Breathing Polluted Air May Raise the Risk of Parkinson’s Disease: What a New Nationwide Study Found

A new study published in October 2025 in the journal Neurology has revealed a troubling link between a widely used industrial solvent, trichloroethylene (TCE), and an increased risk of Parkinson’s disease. The research, led by Dr. Brittany Krzyzanowski and her team at the Barrow Neurological Institute in Phoenix, examined data from over 1.1 million older adults across the United States. The findings point to a 10% higher risk of developing Parkinson’s disease among people exposed to higher levels of TCE in outdoor air.

The study doesn’t prove that TCE causes Parkinson’s, but it adds to a growing body of evidence that long-term exposure to environmental pollutants may contribute to the development of neurodegenerative diseases.

What Exactly Is TCE?

Trichloroethylene (TCE) is a colorless, non-flammable chemical that has been used for decades as an industrial solvent. Its main uses include cleaning metals, degreasing machinery, and dry cleaning fabrics. Although some applications of TCE have been banned or restricted due to safety concerns, the chemical is still found in industrial operations, and contamination remains widespread.

TCE is known to persist in the environment, contaminating air, water, and soil. Because of its long-lasting nature, even sites where TCE use ended decades ago can still release it into the environment. The U.S. Environmental Protection Agency (EPA) has listed TCE as a hazardous air pollutant, and several studies have associated exposure to it with liver and kidney damage, cancer, and now, potentially, neurodegenerative disorders like Parkinson’s.

How the Study Was Conducted

The research team analyzed Medicare data from older adults (aged 67 and above) who were newly diagnosed with Parkinson’s disease between 2016 and 2018. Each diagnosed person was matched with five individuals of similar demographics who did not have Parkinson’s.

After filtering out cases with incomplete data, the study included 221,789 people with Parkinson’s and over 1.1 million without the disease. The researchers then estimated each participant’s exposure to TCE in outdoor air using EPA air monitoring data from 2002.

Participants were assigned to exposure levels based on their ZIP+4 location, which offers very precise geographic data (down to a few city blocks). The analysis divided them into 10 groups, or deciles, depending on how much TCE they were likely exposed to.

Lowest exposure group: 0.005 to 0.01 micrograms per cubic meter (µg/m³)
Highest exposure group: 0.14 to 8.66 µg/m³

By comparing Parkinson’s rates across these groups, the researchers found that people in the highest exposure group were about 10% more likely to develop the disease than those in the lowest group, even after adjusting for other possible risk factors like age, smoking history, and exposure to fine particulate air pollution.

Where the Risk Was Greatest

The researchers also identified several geographic hot spots for high TCE levels, especially in the Rust Belt region — an area known for heavy industry. Smaller pockets of elevated exposure were found across other parts of the country.

To dig deeper, the team looked at the three largest TCE-emitting facilities in the U.S. from 2002 and examined Parkinson’s risk for people living within 10 miles of those sites. In two of these areas, Parkinson’s risk increased the closer residents lived to the facility. In one case, there was a clear gradient — meaning that the closer people lived to the emission source, the greater their risk appeared to be.

This type of spatial analysis is powerful because it visually connects environmental exposure with disease risk, providing a map of how industrial pollutants might affect communities over time.

What the Results Mean

The study shows a modest increase in risk — about 10% — but that doesn’t make it insignificant. Because millions of people are potentially exposed to TCE in the environment, even a small individual risk can translate into a substantial public health concern.

The authors emphasize that their findings should be viewed as associational, not causal. However, the pattern they observed — higher exposure leading to higher risk — strengthens the argument that environmental toxins play a role in the development of Parkinson’s disease.

This aligns with earlier research suggesting that certain chemicals can damage dopaminergic neurons — the brain cells that produce dopamine and are destroyed in Parkinson’s. TCE, in particular, has been shown in laboratory studies to cause oxidative stress, mitochondrial dysfunction, and neural inflammation, all of which can harm these neurons.

The Broader Context: What Is Parkinson’s Disease?

Parkinson’s disease is a progressive neurological disorder that primarily affects movement. It develops when brain cells that produce dopamine, a neurotransmitter that helps coordinate muscle activity, begin to die off.

