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Developmental pesticide exposures and the Parkinson's disease phenotype†

  1. Deborah A. Cory-Slechta1,*,
  2. Mona Thiruchelvam1,
  3. Eric K. Richfield2,
  4. Brian K. Barlow2,
  5. Andrew I. Brooks3

Article first published online: 4 MAR 2005

DOI: 10.1002/bdra.20118

Issue

Birth Defects Research Part A: Clinical and Molecular Teratology

Birth Defects Research Part A: Clinical and Molecular Teratology

Volume 73, Issue 3, pages 136–139, March 2005

Additional Information

How to Cite

Cory-Slechta, D. A., Thiruchelvam, M., Richfield, E. K., Barlow, B. K. and Brooks, A. I. (2005), Developmental pesticide exposures and the Parkinson's disease phenotype. Birth Defects Research Part A: Clinical and Molecular Teratology, 73: 136–139. doi: 10.1002/bdra.20118

Author Information

  1. 1

    Environmental and Occupational Health Sciences Institute and Department of Environmental and Community Medicine, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway, New Jersey

  2. 2

    Department of Pathology, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway, New Jersey

  3. 3

    Department of Environmental Medicine, University of Rochester Medical School, Rochester, New York

*Environmental and Occupational Health Sciences Institute, 170 Frelinghuysen Road, Piscataway, NJ 08854

  1. †

    Presented at The Fetal Basis of Adult Disease: Role of Environmental Exposures, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina.

Publication History

  1. Issue published online: 11 MAR 2005
  2. Article first published online: 4 MAR 2005
  3. Manuscript Accepted: 13 DEC 2004
  4. Manuscript Received: 16 NOV 2004

Funded by

  • National Institute of Environmental Health Sciences (NIEHS). Grant Numbers: ESS01247, ES05017

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Abstract

Whereas Parkinson's disease is a neurodegenerative disorder that typically onsets after 60 years of age, the possibility that it could result from insults sustained during development has been proposed. Experimental evidence based on the combined paraquat + maneb model of the Parkinson's disease (PD) phenotype summarized here provides support for such an assertion. Postnatal exposures of mice to these pesticides led not only to a permanent and selective loss of dopaminergic neurons in the substantia nigra pars compacta but also enhanced the impact of these pesticides administered during adulthood relative to developmental only or adult only treatment. Exposure to maneb alone during gestation resulted in a dramatic response to paraquat in adulthood, including notable reductions in levels of dopamine and metabolites and a loss of nigral dopamine (DA) neurons, despite the fact that paraquat does not share structural similarity to or mechanisms of action with maneb. Collectively, these studies provide developmental environmental models of the PD phenotype. In addition, they demonstrate the fact that silent neurotoxicity produced by developmental insults can be unmasked by challenges later during life as well as the potential for cumulative neurotoxicity over the life span. Birth Defects Research (Part A), 2005. © 2005 Wiley-Liss, Inc.

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