Ethylenediamine dihydrochloride (EDA.2HCl) was fed to groups of 20 (40 controls) timed-pregnant rats on Gestation Days 6 through 15 at 1.0, 0.25, 0.05, or 0 g/kg/day. The day of discovery of a vaginal plug was considered gestation day 0. On Gestation Day 21, the fetuses were delivered by cesarean section, and the standard endpoints for teratogenicity were evaluated. At 1.0 and 0.25 g/kg/day, reductions in maternal diet consumption and weight gain were observed during the exposure period. At 1.0 g/kg/day, fetal weight and crown-rump length were significantly reduced and the percentage of litters with resorptions, with skeletal variants, and with missing or shortened innominate arteries was increased. To circumvent the possible problem of palatability of the diet and/or the effects of reduced food intake, a probe study was performed in which 1.0 or 0 g/kg/day was given to pregnant rats by gavage on Gestation Days 6 through 15. However, food intake was also substantially reduced with gavage dosing of the test substance. To determine whether the arterial defects were the result of reduced food intake, a pair-feeding study was performed in which EDA.2HCl was fed on Gestation Days 6 through 15 at 1.0 g/kg/day. A pair-fed control group received the same amount of diet consumed by the EDA.2HCl-treated rats. An untreated control group was fed ad libitum. All groups contained 20 pregnant females. Maternal weight gain, fetal weight and length, and the length of the innominate artery were all reduced in the EDA.2HCl-treated group compared to both control groups. Two fetuses each in the EDA.2HCl-treated and pair-fed control groups had missing innominate arteries versus none in the untreated controls. The four affected fetuses were from four different litters. Ingestion of EDA.2HCl resulted in reduced maternal weight gain, fetal size, and length of the innominate artery, but the missing innominate artery was not a result of EDA.2HCl treatment. Therefore, there was no evidence of teratogenicity in Fischer 344 rats from EDA.2HCl ingestion during organogenesis.