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Researchers warn that a colorless chemical known as trichloroethylene (TCE) — which has been used to dry-clean clothes, degrease metals and decaffeinate coffee — may be linked to the dramatic increase in Parkinson’s disease (PD) cases.
They recently published a series of seven cases in the Journal of Parkinson’s disease that illustrate TCE’s harmful health effects and the potential PD association.
“TCE is associated with a 500% increased risk of Parkinson’s disease,” lead author Dr. Ray Dorsey, professor of neurology at the University of Rochester in New York and author of “Ending Parkinson’s Disease,” told Online News 72h Digital.
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The chemical reproduces the features of the neurological disease in laboratory animals.
It impairs the function of the energy-producing parts of cells called mitochondria, which are known to be damaged in Parkinson’s disease, Dorsey added.
Widespread applications of TCE
TCE was first synthesized in the lab in 1864 and began to be commercially produced in the 1920s.
Its unique properties inspired many applications, including producing refrigerants, cleaning electronics and degreasing engine parts.
A colorless chemical may be linked to a dramatic increase in Parkinson’s disease cases, according to new research, although the data had some limitations. (Getty Images)
In the 1930s, it began to be used for dry-cleaning clothes, as it evaporated easily but did not shrink fabrics.
But the chemical contaminates up to one-third of the drinking water in the U.S, polluting groundwater in at least 20 different countries on five continents, according to the study.
Numerous military sites have also been previously contaminated, including the Marine Corps base Camp Lejeune in North Carolina.
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There, for 35 years, a million Marines, their families and civilians were exposed to drinking water with levels of TCE that were 280 times the safety standards, per the study.
The U.S. Environmental Protection Agency (EPA) told Online News 72h Digital it recently released its final revised risk determination this January, finding “TCE, as a whole chemical substance, presents an unreasonable risk of injury to human health under its conditions of use.”
What causes PD?
The common signs and symptoms of PD occur after nerve cells in a specific part of the brain that controls movement located in the basal ganglia becomes impaired and/or dies, according to the National Institute on Aging.
But it’s unclear why the nerve cells die.
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While some genetic mutations are known to cause PD, the majority of cases are not inherited, according to the study.
The authors note the number of people with PD has more than doubled in the past 30 years, but Dorsey told Medscape Medical News the “world’s fastest-growing brain disease” might be “largely preventable.”
The “EPA shares the concerns about the risks of TCE to human health,” the agency told Online News 72h Digital. (iStock)
The authors explore TCE specifically because of its “ubiquitous” nature in the environment, starting in the 1970s when “annual U.S. production surpassed 600 million pounds per year, or over two pounds per person.”
The authors estimate 10 million Americans worked with the chemical or other organic solvents daily, but “millions more encounter the chemical unknowingly through outdoor air, contaminated groundwater and indoor air pollution.”
The EPA identified numerous health risks of TCE in the human body, including toxicity to the liver, kidney, reproductive, immune and nervous systems — and possible risk of cancer from inhalation and dermal exposure.
EPA plans to take action
“EPA shares the concerns about the risks of TCE to human health,” the agency told Online News 72h Digital.
Critics argue that TCE should be banned in the U.S.
Before the EPA can put regulations in place, the agency must follow the Toxic Substances Control Act (TSCA), which requires the agency to first conduct a risk evaluation.
The EPA “is now moving quickly to release a proposed rule to take action to regulate TCE so that it no longer presents an unreasonable risk to human health.”
“The risk evaluation includes a determination of whether or not a given chemical poses unreasonable risk to human health or the environment,” EPA noted.
“Then EPA moves to risk management, which is where EPA creates a rule to protect people and/or the environment from the unreasonable risk identified.”
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Since the agency has released its final risk determination, it “is now moving quickly to release a proposed rule to take action to regulate TCE so that it no longer presents an unreasonable risk to human health.”
The agency plans to release this proposed rule this June.
Several actions the agency may take include “regulations prohibiting or limiting the manufacture (including import), processing, distribution in the marketplace, commercial use, or disposal of this chemical substance, as applicable,” the EPA told Online News 72h Digital in an email.
One patient’s story
The authors of the new research discussed seven patients in which TCE may have contributed — through either environmental or work exposure — to the development of PD.
One case included NBA basketball player Brian Grant.
He drank, bathed and swam in contaminated water unaware of its adverse effects.
He started living in Camp Lejeune as a child when he was three, while his father was a Marine around the time the waters had peak TCE levels.
He drank, bathed and swam in contaminated water unaware of its adverse effects.
He started to have symptoms in adulthood while he was playing with the Los Angeles Lakers. He noticed he could no longer jump off his left leg the way he could earlier.
The authors of the new research caution the current data is only “circumstantial but raises worrisome questions about the link between the chemical [TCE] and the disease.” (iStock)
The symptoms progressed the following season with an intermittent tremor in his left hand, but he still was able to take part in playoff game for the Phoenix Suns — although only for two minutes.
In retrospect, the study noted that he likely made history that year by playing an entire basketball season in the NBA without knowing he had PD because he was only diagnosed with the disease two years later.
Limitations of the data
The authors caution the current data is only “circumstantial but raises worrisome questions about the link between the chemical and the disease.”
“There are many research groups currently examining the association and we anticipate more information will be available soon.”
Several factors in the patient cases that make it difficult to establish a strong link between TCE and PD — including that many people were unaware of their exposure and that the duration of time between exposure and disease is long. So other variables could be also responsible.
Other experts who were not part of the research, however, share the report’s concern.
“The collective evidence supporting a strong association between TCE exposure and Parkinson’s disease continues to accumulate,” Dr. Michael S. Okun, medical advisor to the Parkinson’s Foundation, told Online News 72h Digital.
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“There are many research groups currently examining the association and we anticipate more information will be available soon,” added Okun, who is also the executive director of the Norman Fixel Institute for Neurological Diseases University of Florida Health in Gainesville, Florida.
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“Limiting exposure to TCE … could have the potential to lessen our future burden of Parkinson’s disease.”
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