MM1-O-06 Introduction: Maternal bone lead has been shown to be an endogenous source of exposure to the developing fetus and prenatal lead exposure increases the risk of low birth weight. Recent evidence suggests that vitamin D receptor (VDR) polymorphisms may influence the accumulation of lead in bone; however, none of the previously reported studies has evaluated the effects in pregnant women or newborn infants. Methods: We genotyped archived blood of 575 mothers and 419 infants for 2 allelic variants (ApaI and FokI) of the VDR gene. Subjects were participants in a study of lead exposure among peripartum women and children in Mexico City. Maternal and umbilical cord blood lead were measured at delivery and at 1-month postpartum maternal bone lead was measured. Anthropometric data were collected within the first 12 hours following delivery. Results: Genotypes for the mothers and infants, respectively, were: ApaI (AA = 14%, Aa = 44%, aa = 42%); FokI (FF = 22%, Ff = 52%, ff = 27%) and ApaI (AA = 12%, Aa = 45%, aa = 43%); FokI (FF = 23%, Ff = 52%, ff = 25%). Allele frequencies were in Hardy-Weinberg Equilibrium. Umbilical cord lead was significantly higher among those infants with the ApaI AA homozygous variant genotype (7.75 μg/dL), in comparison to those with ApaI Aa or ApaI aa genotype (6.50 μg/dL) (P = 0.03). This relationship was similar, although not statistically significant, for the FokI variant (7.26 vs. 6.47 μg/dL, P = 0.08). Using generalized additive models to explore possible nonlinear associations, while adjusting for maternal age, education, arm circumference, and dietary calcium intake, the presence of ApaI variant (“A”) or FokI variant (“f”) maternal allele resulted in a steeper increase in umbilical cord lead for a given maternal bone lead level, but this effect was attenuated at higher bone lead levels. Mean (SD) infant birth weight among maternal carriers and noncarriers of the variant ApaI allele were not significantly different: 3126 (384) and 3136 (426) g, respectively (P = 0.85). However, after adjusting for maternal age, arm circumference, infant gender, and gestational age, there was a significant interaction between maternal ApaI genotype and patella lead on birthweight (P = 0.027). For every 10 μg/g increase in maternal bone lead, infants born to mothers with the homozygous variant genotype were, on average, 130 g smaller at birth. Discussion and Conclusions: The results of this pilot study suggest that genetic factors modify the distribution of lead during pregnancy. VDR polymorphisms may influence the maternal distribution and placental transfer of lead and, ultimately, may modify the association between prenatal lead exposure and birth outcomes.