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Research Article| Volume 217, ISSUE 2, P169-174, February 15, 2004

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Multiple risk factors for Parkinson's disease

  • Jay M. Gorell
    Correspondence
    Corresponding author. Department of Neurology-K-11, Henry Ford Hospital and Health Sciences Center, 2799 W. Grand Boulevard, Detroit, MI 48202, USA. Tel.: +1-313-916-7323; fax: +1-313-916-3014.
    Affiliations
    Department of Neurology, Henry Ford Health Sciences Center, Henry Ford Health System, Detroit, MI, USA

    Environmental Health Sciences Center in Molecular and Cellular Toxicology with Human Applications, Wayne State University, Detroit, MI, USA
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  • Edward L. Peterson
    Affiliations
    Environmental Health Sciences Center in Molecular and Cellular Toxicology with Human Applications, Wayne State University, Detroit, MI, USA

    Department of Biostatistics and Research Epidemiology, Henry Ford Health Sciences Center, Henry Ford Health System, Detroit, MI, USA
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  • Benjamin A. Rybicki
    Affiliations
    Environmental Health Sciences Center in Molecular and Cellular Toxicology with Human Applications, Wayne State University, Detroit, MI, USA

    Department of Biostatistics and Research Epidemiology, Henry Ford Health Sciences Center, Henry Ford Health System, Detroit, MI, USA
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  • Christine Cole Johnson
    Affiliations
    Environmental Health Sciences Center in Molecular and Cellular Toxicology with Human Applications, Wayne State University, Detroit, MI, USA

    Department of Biostatistics and Research Epidemiology, Henry Ford Health Sciences Center, Henry Ford Health System, Detroit, MI, USA
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      Abstract

      Objective: To determine the relative contribution of various risk factors to the development of Parkinson's disease (PD). Methods: Ten variables that were independently associated with PD in a health system population-based case-control study of epidemiological risk factors for the disease were jointly assessed. Stepwise logistic regression, adjusted for sex, race and age was used to develop a multiple variate model that best predicted the presence of PD. The population attributable risk was estimated for each variable in the final model, as well as for all factors together. Results: The 10 initial variables included >20 years occupational exposure to manganese or to copper, individually; >20 years joint occupational exposure to either lead and copper, copper and iron, or lead and iron; a positive family history of PD in first- or second-degree relatives; occupational exposure to insecticides or herbicides; occupational exposure to farming; and smoking. Logistic regression resulted in a final model that included >20 years joint occupational exposure to lead and copper (p=0.009; population attributable risk [PAR]=3.9%), occupational exposure to insecticides (p=0.002; PAR=8.1%), a positive family history of PD in first- and second-degree relatives (p=0.001; PAR=12.4%), and smoking ≤30 pack-years or not smoking (p=0.005; PAR=41.4%). All four variables combined had a PAR=54.1%. Conclusions: Our final model of PD risk suggests that occupational, environmental lifestyle and, likely, genetic factors, individually and collectively, play a significant role in the etiology of the disease. Clearly, additional risk factors remain to be determined through future research.

      Keywords

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