We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
Prenatal Lead Exposure, δ-Aminolevulinic Acid, and Schizophrenia.
- Authors
Opler, Mark G. A.; Brown, Alan S.; Graziano, Joseph; Desai, Manisha; Wei Zheng; Schaefer, Catherine; Factor-Litvak, Pamela; Susser, Ezra S.
- 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, δ-aminolevulinic acid (δ-ALA), was determined in second-trimester serum samples of 44 cases and 75 controls. δ-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 δ-ALA was 1.83 [95% confidence interval (CI), 0.87–3.87; p = 0.1]. Adjusting for covariates gave an OR of 2.43 (950/o CI, 0.99-5.96; p – 0.051). This finding suggests that the effects of prenatal exposure to lead and/or elevated δ-ALA may extend into later life and must be further investigated as risk factors for adult psychiatric diseases.
- Subjects
ETIOLOGY of diseases; SCHIZOPHRENIA; MENTAL illness; PRENATAL care; SERUM; BIOMARKERS; BLOOD cells
- Publication
Environmental Health Perspectives, 2004, Vol 112, Issue 5, p548
- ISSN
0091-6765
- Publication type
Article
- DOI
10.1289/ehp.6777