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A large U.S. study finds that long-term outdoor exposure to the industrial solvent trichloroethylene (TCE) is associated with a modest but measurable rise in Parkinson’s disease risk. Using detailed ZIP+4 location data and EPA air estimates, researchers linked contamination patterns to diagnoses among older adults.
Researchers have found that long-term exposure to trichloroethylene (TCE), a persistent industrial chemical, is linked to a higher risk of Parkinson’s disease.
Nationwide analysis finds a small but meaningful signal
Published in Neurology on October 1, 2025, the study analyzed Medicare records to identify people aged 67 and older newly diagnosed with Parkinson’s disease between 2016 and 2018. Each case was matched to five controls of similar age and demographics. After excluding records without complete ZIP+4 information, the dataset included 221,789 people with Parkinson’s and over 1.1 million without the disease across the United States.
By combining residential ZIP+4 locations with U.S. Environmental Protection Agency estimates of outdoor TCE concentrations, investigators estimated neighborhood-level exposure for each participant two years before diagnosis. People living in areas with the highest estimated outdoor TCE levels had about a 10% greater risk of Parkinson’s disease than those in the lowest-exposure neighborhoods, after adjusting for age, smoking history and fine particulate air pollution.
Mapping contamination: hotspots and local facility effects
TCE — a chlorinated solvent historically used in metal degreasing, dry cleaning and other industrial processes — persists in air, soil and groundwater even after some uses were banned. The study identified geographic hotspots with elevated outdoor TCE, notably parts of the U.S. Rust Belt and smaller pockets nationwide.
Investigators also examined the area within 10 miles of the three highest TCE-emitting facilities operating in 2002. For two of those regions, Parkinson’s risk was greater closer to the facility; at one location, risk rose incrementally with proximity. These local gradients strengthen the case that industrial emissions can shape community exposure patterns.
Study strengths, limitations and what it does — and doesn’t — prove
The research benefits from its very large, nationwide sample and fine-grained residential data. Using ZIP+4 rather than broader ZIP codes improved spatial precision in exposure estimates, and the team controlled for multiple confounders including smoking and particulate matter pollution.
However, the authors caution the findings are associative, not proof of causation. TCE exposure estimates were based on outdoor levels in 2002 and likely underestimate personal or indoor exposures over a lifetime. The cohort included only Medicare-aged adults, so results may not apply to younger people or those with early-onset Parkinson’s.
"In this nationwide study of older adults, long-term exposure to trichloroethylene in outdoor air was associated with a small but measurable increase in Parkinson’s risk," said Brittany Krzyzanowski, PhD, of Barrow Neurological Institute. "These findings add to a growing body of evidence that environmental exposures may contribute to Parkinson’s disease."
Public health implications and next steps
Even a moderate relative risk can translate into substantial public-health impact when many people are exposed. The study supports calls for more environmental monitoring, tighter regulation of legacy industrial contaminants, and further research into mechanisms by which solvents like TCE might damage dopaminergic neurons involved in Parkinson’s disease.
Future studies that combine personal exposure histories, indoor air measurements and biomarkers of exposure will be needed to clarify causality and guide mitigation. For now, the research highlights how industrial solvents and air pollution remain important considerations for brain health.
Source: scitechdaily
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