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Prenatal Lead Exposure, -Aminolevulinic Acid, and Schizophrenia

Mark G.A. Opler,¹ Alan S. Brown,^1,2 Joseph Graziano,³ Manisha Desai,⁴ Wei Zheng,³ Catherine Schaefer,⁵ Pamela Factor-Litvak,⁶ and Ezra S. Susser^2,6

¹Department of Psychiatry, College of Physicians and Surgeons, Columbia University, New York, New York, USA; ²New York State Psychiatric Institute, New York, New York, USA; ³Department of Environmental Health Sciences and ⁴Department of Biostatistics, Mailman School of Public Health, Columbia University, New York, New York, USA; ⁵Division of Research, Kaiser Permanente Health Care, Oakland, California, USA; ⁶Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, New York, USA

Abstract
Schizophrenia is a severe mental disorder of unknown etiology. Recent reports suggest that a number of environmental factors during prenatal development may be associated with schizophrenia. We tested the hypothesis that environmental lead exposure may be associated with schizophrenia using archived serum samples from a cohort of live births enrolled between 1959 and 1966 in Oakland, California. Cases of schizophrenia spectrum disorder were identified and matched to controls. A biologic marker of lead exposure, -aminolevulinic acid (-ALA) , was determined in second-trimester serum samples of 44 cases and 75 controls. -ALA was stratified into high and low categories, yielding 66 subjects in the high category, corresponding to a blood lead level (BPb) 15 µg/dL, and 53 in the low category, corresponding to BPb < 15 µg/dL. Using logistic regression, the odds ratio (OR) for schizophrenia associated with higher -ALA was 1.83 [95% confidence interval (CI) , 0.87-3.87 ; p = 0.1]. Adjusting for covariates gave an OR of 2.43 (95% CI, 0.99-5.96 ; p = 0.051) . This finding suggests that the effects of prenatal exposure to lead and/or elevated -ALA may extend into later life and must be further investigated as risk factors for adult psychiatric diseases. Key words: -aminolevulinic acid, developmental, lead, Pb, prenatal, prospective, psychosis, schizophrenia. Environ Health Perspect 112:548-552 (2004) . doi:10.1289/ehp.6777 available via http://dx.doi.org/ [Online 8 January 2004]

Address correspondence to M.G.A. Opler, Department of Epidemiology, Columbia University, 722 West 168th St., New York, NY 10032 USA. Telephone: (646) 234-3607. Fax: (212) 305-9413. E-mail: mgo4@columbia.edu

Work reported in this article was supported in part by National Institutes of Health training grant 5 T32 MH 13043 (M.O.) , a NARSAD (National Alliance for Research on Schizophrenia and Depression) Independent Investigator Award (A.S.B.) , the Lieber Center for Schizophrenia Research, and a NARSAD Young Investigator Award (M.O.) .

The authors declare they have no competing financial interests.

Received 1 October 2003 ; accepted 8 January 2004.