Parkinson’s disease, a neurodegenerative condition affecting millions worldwide, may have a surprising link to a common chemical solvent. While the exact cause of Parkinson’s remains unknown, emerging research suggests exposure to certain chemicals could play a significant role in its development. Understanding potential environmental factors is crucial for both prevention and early detection of this debilitating disease.
A study published in the Journal of Parkinson’s Disease points to trichloroethylene (TCE) as a potential contributor to the increasing incidence of Parkinson’s. TCE is a widely used solvent found in industrial settings, consumer products, military applications, and medical procedures, commonly used for tasks like paint removal, correcting writing errors, cleaning engines, and even as an anesthetic.
The research was conducted by a collaborative team of experts from institutions including the University of Rochester Medical Center, Radboud University Medical Center, the Parkinson’s and Movement Disorders Center of Expertise in Nijmegen, the Weill Institute for Neurosciences at the University of California-San Francisco, and the University of Alabama at Birmingham’s Center for Neurodegeneration and Therapeutics. These specialists propose that TCE exposure could be a causative factor in the development of Parkinson’s disease.
The Link Between TCE and Parkinson’s Disease
The report details the widespread presence of TCE, evidence linking it to the disease, and the cases of seven individuals – including a former NBA player, a U.S. Navy captain, and a deceased U.S. Senator – who developed Parkinson’s after working with or being exposed to the substance.
The connection between TCE and Parkinson’s was first suggested by case studies over 50 years ago. Subsequent research on mice and rats has demonstrated that TCE readily enters the brain and body tissue, and at high doses, damages mitochondria – the energy-producing components of cells.
Animal studies have shown that TCE exposure leads to the selective loss of dopamine-producing nerve cells, a hallmark characteristic of Parkinson’s disease in humans.
However, the authors cautioned that “millions more encounter the chemical unknowingly through outdoor air, contaminated groundwater, and indoor air pollution.”
The chemical can contaminate soil, creating underground plumes that can travel long distances and migrate over time. One such plume, associated with an aerospace company in Long Island, Fresh York, spans over 6 kilometers in length and 3 kilometers in width, contaminating the drinking water of thousands of residents.
The article highlighted the cases of seven individuals where TCE may have contributed to the development of Parkinson’s. While the evidence linking exposure to the substance and the disease in these individuals is circumstantial, their stories underscore the challenges of establishing definitive proof against the chemical.
The research included professional basketball player Brian Grant, who played for 12 years in the NBA and was diagnosed with Parkinson’s at age 36. Grant’s exposure to TCE likely occurred when he was three years aged, as his father was stationed at Camp Lejeune as a Marine.
