4.7 Article

Prenatal Exposure to Lead, δ-Aminolevulinic Acid, and Schizophrenia: Further Evidence

Journal

ENVIRONMENTAL HEALTH PERSPECTIVES
Volume 116, Issue 11, Pages 1586-1590

Publisher

US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE
DOI: 10.1289/ehp.10464

Keywords

delta-aminolevulinic acid; developmental; lead; Pb; prenatal; prospective; psychosis; schizophrenia

Funding

  1. National Institutes of Health [5 T32 MH 13043]
  2. National Alliance for Research on Schizophrenia and Depression Young Investigator Award
  3. National Institute of Environmental Health Sciences Center [P30 ES 09089]
  4. National Institute of Child Health and Human Development [NO1-HD-1-3334, NO1-1-HD-6-3258]
  5. Public Health Institute, Berkeley, California

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BACKGROUND: A previously conducted study of prenatal lead exposure and schizophrenia using delta-aminolevulinic acid, a biologic marker of Ph exposure, in archived maternal serum samples collected from subjects enrolled in the Childhood Health and Development Study (1959-1966) based in Oakland, California, suggested a possible association between prenatal Ph exposure and the development of schizophrenia in later life. OBJECTIVES: In the present study we extend these findings using samples collected from the New England cohort of the National Collaborative Perinatal Project (1959-1966). Using similar methods, in this study we found results that suggest a comparable association in this cohort. METHODS: We pooled matched sets of cases and controls from both the California and New, England sites using a multilevel random-intercept logistic regression model, accounting for matching and site structure as well as adjusting for maternal age at delivery and maternal education. RESULTS: The estimated odds ratio for schizophrenia associated with exposure corresponding to 15 mu g/dL of blood Pb was 1.92 (95% confidence interval, 1.05-3.87; p = 0.03). CONCLUSION: Although several limitations constrain generalizability, these results are consistent with previous findings and provide further evidence for the role of early environmental exposures in the development of adult-onset psychiatric disorders.

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