OBJECTIVE: To determine the relative contribution of residential lead hazards to children's blood lead concentrations during early childhood. METHODS: We enrolled children 6 months of age and followed them until 24 months of age. Blood and samples of dust, soil, water and paint were analyzed for lead at 6-month intervals, and interviews were conducted to estimate nutritional, behavioral, and demographic factors linked with lead exposure. RESULTS: Of the 276 children enrolled, 249 (90%) were followed until 24 months of age. The geometric mean blood lead concentration of children at 6 months of age was 2.9 microg/dL (95% CI, 2.7-3.1). At 24 months of age, children's mean blood lead was 7.5 microg/dL; 82 (33%) had a blood lead level of > or = 10 microg/dL. In adjusted analyses, lead-contaminated floor dust, soil, and water contributed to children's lead intake throughout the first 2 years of life (P < .05). Lead-contaminated dust from window troughs was a source of lead exposure, especially in the second year of life. Dietary iron intake, but not calcium intake, was inversely associated with blood lead levels (P < .05). Blood lead concentration was over 50% higher in black than in white children (P = .0001). CONCLUSION: Lead-contaminated house dust is the major source of lead intake during early childhood. Black children remain at increased risk for higher blood lead concentration after adjusting for environmental lead exposures and dietary intake.
OBJECTIVE: To determine the relative contribution of residential lead hazards to children's blood lead concentrations during early childhood. METHODS: We enrolled children 6 months of age and followed them until 24 months of age. Blood and samples of dust, soil, water and paint were analyzed for lead at 6-month intervals, and interviews were conducted to estimate nutritional, behavioral, and demographic factors linked with lead exposure. RESULTS: Of the 276 children enrolled, 249 (90%) were followed until 24 months of age. The geometric mean blood lead concentration of children at 6 months of age was 2.9 microg/dL (95% CI, 2.7-3.1). At 24 months of age, children's mean blood lead was 7.5 microg/dL; 82 (33%) had a blood lead level of > or = 10 microg/dL. In adjusted analyses, lead-contaminated floor dust, soil, and water contributed to children's lead intake throughout the first 2 years of life (P < .05). Lead-contaminated dust from window troughs was a source of lead exposure, especially in the second year of life. Dietary iron intake, but not calcium intake, was inversely associated with blood lead levels (P < .05). Blood lead concentration was over 50% higher in black than in white children (P = .0001). CONCLUSION: Lead-contaminated house dust is the major source of lead intake during early childhood. Black children remain at increased risk for higher blood lead concentration after adjusting for environmental lead exposures and dietary intake.
Authors: Bruce P Lanphear; Richard W Hornung; Jane Khoury; Kim N Dietrich; Deborah A Cory-Slechta; Richard L Canfield Journal: Sci Total Environ Date: 2008-03-07 Impact factor: 7.963
Authors: Sherry L Dixon; Joanna M Gaitens; David E Jacobs; Warren Strauss; Jyothi Nagaraja; Tim Pivetz; Jonathan W Wilson; Peter J Ashley Journal: Environ Health Perspect Date: 2008-11-14 Impact factor: 9.031