Interrelations of lead levels in bone, venous blood, and umbilical cord blood with exogenous lead exposure through maternal plasma lead in peripartumwomen

Recent research has raised the possibility that fetal lead exposure is not estimated adequately by measuring lead content in maternal whole blood lead because of the variable partitioning of lead in whole blood between plasma and red blood cells. Lead in maternal plasma may derive in large part from maternal bone lead stores. In this study we aimed to estimate the contribu tion of maternal whole blood lead, maternal bone lead levels, and environme ntal lead to umbilical cord blood lead levels (as a measure of fetal lead e xposure). In the model, we assumed that lead from all of these sources reac hes the fetus through the maternal plasma lead pathway. In 1994-1995, we re cruited 615 pregnant women for a study of lead exposure and reproductive ou tcomes in Mexico City. We gathered maternal and umbilical cord blood sample s within 12 hr of each infant's delivery and measured maternal lead levels in cortical bone and trabecular bone by a K-X-ray fluorescence (K-XRF) inst rument within 1 month after delivery. We administered a questionnaire to as sess use of lead-glazed ceramics (LGC) to cook food and we obtained data on regional air lead levels during the 2 months before delivery. We used stru ctural equation models (SEMs) to estimate plasma lead as the unmeasured (la tent) variable and to quantify the interrelations of plasma lead, the other lead biomarkers, and environmental lead exposure. In the SEM analysis, a m odel that allowed plasma lead to vary freely from whole blood lead explaine d the variance of cord blood lead (as reflected by a total model R-2; R-2 = 0.79) better than did a model without plasma lead (r(2) = 0.67). Cortical bone lead, trabecular bone lead, use of LGC, and mean air lead level contri buted significantly to plasma lead. The exchange of lead between plasma and red blood cells was mostly in the direction of plasma to cells. According to the final model, an increase in trabecular bone lead and cortical bone l ead was associated with increases in cord blood lead of 0.65 and 0.25 mug/d L, respectively. An increase of 0.1 mug/m(3) in air lead was associated wit h an increase in the mean level of fetal cord blood lead by 0.67 mug/dL. Wi th one additional day of LCG use per week in the peripartum period, the mea n fetal blood lead level increased by 0.27 mug/dL. Our analyses suggested t hat maternal plasma lead varies independently from maternal whole blood lea d and that the greatest influences on maternal plasma lead are maternal bon e lead stores, air lead exposures, and recent cooking with LGC. The contrib utions from endogenous (bone) and exogenous (environmental) sources were re latively equal. Measurement of plasma and bone lead may be important in acc urately assessing fetal lead exposure and its major sources, particularly i f exogenous exposures decline.