Pregnant rats received betamethasone 0.02, 0.05, 0.10, or 0.20 mg/kg body weight/day or saline (controls) for three days before delivery of fetuses at day 19 of gestation. Dose related effects on morphology, dipalmitoyl phosphatidylcholine content, and phosphatidylcholine species composition of the fetal lungs were evaluated. Injection of 0.02 and 0.05 mg/kg body weight betamethasone resulted in cellular differentiation of some cells, but the increase in dipalmitoyl phosphatidylcholine content was not significant. Dosages of either 0.10 or 0.20 mg/kg body weight resulted in markedly accelerated organ differentiation, complete cytodifferentiation of type II cells, and markedly increased numbers of lamellar bodies per alveolar type II cell. Compared to the controls, maternal administration of 0.10 or 0.20 mg/kg betamethasone caused significant increases of both fetal lung dipalmitoyl phosphatidylcholine content, and the fraction of dipalmitoyl phosphatidylcholine of total phosphatidylcholine. None of the parameters differed between the groups that were treated with 0.10 or 0.20 mg/kg body weight betamethasone respectively. Diminution of lung DNA content was significant after treatment with betamethasone in doses of 0.05, 0.10, and 0.20 mg/kg body weight. The results of the present study suggest that maternal treatment with lower doses than those in common usage may be successful in prevention of respiratory distress syndrome, and that higher dosages do not confer any additional advantage.