Trichloroethylene: An Invisible Cause of Parkinson’s Disease?

Author:

Dorsey E. Ray12,Zafar Maryam1,Lettenberger Samantha E.1,Pawlik Meghan E.1,Kinel Dan12,Frissen Myrthe3,Schneider Ruth B.12,Kieburtz Karl12,Tanner Caroline M.4,De Miranda Briana R.5,Goldman Samuel M.6,Bloem Bastiaan R.3

Affiliation:

1. Center for Health + Technology, University of Rochester Medical Center, Rochester, NY, USA

2. Department of Neurology, University of Rochester Medical Center, Rochester, NY, USA

3. Radboud University Medical Centre; Donders Institute for Brain, Cognition and Behaviour; Department of Neurology; Centre of Expertise for Parkinson & Movement Disorders; Nijmegen, the Netherlands

4. Weill Institute for Neurosciences, Department of Neurology, University of California-San Francisco, San Francisco, CA, USA

5. Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, Birmingham, AL, USA

6. Division of Occupational and Environmental Medicine, San Francisco Veterans Affairs Health Care System, School of Medicine, University of California–San Francisco, San Francisco, CA, USA

Abstract

The etiologies of Parkinson’s disease (PD) remain unclear. Some, such as certain genetic mutations and head trauma, are widely known or easily identified. However, these causes or risk factors do not account for the majority of cases. Other, less visible factors must be at play. Among these is a widely used industrial solvent and common environmental contaminant little recognized for its likely role in PD: trichloroethylene (TCE). TCE is a simple, six-atom molecule that can decaffeinate coffee, degrease metal parts, and dry clean clothes. The colorless chemical was first linked to parkinsonism in 1969. Since then, four case studies involving eight individuals have linked occupational exposure to TCE to PD. In addition, a small epidemiological study found that occupational or hobby exposure to the solvent was associated with a 500% increased risk of developing PD. In multiple animal studies, the chemical reproduces the pathological features of PD. Exposure is not confined to those who work with the chemical. TCE pollutes outdoor air, taints groundwater, and contaminates indoor air. The molecule, like radon, evaporates from underlying soil and groundwater and enters homes, workplaces, or schools, often undetected. Despite widespread contamination and increasing industrial, commercial, and military use, clinical investigations of TCE and PD have been limited. Here, through a literature review and seven illustrative cases, we postulate that this ubiquitous chemical is contributing to the global rise of PD and that TCE is one of its invisible and highly preventable causes. Further research is now necessary to examine this hypothesis.

Publisher

IOS Press

Subject

Cellular and Molecular Neuroscience,Neurology (clinical)

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