Dry Cleaning Chemical Found to Harm Brain Cells and Raise Parkinson's Risk
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STORY AT-A-GLANCE
A study of more than 1.3 million Americans found that people living in areas with high trichloroethylene (TCE) levels had a 10% greater risk of Parkinson’s disease than those in cleaner regions
TCE, a solvent once used in dry cleaning and degreasing, persists in air, soil, and groundwater for decades, exposing people through contaminated water and indoor air — even far from industrial sites
Laboratory research revealed that TCE damages dopamine-producing neurons, disrupts mitochondrial energy production, and causes toxic protein buildup like that seen in Parkinson’s patients
The studies show that chronic, low-level exposure to environmental toxins silently erodes brain health over time, especially in older adults with weakened cellular repair systems
Reducing exposure through clean water, good ventilation, and low-toxin household choices — while supporting your cells through restorative sleep, regular movement, and whole, unprocessed foods — helps protect mitochondrial energy production and strengthen long-term neurological resilience
Parkinson’s disease is the fastest-growing neurological disorder in the world,1 and new research shows that a common dry-cleaning solvent used for nearly a century is contributing to that rise. The chemical — trichloroethylene, or TCE — has been detected in up to 30% of U.S. drinking water supplies and lingers in soil and air long after industrial use stops.2
TCE exposure doesn’t require working in a factory or chemical plant — it also occurs simply from breathing outdoor air near contaminated sites or using tainted groundwater. TCE was once prized for its ability to dissolve grease and dry-clean fabrics, but it’s now recognized as a persistent neurotoxin.
When inhaled or ingested, it passes quickly through your blood-brain barrier and damages the same neurons destroyed in Parkinson’s. Evidence from both human and animal research shows that even moderate, chronic exposure disrupts mitochondrial function — the energy engine inside your cells — triggering oxidative stress and inflammation that gradually erode brain health.
These discoveries point to a deeper issue: environmental toxins are silently undermining neurological health across generations. Understanding how exposure to this solvent alters brain chemistry and increases Parkinson’s risk is the first step toward protecting yourself and those you love.
Large US Study Connects TCE Exposure to Higher Parkinson’s Risk
Parkinson’s disease, characterized by tremors, muscle stiffness, slow movement, and balance problems, develops when dopamine-producing brain cells begin to die. Most people notice early symptoms such as reduced arm swing, changes in handwriting, or sleep disturbances long before diagnosis. Over time, it progresses to more serious complications affecting speech, memory, and mobility. In a study published in Neurology, researchers linked long-term solvent exposure to rising Parkinson’s rates.3
Researchers analyzed medical records from more than 1.3 million older adults across the U.S. to determine whether living in areas with high levels of TCE in the air was associated with greater risk of Parkinson’s disease. Because it lingers in the environment for decades, even communities far from active factories remain exposed through soil, air, and groundwater.
Older adults exposed to more TCE faced a measurable increase in Parkinson’s diagnoses — Individuals living in the top 10% of areas for TCE concentration had about a 10% higher risk of developing Parkinson’s disease than those in the lowest exposure regions.
<label class="hide-text" contenteditable="false">Text within this block will maintain its original spacing when published</label>The association remained significant even after adjusting for age, sex, and regional demographics. The finding is important because Parkinson’s disease usually develops over decades. This suggests that chronic, low-level TCE exposure contributes to disease onset long before symptoms appear.
The study revealed early neurological warning signs in high-exposure areas — Residents from regions with higher TCE levels were more likely to report balance issues, falls, and mild cognitive decline — precursors that often precede Parkinson’s diagnosis by several years. These early signs serve as clues that environmental exposure is harming brain health long before full disease develops.
Geographic data exposed chemical hotspots of neurological risk — When researchers mapped Parkinson’s cases across the U.S., they found distinct clusters surrounding industrial areas and known TCE-emitting facilities, including in Oregon, Indiana, and parts of the Midwest. Risk decreased steadily the farther people lived from these emission sites. This pattern provides strong real-world evidence that environmental pollution directly contributes to neurological disorders.
TCE persists in your body and environment, making exposure difficult to avoid — Even after factories shut down, TCE residues remain trapped in soil and groundwater for decades. Vaporized fumes leak into homes and workplaces through basements or plumbing systems, exposing people without their knowledge. Because of this, simply living near an old industrial site carries long-term neurological consequences.
<label class="hide-text" contenteditable="false">Text within this block will maintain its original spacing when published</label>Knowing that Parkinson’s risk rises even with small, repeated exposure underscores the need to filter your home’s air and water, avoid using chemical-based degreasers, and support cleanup of contaminated sites. The research makes it clear that protecting your environment is inseparable from protecting your brain health.
Laboratory Research Reveals How TCE Triggers Neuronal Damage at the Cellular Level
Before researchers examined TCE’s effects in humans, earlier lab experiments revealed what this solvent does inside the brain itself. Published in Neurobiology of Disease, this study explored how TCE affects the brain’s motor control centers using aged rats, which closely mimic human vulnerability to Parkinson’s disease.4
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