyperactivity and attention deficit in BPA-rats. Microarray analysis is an effective way to explore possible mechanisms and has been used to study the molecular pathway of reproductive toxicity of BPA exposure in animal models. However, few studies evaluated childhood neuronal development in exposure to BPA with human data. In human samples, umbilical cord blood is a postpartum placental remnant containing fetal blood which can be used as a surrogate for childhood study. In this study, we used meta-analysis of publicly available microarray datasets to find the neuronal target genes in exposure to BPA, and explored whether trans-placental BPA exposure in mothers would alter gene expression on their progeny in human umbilical cord blood and the potential underlying mechanism from gene network analysis to childhood neuronal development. Although some studies have found that BPA affects growth and development of reproductive organ, potential adverse effects of BPA on childhood neuronal development are not fully understood yet. In this study, we identified Sox2 and Pax6 as neuronal development biomarkers whose gene expression was appeared in response to trans-placental BPA exposure. Such a biomarker holds promise in assessing BPA exposure and acts as a clinically relevant predictor for neurogenesis in children underlying maternal BPA exposure. In general, it’s hard to explore the health effect of prenatal exposure in human subjects. A biomarker is found from a costly method because of the need for several gene chips with sufficient amount of samples; childhood neuronal development research takes time to prospectively follow up a cohort which generates additional challenges. The method described in this study offered an alternative strategy to examine the molecular effect of prenatal BPA exposure on child development. Candidate biomarkers were surveyed from the use of microarray meta-analysis and the gene expression of biomarkers were investigated in human samples from fetal umbilical cord blood for potential impact research.