The effect of maternal nicotine exposure on fetal and neonatal lung metabolism was investigated. Nicotine (0.25 and 1.0 mg/kg body weight/day) administered subcutaneously to the mother animal from day 7 of gestation until weaning led to retarded glycogenolysis of fetal lung. This was due to an inhibition of lung glycogen phosphorylase. Exposure until 2 weeks after birth had no effect on the in vitro oxygen consumption of lung tissue, but the total glucose turnover of rat neonates exposed to 0.25 and 1.0 mg nicotine/kg body weight per day was increased to 78.96 +/- 3.92 and 121.09 +/- 7.36 mumol/g per h, respectively, as compared to controls (64.95 +/- 4.56 mumol/g per h). In contrast to the marked increase in total glucose turnover, the in vitro lactate production was significantly lowered, suggesting an inhibition of the glycolytic pathway. The lung lecithin content of control neonates (day 1 post-partum) was 1.94 +/- 0.30 mg/g wet tissue mass. Nicotine administration to the mother resulted in a 92% higher lung lecithin content (3.72 +/- 0.06 mg/g). The results suggest that although nicotine will have no effect on the incidence of respiratory distress syndrome due to a lack of lecithin, it may have a detrimental effect on the functional development of the lung as a result of its inhibitory effect on glucose oxidation via the glycolytic pathway.