COULD PARKINSON’S DISEASE DRAMATIC RISE result from exposure to a common chemical? An international team of researchers recently concluded that the chemical trichloroethylene is associated with as much as a 500 percent increased risk for Parkinson’s disease. Today we explore what’s behind the world’s fastest-growing brain disease.
Trichloroethylene (TCE) is a common chemical in paint removers, gun cleaners, correction fluid, aerosol cleaning products, and dry cleaning.
“Earth provides enough to satisfy every man’s needs, but not every man’s greed.” ― Mahatma Gandhi.
What is Parkinson’s disease?
Parkinson’s disease is a progressive neurological disorder that affects movement. A loss of dopamine-producing cells in the brain causes the condition, which leads to a lack of dopamine, a neurotransmitter responsible for coordinating movement.
Common symptoms of Parkinson’s disease include the following:
- Tremors in the arms, hands, legs, or head
- Stiff muscles with contractions for a long time
- Slow movements
- Balance and coordination challenges, sometimes resulting in falls
- Impaired balance and coordination, sometimes leading to falls
Other symptoms may include:
- Emotional changes such as depression
- Swallowing, speaking, or chewing challenges
- Constipation or urinary problems
- Skin problems
Individuals with Parkinson’s disease often develop a so-called Parkinsonian gait. Here, the patient tends to lean forward, taking small and quick steps. There may be reduced arm swinging, too. Many need help initiating (or continuing) movement.
There is no cure for Parkinson’s disease, but tools are available to help manage symptoms and improve quality of life. Such interventions may include medications (for example, dopamine agonists or levodopa, and non-medication interventions, including physical therapy, exercise, and speech therapy.
What causes Parkinson’s disease?
The basal ganglia is a brain region that regulates movement. The most prominent Parkinson’s disease symptoms occur when nerve cells in the basal ganglia, an area of the brain that controls movement, become impaired or die.
These nerve cells (neurons) normally produce an important brain chemical — dopamine. When the neurons die or become impaired, they produce less dopamine, which causes movement problems associated with the disease.
Second, patients with Parkinson’s disease also lose nerve endings that make norepinephrine. This neurotransmitter is a primary chemical messenger of the sympathetic system, controlling functions such as blood pressure and heart rate.
This neurotransmitter loss may contribute to some of the non-movement Parkinson’s features, including irregular blood pressure, fatigue, diminished food movement through the gut, and a sudden blood pressure drop upon sitting or lying.
Third, those with Parkinson’s disease have many brain cells with Lewy bodies and unusual clumps of the protein alpha-synuclein. Researchers are working to understand better the relationship between alpha-synuclein and genetic variants impacting Parkinson’s and Lewy body dementia.
Researchers believe Parkinson’s disease is the product of a combination of environmental and genetic factors. There are several risk-increasing genes, with mutations causing the brain’s hallmark loss of dopamine-producing cells. The Mayo Clinic reminds us that such mutations are uncommon (except in rare cases with many family members affected by Parkinson’s disease).
Environmental factors such as exposure to toxins (including pesticides) and head injuries are associated with an increased risk of Parkinson’s disease.
Aging is another risk factor for Parkinson’s disease. The disease is more common in people over the age of 60. Finally, men are more likely than women to develop the condition.
Parkinson’s disease is probably secondary to a complex interplay between genetics, aging, and environmental exposures.
A common chemical and Parkinson’s disease risk
The number of individuals with Parkinson’s disease has doubled over the last three decades. It may double again (from 6.9 million in 2015 to 14.2 million) by 2040.
The causes of Parksin’s disease are entirely clear. As discussed above, certain genetic mutations can increase risk, as can head trauma. However, these risk factors don’t explain the vast majority of cases. There are some less visible factors.
Could a common chemical used in paint removers, gun cleaners, dry cleaning, aerosol cleaning products, decaffeinating coffee, and correction fluid be a key to understanding the recent dramatic increase in Parkinson’s disease?
An international group of researchers recently reported the disturbing results of its review of previous research:
Trichloroethylene is associated with as much as a 500 percent increased risk for Parkinson’s disease.
What is TCE?
It is invisible, a highly volatile liquid, and seemingly everywhere. It is invisible, a highly volatile liquid, and seemingly everywhere. First synthesized in a lab in 1864, the chemical trichloroethylene (TCE) was first used for commercial production in 1920. TCE has commercial, industrial, military, and medical applications.
Among its uses are:
- Producing refrigerants
- Cleaning electronics
- Degreasing engine parts
- Anesthetic and analgesic (limited use)
- Gun cleaners
- Correction fluid
- Dry cleaning. A similar chemical (perchloroethylene) is currently more widely used. The current researchers pointedly observe that, in anaerobic conditions, perchloroethylene often transforms into TCE.”
The researchers remind us that we don’t have to have occupational exposure to come into contact with TCE. Exposure can occur through the air (indoor or outdoor) or groundwater. The substance evaporates from the underlying solid and groundwater and often enters our workplaces, homes, and schools undetected.
Animal studies indicate the potential peril, with TCE exposure causing selective loss of dopamine-producing nerve cells. Studies dating back to 1960 show a TCE: Parkinson’s disease association.
Unfortunately, the chemical was ubiquitous in the 1970s; 10 million Americans worked with chemical or organic solvents daily. If you want to see an exhaustive list of the occupations and industries in which TCE exposure still occurs, please go here:
Trichloroethylene: An Invisible Cause of Parkinson’s Disease?
The etiologies of Parkinson’s disease (PD) remain unclear. Some, such as certain genetic mutations and head trauma, are…
TCE problem scope
I decided to write this piece after seeing this figure from the research paper:
“TCE contaminates up to one-third of US drinking water, and has polluted groundwater in over 20 countries on five continents. The substance is found in half of the 1300 most toxic “Superfund” sites that are in a federal cleanup program, including 15 in California’s Silicon Valley; there TCE was used to clean electronics.”
While the United States military no longer uses TCE, several contaminated sites exist, including Marine Corps Base Camp Lejeune in North Carolina. Researchers discovered TCE and PCE in drinking water at 280 times the recommended safety standards at Camp Lejeune.
The current review highlights seven cases of people who developed Parkinson’s disease after likely exposure to TCE. For example, National Basketball Association player Brian Grant developed symptoms of Parkinson’s disease in 2006 at age 34.
Grant lived at Camp Lejeune as a child. He bathed in, drank, and swam in contaminated water. His father died of esophagus carcinoma, cancer that is associated with TCE. Grant created a foundation to support and inspire folks with Parkinson’s disease.
In 2014, the International Agency for Research on Cancer updated its classification of TCE to Group 1. This assignment means that there is sufficient evidence that the substance causes kidney cancer (and that there is some evidence that it leads to liver cancer and non-Hodgkin’s lymphoma.
My take — TCE and Parkinson’s disease
This study was eye-opening, even as these authors acknowledge that TCE’s role in Parkinson’s disease is “far from definitive.” For example, TCE exposure is often combined with toxin exposure or unmeasured genetic risk factors. No causal relationship is proven; most of us exposed to TCE never get Parkinson’s disease.
Secondly, there can be recall bias: Those with Parkinson’s disease may be more likely to recall their exposure to the toxin.
Of course, we need more research and cleanup of contaminated sites. I hope to have contributed to spreading the word about the potential harms of TCE exposure. Still, given the known connection with some cancer types, I hope to stay clear of trichloroethylene.
