The skin surface of the newborn rat at term is highly hydrophobic. This surface hydrophobicity plays a putative role in the transition from an aqueous to a gaseous environment at birth and is dependent on the presence of an intact periderm. Glucocorticoids given to pregnant dams, during late gestation, will accelerate formation of the stratum corneum and reduce transepidermal water loss in prematurely delivered pups. We tested the related hypotheses that surface hydrophobicity and maturation of the periderm are developmentally accelerated by prenatal exposure to steroids. Thirty pregnant Sprague-Dawley rats received either normal saline or 0.5 mg/kg betamethasone on d 17 of gestation. After cesarean delivery on d 18, 19, and 20, dorsal skin surface hydrophobicity was quantified by direct surface electrical capacitance (SEC) measurement. Initial skin surface hydration at birth was significantly lower in steroid-treated pups than in control pups at gestational ages 19 and 20 d (3060 +/- 1379 versus 4441 +/- 153 pF and 646 +/- 295 versus 1493 +/- 1019 pF, respectively, p < 0.001, mean +/- SD). Likewise, after desorption of amniotic fluid, baseline skin hydration was significantly lower in steroid-treated pups than in control pups at gestational ages 19 and 20 d (1862 +/- 1560 pF versus 4278 +/- 97 pF and 60 +/- 56 pF versus 128 +/- 264 pF, p < 0.001). Scanning and transmission electron microscopy showed morphologic maturation of the periderm after steroid treatment. These results demonstrate accelerated development of both functional and structural correlates of skin surface hydrophobicity in the premature rat after prenatal exposure to steroids.