Trichloroethylene (TCE) is ubiquitous in our living environment as a contaminant in air, water and food.Prenatal exposure to TCE is reported to cause congenital heart disease in humans.However, the mechanisms of TCE-induced cardio-teratogenicity remain largely unknown.In the current study, human embryonic stem cells (hESCs) and cardiomyocytes (derived from the hESCs) were used to evaluate the developmental toxicity of TCE in cardiogenesis.The expression of genes relating to cardiac development at four different time points (day 0, day 6, day 12 and day 21) was examined to monitor the effect of TCE on cardiogenesis.The overall data indicated the following: (1) significant cardiac inhibition,which was characterized by decreased beating clusters and beating rates, following treatment with a non-toxic dose of TCE;(2) significant up-regulation of the Nkx2.5/Handl gene in cardiac progenitors and down regulation of the Mhc-7/cTnT gene in cardiac cells;and (3) significant interference with Ca2+ channel pathways in cardiomyocytes, which contributes to the adverse effect of TCE on cardiac differentiation during early embryo development.Our findings provide new insight into TCE biology in humans, which may help to explain the development of congenital heart defects after TCE exposure.