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

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

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Title: Prenatal Exposure to Lead, δ-Aminolevulinic Acid, and Schizophrenia: Further Evidence
Author: Opler, Mark G.A.; Groeger, Justina; McKeague, Ian; Wei, Catherine; Factor-Litvak, Pam; Bresnahan, Michaeline; Graziano, Joseph; Brown, Alan S.; Susser, Ezra S.; Buka, Stephen L.; Goldstein, Jill M.; Seidman, Larry Joel

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Citation: Opler, Mark G.A., Stephen L. Buka, Justina Groeger, Ian McKeague, Catherine Wei, Pam Factor-Litvak, Michaeline Bresnahan, et al. 2008. Prenatal exposure to lead, δ-aminolevulinic acid, and schizophrenia: further evidence. Environmental Health Perspectives 116(11): 1586-1590.
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Abstract: Background: A previously conducted study of prenatal lead exposure and schizophrenia using δ-aminolevulinic acid, a biologic marker of Pb 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 Pb 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 μg/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.
Published Version: doi:10.1289/ehp.10464
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