Maturation of the fetal lung is accelerated by in utero treatment with corticosteroids and thyroid hormones. Other agents such as catecholamines, thyrotropin-releasing hormone, oestradiol, heroin and cyclic AMP also influence pulmonary phospholipid metabolism. Glucocorticoids cause precocious development of both lung morphology and the surfactant system in type II cells, resulting in more stable lungs with increased air space. The properties of glucocorticoid action are consistent with enzyme induction mediated by interaction of steroid with cytoplasmic glucocorticoid receptors. Receptors are present in lung of many species, including the human fetus, and in both pulmonary fibroblasts and type II cells. Corticosteroid therapy of women in premature labour is currently used to reduce the incidence of infant respiratory distress syndrome (RDS). Treatment of the mother with 12 mg betamethasone causes an approximately four-fold maximal increase in unbound glucocorticoid activity in fetal plasma which is calculated to cause 80% nuclear occupancy by receptor-steroid complex. It is likely that endogenous corticoids influence normal lung development; possible sources of cortisol include the fetal adrenal, maternal adrenal, and conversion of cortisone to cortisol by amniotic membranes and lung fibroblasts. Thyroid hormones have effects similar to corticosteroids, but appear to influence different biochemical steps. Synthetic analogues of triiodothyronine (T3) are available which readily cross the placenta, in contrast to T3 and thyroxine, and accelerate surfactant synthesis and release. Thyroid hormones probably act through nuclear receptors which are present in lung of both animals and the human. Thyroid treatment in utero also appears to accelerate lung maturation and prevent RDS in premature infants.