A B S T R A C T Serumii glucocorticoid levels were (letermined in 20 inothers andI 43 premature infalnts wh-lio r-eceived prenatal betamnetlhasonie therapy for preventionl of respiratory distress syndrome (RDS). 'Maternal betamethasone peaked at 75 ,ug cortisol equivalents per 100 ml 1 h after injection of 12 mg steroid and declined to half by 6 h. Betamethasone in cord blood w-as 14.3 tig cortisol equivalents per 100 ml at 1 h, decreased to a level of 4.7 at 20 h, aand was not detected 2 days after a second dose at 24 h. After the second dose, the mean level of cortisol in cord blood was 5.9 yg per 100 ml compared witlh 13.05 y-per 100 ml (P < 0.001) in untreated premature infanits. The unbound glucocorticoid activity in treated infants delivered 1-10 h after the second dose (mean, 8.4 Ag per 100 nil) is simlilar to the unbound cortisol level after birth in untreated premature infants who develop RDS.These findings indicate that (a) serlum glucocorticoid levels in the physiologic stress range can induce lung mnaturationi in the human aind (b) antenatal treatment with this dose of betaimietlhasoine does not expose the lhuman fetuis to potentially hiarmiftil pharmacologic levels of steroid.