Trichloroethylene (TCE) and dichloroethylene (DCE) are related halogenated aliphatic hydrocarbon industrial solvents that are frequently found as drinking water contaminants. TCE has been implicated as a cardiac teratogen in an epidemiologic study and in a chick model. The purpose of this study was to determine whether DCE was also a cardiac teratogen in the chick embryo. Fertilized White Leghorn chick eggs (n = 418) were inoculated just above the embryo with 30 μL of a test solution on d 3 of incubation. Two control groups were studied: normal saline (n = 96) and the diluent for the DCE, miners' oil (n = 108). DCE was studied at three doses: 5, 20, and 25 μM (n = 76, 62, and 76, respectively). Eggs were coded with a seven-digit number to mask identity. Chicks were terminated on d 18 of incubation, and, after external inspection, hearts and great vessels were dissected macroscopically according to a detailed protocol. Abnormal hearts were reviewed and the diagnosis was agreed upon by three investigators before decoding the seven-digit number and photographing the abnormality. Some embryo death and subsequent tissue autolysis occurred in all groups, but, compared to controls, it was not significantly greater in the treatment group. However, combining all controls and all experimentals, significantly more (p = 0.02) embryonic death occurred in the experimental group. Noncardiac anomalies occurred in 17 embryos and were highest in the saline (four), 5 μM (four), and 20 μM (seven) DCE groups. Cardiac and great vessel anomalies occurred in 4% of saline controls, 4% of mineral oil controls, 17% of the DCE 5 μ group (p < 0.05), 19% of the DCE 20 μM group (p < 0.05), and 2% of the DCE 25 μM group (p = 0.1). Cardiac anomalies included atrial and ventricular septal defects, malformations of all valves, and great vessel abnormalities. Results suggest that DCE is a more potent cardiac teratogen than a general teratogen in the chick. Results for DCE, including the marked decrease in cardiac teratogenicity between 20 and 25 μM treated groups, are almost identical to results found for TCE, which suggests that the cardiac teratogenic effect may be exerted through a common mechanism, possibly a common or similar metabolite.