A large nationwide study published in Neurology suggests that long-term outdoor exposure to the industrial solvent trichloroethylene (TCE) may increase the risk of Parkinson’s disease, reinforcing growing concerns over environmental contributors to neurological disorders.
- A large nationwide study found that long-term outdoor exposure to trichloroethylene (TCE), an industrial solvent and environmental pollutant, was linked to a 10% increased risk of Parkinson’s disease among older adults.
- Researchers analyzed Medicare data from over 1.3 million people and used EPA air quality data to map TCE exposure by neighborhood, finding higher risks in areas with greater concentrations of the chemical.
- Geographic "hot spots" of elevated TCE exposure were identified, particularly in the U.S. Rust Belt and near major TCE-emitting facilities, where Parkinson’s risk rose the closer residents lived to the source.
- While the association does not prove causation, experts warn that widespread exposure means even modest increases in risk could have significant public health implications, highlighting the need for stronger monitoring and regulation.
Outdoor Air Exposure to Industrial Solvent Trichloroethylene May Raise Risk of Parkinson's Disease
TCE is a chemical commonly used in metal degreasing, dry cleaning, and other industrial applications. While some uses have been banned, it remains present in certain industries and persists as a widespread pollutant in U.S. air, water, and soil. The new study does not establish causation but identifies a significant association between outdoor TCE exposure and Parkinson’s disease risk.
The research team, led by Brittany Krzyzanowski, Ph.D., of the Barrow Neurological Institute in Phoenix, examined Medicare data from individuals aged 67 and older who were newly diagnosed with Parkinson’s disease between 2016 and 2018. Each case was matched with five control participants without the disease. After refining the dataset to include only those with valid ZIP+4 residential information, the study analyzed 221,789 individuals with Parkinson’s and more than 1.1 million controls.
To estimate environmental exposure, researchers mapped outdoor TCE concentrations using U.S. Environmental Protection Agency data. Exposure levels were calculated based on U.S. Census tracts, with each participant’s exposure assessed two years prior to diagnosis. Participants were then divided into 10 groups according to TCE exposure, ranging from 0.005–0.01 micrograms per cubic meter (?g/m³) in the lowest group to 0.14–8.66 ?g/m³ in the highest group.
After adjusting for potential confounders—including age, smoking history, and exposure to fine particulate matter—the study found that participants in the highest TCE exposure group had a 10% higher risk of developing Parkinson’s disease compared to those in the lowest exposure group. While the relative risk increase is modest, the researchers emphasized the broad population-level impact given the number of people potentially exposed.
The study also identified geographic "hot spots" of higher TCE exposure, particularly in the Rust Belt region of the United States, with additional pockets across the country. To further investigate, researchers assessed Parkinson’s risk within 10 miles of the top three TCE-emitting facilities in 2002. In two of these regions, risk was elevated closer to the facilities, with one site showing a clear incremental increase in risk the nearer individuals lived to the emissions source.
Dr. Krzyzanowski noted that although the observed increase in Parkinson’s risk was small, the widespread presence of TCE makes the findings significant for public health. She emphasized the need for stronger regulations, improved monitoring of industrial emissions, and additional research to understand the long-term impacts of exposure.
The study does have limitations. It focused exclusively on older adults covered by Medicare, leaving uncertain whether similar risks apply to younger individuals or those with early-onset Parkinson’s disease. Additionally, exposure estimates were based solely on outdoor air levels from 2002, which may not reflect lifetime exposure or indoor contamination, both of which could influence disease risk.
Despite these limitations, the findings contribute to growing evidence that environmental pollutants like TCE may play a role in the development of Parkinson’s disease. The research underscores an urgent need for policies aimed at reducing exposure and protecting vulnerable populations from preventable environmental risks.
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