New research has shown that continued exposure to the chemical solvent trichloroethylene (TCE) is linked to developing Parkinson’s disease – the fastest-growing neurodegenerative disease in the world.
A new study published in JAMA Neurology presents substantial evidence that prolonged exposure to the chemical solvent trichloroethylene (TCE) is strongly linked to the potential of developing Parkinson’s disease. Concerns are raised worldwide as TCE remains in various groundwater sources.
The study focused on the medical records of tens of thousands of Marine Corps and Navy veterans who underwent training at Marine Corps Base Camp Lejeune in North Carolina between 1975 and 1985.
It was found that veterans exposed to TCE-contaminated water at Camp Lejeune had 70% higher risk of developing Parkinson’s disease compared to similar veterans who trained elsewhere. Moreover, these exposed veterans exhibited elevated rates of early Parkinson’s symptoms, including erectile dysfunction, loss of smell, tremors, difficulties with movement, speech, and balance, as well as dementia and swallowing issues that can lead to fatal pneumonia.
What is Parkinson’s disease?
Parkinson’s disease is a movement disorder recognised as the fastest-growing neurodegenerative disease worldwide. Over the past 25 years, its global prevalence has doubled.
Although genetics explain only about 10% of Parkinson’s cases, previous research has hinted at the potential role of TCE exposure in triggering the disease.
However, the study conducted by researchers at the University of California, San Francisco (UCSF) establishes the strongest environmental link between TCE and Parkinson’s disease to date. Prior to this study, the epidemiological literature included fewer than 20 reported cases of Parkinson’s resulting from TCE exposure.
Prevalence of TCE
TCE is a colourless liquid that easily permeates biological membranes and can be absorbed through ingestion, skin contact, or inhalation. It quickly vaporizes and is currently employed primarily in refrigerant production and heavy industry degreasing.
In the past, TCE had various applications, such as decaffeinated coffee, dry cleaning, carpet cleaning, and as an inhaled surgical anaesthetic for children and women in labour.
TCE exhibits significant persistence in soil and groundwater, and inhalation of vapour from these hidden sources is believed to be the primary route of exposure today.
However, TCE can also be detected in many food items, up to one-third of drinking water, breast milk, blood, and urine.
Implications of the study
The Camp Lejeune analysis “is exceptionally important”, says Briana De Miranda, a neurotoxicologist at the University of Alabama at Birmingham who studies TCE’s pathological impacts in the brains of rats.
“It gives us an extremely large population to assess a risk factor in a very carefully designed epidemiological study,” De Miranda adds.
Studies on animals have shown that TCE acts in an area of the midbrain responsible for movement control.
It inhibits complex 1, the leading enzyme in a chain of reactions that convert food to energy in cellular organelles called mitochondria.
In rodents exposed to TCE, the dopamine-generating neurons in the midbrain’s substantia nigra are destroyed, as happens in human Parkinson’s disease. Pesticides such as paraquat and rotenone that have been associated with Parkinson’s disease also leave that pathological signature in rodents.
The new study will likely add ammunition to class action lawsuits that were launched after Congress last year enabled veterans from Camp Lejeune to sue the government for health damage they suffered from exposure to the contaminated water there decades ago.
“This is increasing evidence that environmental factors are important causes of Parkinson’s disease,” Miller says. “But we are just scratching the surface. We need to continue studying this.”