A large nationwide study of more than a million older adults in the U.S. has found an association between long-term exposure to trichloroethylene, or TCE, in outdoor air and a heightened risk of developing Parkinson’s disease. The research, which analyzed Medicare beneficiary data, determined that individuals living in areas with the highest concentrations of the industrial solvent faced a 10% greater risk of a Parkinson’s diagnosis compared to those in the least-exposed areas.
Published on October 1, 2025, in Neurology, the medical journal of the American Academy of Neurology, the findings add to a growing body of evidence suggesting environmental pollutants play a role in the development of the neurodegenerative disorder. “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 study author Brittany Krzyzanowski of the Barrow Neurological Institute in Phoenix. While the study establishes a strong correlation, its authors caution that it does not definitively prove that TCE exposure causes Parkinson’s disease.
A Pervasive Environmental Toxin
Trichloroethylene is a chemical compound widely used in industrial applications, primarily for degreasing metal parts and in dry cleaning. Despite some restrictions on its use, TCE remains a common solvent and a persistent environmental contaminant found across the United States. Because of its chemical stability, it does not break down easily and can pollute soil, groundwater, and outdoor air for long periods, leading to sustained, low-level population exposure. This persistence makes understanding its long-term health effects a critical public health issue. The U.S. Environmental Protection Agency has tracked its release, and many contaminated sites remain nationwide.
Nationwide Study Design and Methods
Analyzing Health and Environment Data
To investigate the link between ambient TCE and Parkinson’s disease, researchers turned to a massive dataset from the U.S. Medicare program. They identified 221,789 people over the age of 67 who were newly diagnosed with Parkinson’s between 2016 and 2018. This group was then compared against a large control population of more than 1.1 million Medicare beneficiaries who did not have the disease. Each person with Parkinson’s was matched with five individuals without the condition to ensure a robust comparison.
Mapping Toxin Exposure
The research team estimated historical TCE exposure levels by linking participants’ residential information, identified by their ZIP+4 code, to U.S. Environmental Protection Agency data on outdoor air pollution. This allowed them to calculate the concentration of ambient TCE in the neighborhoods where the individuals lived. To isolate the potential effect of the solvent, the scientists statistically adjusted for other factors known to influence Parkinson’s risk. These variables included age, a history of smoking, and exposure to fine particulate matter, another form of air pollution.
Quantifying the Neurological Risk
After performing their analysis, the researchers found a clear, dose-dependent relationship between TCE exposure and Parkinson’s risk. People living in the top 10% of areas with the highest estimated TCE concentrations had a 10% higher relative risk of a subsequent Parkinson’s diagnosis compared with those living in the bottom 10% of exposure levels. The exposure levels ranged from as low as 0.005 micrograms per cubic meter to more than 8 micrograms per cubic meter in the most polluted locations. The study demonstrates that even outdoor air pollution, not just high-level occupational exposure, presents a measurable risk.
Geographic Hot Spots and Previous Research
Identifying High-Risk Areas
The study also identified geographic “hot spots” where ambient TCE levels were highest. These areas were concentrated primarily in the Rust Belt region of the U.S., with smaller pockets of high concentration scattered across the country. Further analysis focused on the areas surrounding the three U.S. industrial facilities that emit the highest levels of TCE. In these locations, Parkinson’s risk was notably higher for individuals living closer to the facilities, with the risk decreasing as the distance from the pollution source increased.
Building on Prior Evidence
This research builds on previous studies that have linked TCE to Parkinson’s disease in more direct exposure scenarios. A widely cited 2023 study, for example, found that U.S. Marines exposed to TCE and other volatile organic compounds in contaminated drinking water at Camp Lejeune had a 70% increased risk of developing Parkinson’s later in life. The new study on ambient air exposure complements these earlier findings from military and occupational cohorts, suggesting that widespread, low-level environmental pollution may also contribute to the development of the disease.
Biological Mechanisms and Study Limitations
The statistical association is supported by existing biological evidence. Experimental studies have shown that TCE and its metabolites can be toxic to the nervous system. The chemical is believed to induce oxidative stress, impair the function of mitochondria—the energy-producing centers of cells—and trigger the degeneration of dopamine-producing neurons. These are the same pathological hallmarks observed in the brains of individuals with Parkinson’s disease, providing a plausible mechanism for how the solvent could contribute to the disease process. The investigators noted that their study relied on estimated air pollution data and could not account for individual mobility or occupational exposures, framing the need for future research with more detailed exposure tracking.
Implications for Public Health
While a 10% increase in relative risk may seem modest for an individual, the public health implications are significant due to the ubiquity of TCE as an environmental contaminant. Millions of Americans may live in areas with elevated levels of the solvent, potentially increasing their vulnerability to a debilitating neurodegenerative condition that has no cure. The findings amplify calls from public health advocates and scientists for more stringent environmental regulations, better monitoring of industrial emissions, and a greater focus on remediation efforts to clean up legacy TCE contamination in communities across the country.
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