Dibutyl phthalate (DBP), a phthalate congener, is widely utilized in consumer products and medication coatings. Women of reproductive age have a significant burden of DBP exposure through consumer products, occupational exposure, and medication. Prenatal DBP exposure is associated with adverse pregnancy/fetal outcomes and cardiovascular diseases in the offspring. However, the mechanisms underlying DBP exposure-associated adverse pregnancy outcomes are unclear. We hypothesize that prenatal exposure to environmentally relevant low dosage DBP adversely affects fetal-placental vascular function and development during pregnancy. Adult female CD-1 mice (8-10wks) were orally treated with vehicle (control) or with environmentally relevant DBP dosages (100, 10, and 0.1 μg/kg/day; DBP100, DBP10, DBP0.1) daily from 30 days before pregnancy through gestational day (GD) 18.5. Dam body mass composition (fat/lean mass) was measured non-invasively using the echo-magnetic resonance imaging system. Placental lipid disposition was examined using Oil Red O staining. DBP100 and 10 dose dependently increased weight of non-pregnant female mice, while DBP0.1 did not affect their weight. DBP0.1 exposure also did not affect the maternal weight gain pattern and body fat % during pregnancy. However, DBP0.1 exposure significantly increased the placental weight and decreased the fetal/placental weight ratio (indicative of decreased placental efficiency) at GD18.5. We further observed that while DBP0.1 did not affect lipid disposition in maternal decidual, it significantly decreased lipid disposition in fetal labyrinth of female, but not male placentas. Prenatal DBP exposure to environmentally relevant low-dosage adversely impacts the fetal-placental efficiency and lipid disposition in a fetal sex specific manner.