title: Serum vitamin D metabolites and bone mineralization in young children with chronic low to moderate lead exposure.
abstract: One hundred five children (49 male, 99 black) with known lead exposure indices from birth and adequate nutrient intake of calcium, phosphorus, and vitamin D were studied at 1 of 3 ages (21, 27, or 33 months) to determine the effects of chronic low to moderate lead exposure on circulating concentrations of vitamin D metabolites and bone mineral content as determined by photon absorptiometry. Univariate multiple regression analyses showed no direct relationship of blood lead levels to vitamin D metabolites or bone mineral content. Structural equation analyses which took into account potential covariates of age, season, race, and sex showed estimated declines in serum concentrations of total calcium (from 9.72 to 9.61 mg/dL), phosphorus (from 5.4 to 4.67 mg/dL), and 25-hydroxyvitamin D (from 27.24 to 25.8 ng/mL) and estimated increases in concentrations of parathyroid hormones (from 73.03 to 83.14 microL Eq/mL), 1,25-dihydroxyvitamin D (from 62.39 to 62.69 pg/mL), and bone mineral content (from 222.66 to 234.91 mg/cm) over the observed range of average lifetime blood lead concentrations (4.76 to 23.61 micrograms/dL, geometric mean 9.74 micrograms/dL). However, the only statistically significant effect of average lifetime blood lead concentration was that for phosphorus, and the multivariate test of the combined effects of lead on these six outcomes was not statistically significant (P = .2). It is concluded that significant alterations in vitamin D metabolism, calcium and phosphorus homeostasis, and bone mineral content are not present in children whose nutritional status is adequate and who experience low to moderate lead exposure.
authors.affiliation: Division of Neonatology, University of Cincinnati, Ohio.
authors.forename: W W
authors.initials: WW
authors.lastname: Koo
authors.forename: P A
authors.initials: PA
authors.lastname: Succop
authors.forename: R L
authors.initials: RL
authors.lastname: Bornschein
authors.forename: S K
authors.initials: SK
authors.lastname: Krug-Wispe
authors.forename: J J
authors.initials: JJ
authors.lastname: Steinchen
authors.forename: R C
authors.initials: RC
authors.lastname: Tsang
authors.forename: O G
authors.initials: OG
authors.lastname: Berger
mesh_terms: D015519:Bone Density / Q000502:physiology*; D002113:Calcification, Physiologic / Q000502:physiology*; D002116:Calcitonin / Q000097:blood; D002118:Calcium / Q000097:blood; D002675:Child, Preschool; D002908:Chronic Disease; D015331:Cohort Studies; D005260:Female; D006801:Humans; D006887:Hydroxycholecalciferols / Q000097:blood*; D007223:Infant; D007854:Lead / Q000097:blood; D007855:Lead Poisoning / Q000097:blood / Q000378:metabolism*; D008274:Magnesium / Q000097:blood; D008297:Male; D010281:Parathyroid Hormone / Q000097:blood; D010758:Phosphorus / Q000097:blood; D012044:Regression Analysis
chemical_list: D006887:Hydroxycholecalciferols; D010281:Parathyroid Hormone; D010758:Phosphorus; D007854:Lead; D002116:Calcitonin; D008274:Magnesium; D002118:Calcium