Enormous increase of use of herbicide was brought to problem with adverse effect on environment and its inhabitant. And the refatogenic effects of a few herbivides were reported. Nitrofen, 2,3-dichlorphenyl-p-nitrophenyl ether is an organic chemical placed in nitrophenol/aniline group. This chemical has been one of most widely used herbicides in Korea. Initial toxicity study of nitrofen was done by Ambrose with lung toxicity. Respiratory distress and cyanosis of neonatal rats following nitrofen exposure in uterus was descibed by Kimbrough et al and suggested that nitrofen might be affecting surfactant production. Later, it was reported that cardiac naomaly accounted for the neomatal distress and death. This experiment was attempted to produce diaphragmatic defect in offsprings of rats by nitrofen administration orally in early developmental stage and to find characteristics of diaphragmatic defect. Following results and conclusions were made. 1) Nitrofen was a potent teratogenic agent in rats in dose of 350 mg/kg at 10th day of gestation. It was fairly selective in producing diaphragmatic defect. The overall frequency of diaphragmatic defect was 66.3%. 2) Diaphragm was the primary target organ in nitrofen induced neonatal death, and pulmonary hypoplasia due to diaphramatic defect was major contributor of direct cause of neonatal death. 3) In majority the defect was in the posterolateral(Bochdalek) portion of the ddiaphragm and in some cases, diaphragmatic defect was due to attenuation of central tendon. 4) The difference in the sidedness of the defect was obviously noted; in group of administration of 250 mg/ kg at gestation 11th day, the great majority were right sided(92%), while in group of administration of 350 mg/kg at gestation 10th day no difference was observed. 5) Pathogenesis of nitrofen induced diaphragmatic defect was thought probable due to delay or arrest of development of pleuroperitoneal fold.