Where Is My Mind?
Researchers Have Found This Chemical May Be Driving Up Cases Of The Fastest-Growing Neurological Condition In The World
Yesterday (April 11) was World Parkinson’s Day.
Parkinson’s disease (PD) is a progressive and debilitating neurological disorder affecting millions of people throughout the world.
Despite significant advancements in treatment, there is still no known cure for the disease, and those living with Parkinson’s must navigate its ongoing impact on their health and well-being.
The number of people with PD has more than doubled in the past 30 years, and experts believe it will double again by 2040, making it the fastest growing brain disease in the world.
Today, PD affects an estimated 10 million people worldwide.
Yet the causes of this degenerative condition remain unclear. Researchers theorize that a combination of genetic and environmental factors are at play.
A new study published last month, calls out an invisible cause—trichloroethylene (TCE), a ubiquitous chemical that has contaminated countless sites, tainted drinking water, and posed health risks to those who are, often unknowingly, exposed via their work or their environment.
For the study, a team of international researchers reviewed previous research and cited data that suggests TCE is associated with as much as a 500 percent increased risk for PD.
Lead investigator Ray Dorsey, MD, professor of neurology at the University of Rochester, New York, told Medscape Medical News that PD “may be largely preventable.”
“Countless people have died over generations from cancer and other disease linked to TCE [and] Parkinson’s may be the latest,” he said. “Banning these chemicals, containing contaminated sites, and protecting homes, schools, and buildings at risk may all create a world where Parkinson's is increasingly rare, not common.”
He noted that the rapid growth in PD incidence cannot be explained by genetics or aging alone, and I would agree.
Right now, about 15 percent of patients have a genetic factor.
“Certain pesticides…are likely causes but would not explain the high prevalence of PD in urban areas, as is the case in the U.S.” and “TCE is likely one such factor.”
A Closer Look At TCE
TCE is a colorless, nonflammable liquid solvent used in both industrial and household items. While this chemical’s name doesn’t roll off the tongue, its widespread use in multiple industries means that most of us have been exposed to it.
Starting in the early 1900s, it was used to remove grease and dirt from metal parts and was a favorite in the aircraft industry from the 1950s to 1980s. It was also used as an industrial solvent in the rubber industry—in paints, varnishes, adhesives, and paint strippers—and to produce agricultural chemicals such as fungicides and insecticides.
It was used again in the dry-cleaning industry, as a carpet cleaner, and in spray fixatives for arts and crafts. Until the 1970s, it was used to help decaffeinate coffee.
“From getting stains out of favorite shirts to baking cookies and everything in between, Whirlpool® appliances are there to help you keep the day moving” reads the company’s website, a corporation as American as apple pie with more than $20 billion in annual sales.
For 45 years, the Whirlpool refrigeration production facility was based in Fort Smith, Arkansas. In 1967, they started using TCE as a degreaser and discontinued its use in 1981. Yet, in 2001 the company became aware that a plume of TCE had been found in the groundwater beyond its property and underneath homes in a nearby neighborhood.
TCE is known to have a latency period of twenty years or more. When I worked with the community in Arkansas, people reported brain tumors, throat cancers, and nasopharyngeal cancer, and these rare cancers always raise a red flag for me. The Fort Smith plant closed in June 2012, and the company has been working to clean up the contamination.
Most people get exposed to TCE by consuming contaminated drinking water. It breaks down slowly and can move through soil to find its way into drinking water sources.
The water is contaminated from some combination of industry discharge/spills and existing hazardous-waste sites. TCE has polluted the groundwater in more than 20 different countries on five continents.
In November 2016, it was added to the list of substances known to cause cancer in the “14th Report on Carcinogens” released by the U.S. Department of Health and Human Services.
TCE and its health effects made the cover of Newsweek in 2014 because it was one of the top pollutants at Camp Lejeune, a North Carolina military base that is considered one of the worst toxic sites in the U.S.
TCE was found in the drinking water of the 240-square-mile base as part of what was described as “a toxic cocktail of industrial solvents, dry-cleaning chemicals, and gas.”
TCE contaminates countless industrial, commercial, and military sites. It’s found in half of the 1300 most toxic Superfund sites in the U.S. that are part of a federal clean-up program, including 15 in California’s Silicon Valley where TCE was used to clean electronics, according to the new study.
The study also examines another route of exposure for TCE and other chemicals. Starting in 1978, researchers began to understand vapor intrusion and that TCE, much like radon, could evaporate from contaminated soil and groundwater and enter homes, schools, and workplaces.
The researchers in the study focus on 7 cases of individuals who developed PD after likely exposure to TCE, including NBA basketball player Brian Grant, who developed PD symptoms in 2006 at the age of 34.
Grant and his family lived in Camp Lejeune when he was a child, during which time he drank, bathed, and swam in contaminated water. His father also died of esophageal cancer, "which is linked to TCE," the authors of the study write.
Grant created a foundation to inspire and support patients with PD.
The study authors acknowledge that the role of TCE in PD, as illustrated by the cases, is “far from definitive.”
I would argue part of that knowledge gap is based on so little study of toxic exposures. Plus, exposure to TCE is often combined with exposure to other toxins.
Take Action on TCE
The study discusses future actions to help address the role TCE may play in the increase of PD cases, and we’ve highlighted them below.
Conduct more research. A search of TCE and PD on PubMed yields only 15 papers in the past decade. By contrast, a search of the genetic risk factors for PD returns more published papers in just the last two months. Further work is also needed to estimate the risk of TCE exposure in conjunction with other known neurotoxicants, such as pesticides, and risk factors like traumatic brain injury.
Clean and contain contaminated sites. Hundreds of thousands of sites are contaminated across the U.S. and globally. They are found in strip malls where dry cleaners used to operate, on military bases where use was widespread, in cities near old manufacturing sites (especially those near rivers or streams), and in rural areas where landfills were created to dump hazardous waste. Local, regional, and national authorities should take responsibility in overseeing rapid control of contaminated sites.
Monitor TCE levels and publicly communicate risk. Most databases monitor emissions, not current levels, and monitoring tends to be sporadic and reactive. TCE testing in groundwater, drinking water, soil, and in outdoor and indoor air should be widespread, frequent, and part of routine water quality testing. The results should be readily and publicly available. Polluted sites need to be marked as such, and the dangers to health clearly communicated to all parties at risk.
Ban trichloroethylene. TCE has a long-established list of health risks. TCE causes cancer, increases the risk of miscarriages, contributes to birth defects, and is associated with diseases in nearly every organ system. The chemical is more than a century old. It’s time to find a better solution for solvents.
Listen to patients. Finally, we should listen to patients more! Medicine often moves from diagnosis to treatment without considering the cause. The vast majority of individuals with PD do not have a family history of the disease or carry an identifiable genetic risk factor. Listening to their life stories or occupational histories can help identify TCE or other factors contributing to PD and could help develop etiology-specific treatments. This information can also inform their care (e.g., cancer screening), provide guidance to family members, co-workers, and classmates, and advance our understanding of the potential causes of this debilitating and likely very preventable disease.
What do you think about the role these toxic chemicals play in our health? Let us know in the comments below.