The recognition and implementation of the new criteria for a safe level of childhood blood lead as below 10 micrograms/dl is primarily based on risk of increased fetal transfer at higher levels of maternal blood lead. The first two years of this study of 22 children 18-36 months old provide unique quantitation of duplicate diet, handwipe, blood, plasma and urine lead and identify housedust as the primary source of exogenous lead and a major contaminant of food lead. It establishes the (206/207) lead ratio of carefully collected, bagged urine as identical with the isotopic ratio of the simultaneous blood and plasma lead. The isotopic ratio analyses of selected subjects defines mobilized endogenous lead as the dominant fraction of circulating blood lead. It is obvious that we began the study at least 18 to 36 months too late. The four year competitive renewal thus goes back in time to quantitate the mobilization of endogenous maternal and neonatally acquired lead and its contribution to the blood lead of children. This is a longitudinal study, employing thermal ionization/mass spectrometry (TI/MS) isotopic dilution analysis in an ultraclean laboratory, of endogenous and exogenous sources of blood lead during pregnancy, lactation and post lactation and from birth to two years. This study will be conducted on 24 women from the first trimester of their first or second pregnancy and on their infants from birth through 24 months. The subjects will be women in pre-1950 housing who will exclusively breast feed or bottle feed their infants through at least 4 months of age, anticipate the same residence throughout pregnancy and the child's first two years and do not expect the child to be out of the home for more than 20 h/wk. All subjects will live in urban Omaha, a smelter city with relatively high residual soil lead but where air and water lead are negligible. Determination of the relative contribution of prenatally and postnatally acquired endogenous lead and of current exogenous lead is critical to the prevention of adverse sequelae to prenatal and postnatal increases in the blood lead.
| Manton, William I; Angle, Carol R; Krogstrand, Kaye L Stanek (2005) Origin of lead in the United States diet. Environ Sci Technol 39:8995-9000 |
| Manton, W I; Angle, C R; Stanek, K L et al. (2003) Release of lead from bone in pregnancy and lactation. Environ Res 92:139-51 |
| Manton, W I; Angle, C R; Stanek, K L et al. (2000) Acquisition and retention of lead by young children. Environ Res 82:60-80 |
| Stanek, K; Manton, W; Angle, C et al. (1998) Lead consumption of 18- to 36-month-old children as determined from duplicate diet collections: nutrient intakes, blood lead levels, and effects on growth. J Am Diet Assoc 98:155-8 |
| Angle, C R; Manton, W I; Stanek, K L (1995) Stable isotope identification of lead sources in preschool children--the Omaha Study. J Toxicol Clin Toxicol 33:657-62 |