Common symptoms include tremors, muscle stiffness, slow movement, and balance problems. As the disease progresses, it can also lead to depression, memory issues, and sleep disorders.

There is no known cure, and while genetics play a role, environmental exposures are increasingly being recognized as major contributors. Scientists estimate that up to 85% of Parkinson’s cases may have some environmental or lifestyle component.

Why TCE Is So Concerning

TCE is not a new problem — in fact, it has a long and troubling history. It has been detected in groundwater at thousands of sites, including former military bases, factories, and Superfund cleanup locations.

One of the most infamous examples is the Camp Lejeune contamination case in North Carolina, where TCE (along with other chemicals) was found in drinking water for decades. Studies of people exposed at Camp Lejeune later showed higher rates of Parkinson’s disease and other neurological issues.

The current study differs in that it focuses on ambient air exposure, not direct occupational or water contamination. That makes its findings especially concerning, because it suggests that even low-level exposure in everyday environments might contribute to health risks over time.

Study Strengths and Limitations

Strengths:

The study’s massive sample size gives it significant statistical power.
The nationwide scope means the findings are broadly applicable to older adults in the U.S.
Using ZIP+4 geographic precision allowed for fine-grained exposure mapping.
Researchers adjusted for multiple variables that could affect risk, including smoking, age, and particulate air pollution.

Limitations:

The study included only older adults (67+), so results may not apply to younger people.
TCE exposure was estimated from 2002 air quality data, not individual lifetime exposure.
The researchers couldn’t account for indoor or occupational exposure, which may differ greatly between individuals.
As an observational study, it cannot prove causation — only correlation.

Despite these limitations, experts see this as a critical piece of evidence linking long-term exposure to industrial pollutants with neurological disease.

Environmental and Health Policy Implications

Given how widely TCE persists in the environment, even a modest risk increase has serious policy implications. The study’s authors urge stronger regulation, more frequent monitoring, and better cleanup of contaminated sites.

The EPA has already classified TCE as a human carcinogen and has been evaluating stricter rules for its use. However, enforcement and monitoring vary widely by region, and many older industrial areas still face ongoing contamination.

If these findings are confirmed by further research, TCE could become a key target in public health efforts to reduce environmental contributions to neurodegenerative diseases.

The Bigger Picture: Environmental Toxins and the Brain

The human brain is extremely sensitive to chemical pollutants. Substances like pesticides, herbicides, and solvents can cross the blood-brain barrier, damaging neurons over time.

TCE is part of a growing list of neurotoxic chemicals that have been linked to Parkinson’s. Others include paraquat, a widely used herbicide, and manganese, a metal that can accumulate in the brain and cause Parkinson’s-like symptoms.

These chemicals may act through similar mechanisms — disrupting mitochondrial function, increasing oxidative stress, and triggering inflammation in the nervous system. Researchers are now exploring whether combined exposure to multiple pollutants amplifies risk even further.

What Can Be Done

While the average person can’t easily test for TCE in their neighborhood air, there are ways to reduce overall exposure:

Avoid using solvents or degreasers that contain TCE.
Check your local EPA Superfund map to see if your area has a history of TCE contamination.
Ensure good ventilation if you work with cleaning chemicals or industrial equipment.
Support policies and community actions aimed at cleaning up polluted industrial zones.

Parkinson’s disease takes years to develop, and exposures often occur decades before symptoms appear. That’s why identifying and mitigating environmental risks now could prevent cases in the future.

Final Thoughts

This study is not the final word on TCE and Parkinson’s, but it’s a strong signal that our environment plays a measurable role in brain health. A 10% increase in risk might seem small, but when applied to millions of people exposed to industrial pollutants, the impact could be significant.

It also raises an important question: how many other chemicals in our air, water, and soil are quietly shaping the future of public health? The answer may depend on how seriously we take studies like this — and how quickly we act on them.

Research Reference:
Ambient Trichloroethylene Exposure and Parkinson Disease Risk in Medicare Beneficiaries — Neurology (October 1, 2025)