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The association between ambient exposure to organophosphates and Parkinson's disease risk
  1. Anthony Wang1,
  2. Myles Cockburn2,3,
  3. Thomas T Ly2,3,
  4. Jeff M Bronstein4,
  5. Beate Ritz1,4,5
  1. 1Department of Epidemiology, University of California, Los Angeles (UCLA) Fielding School of Public Health, Los Angeles, California, USA
  2. 2Department of Preventive Medicine, University of Southern California (USC) Keck School of Medicine, Los Angeles, California, USA
  3. 3Department of Geography, University of Southern California (USC), Los Angeles, California, USA
  4. 4Department of Neurology, University of California, Los Angeles (UCLA) Geffen School of Medicine, Los Angles, California, USA
  5. 5Department of Environmental Sciences, University of California, Los Angeles (UCLA) Fielding School of Public Health, Los Angeles, California, USA
  1. Correspondence to Professor Beate Ritz, Department of Epidemiology, Fielding School of Public Health, University of California, Los Angeles (UCLA), Box 951772, Los Angeles, CA 90095-1772, USA; britz{at}ucla.edu

Abstract

Objectives There is a general consensus that pesticides are involved in the aetiology of Parkinson's disease (PD), although associations between specific pesticides and the risk of developing PD have not been well studied. This study examines the risk of developing PD associated with specific organophosphate (OP) pesticides and their mechanisms of toxicity.

Methods This case–control study uses a geographic information system-based exposure assessment tool to estimate ambient exposure to 36 commonly used OPs from 1974 to 1999. All selected OPs were analysed individually and also in groups formed according to their presumed mechanisms of toxicity.

Results The study included 357 incident PD cases and 752 population controls living in the Central Valley of California. Ambient exposure to each OP evaluated separately increased the risk of developing PD. However, most participants were exposed to combinations of OPs rather than a single pesticide. Risk estimates for OPs grouped according to different presumed functionalities and toxicities were similar and did not allow us to distinguish between them. However, we observed exposure-response patterns with exposure to an increasing number of OPs.

Conclusions This study adds strong evidence that OPs are implicated in the aetiology of idiopathic PD. However, studies of OPs at low doses reflective of real-world ambient exposure are needed to determine the mechanisms of neurotoxicity.

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