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Parkinson’s Disease and the Environment: Opportunities for Prevention

by Ted Schettler MD, MPH, Science Director

Parkinson’s disease was probably uncommon when first described about 200 years ago. Now however, the Global Burden of Disease Study, published in The Lancet Neurology, estimates that Parkinson’s disease afflicts more than six million people throughout the world, and projections suggest over 12 million cases by 2040. Although registries are incomplete, an estimated 90,000 new cases in people 65 and older are diagnosed annually in the United States alone.

Aging populations and genetic susceptibility explain only a portion of this growing disease burden. Geographic “hot spots,” where the disease is more common, and a rapidly growing number of epidemiologic and laboratory studies make it clear that environmental factors, many now identified, are largely responsible for what some call a Parkinson’s pandemic.   

Parkinson’s disease, now among the most common neurological disorders, is characterized by slowed movements, tremor, rigidity, and difficulties with gait and balance. Changes in smell, cognition, affect, and sleep are also common. These symptoms are due to degenerative changes in neurons along with deposition of aggregates of a protein, alpha-synuclein. Dopamine-producing cells in a portion of the brain called the substantia nigra have received the most attention because dopamine replacement can alleviate some of the symptoms. However, other cells in the nervous system are also involved, and the disorder may actually begin in the nose or gastrointestinal tract long before neurological symptoms appear.   

Initial links to environmental agents

Case reports linking Parkinson’s disease with occupational exposure to the solvent trichloroethylene (TCE) appeared as early as 1969. It wasn’t until 1982, however, that neurologist Dr. William Langston encountered a group of young people with sudden onset of Parkinson-like symptoms—and a search for environmental risk factors gained traction. Langston traced the cause to a synthetic heroin contaminated with MPTP that had been injected by the victims. When they were given dopamine, their symptoms rapidly but temporarily improved.  

Soon after Langston identified MPTP as a cause of Parkinsonian symptoms, neurologist Dr. Caroline Tanner and her colleagues conducted a large study of identical and fraternal twins showing that genetics played only a minor role in determining the risk of developing Parkinson’s disease.   

Together, the identification of MPTP as an agent that could cause Parkinson’s disease and demonstration that genetic inheritance did not explain disease patterns encouraged a more vigorous search for other environmental agents. Paraquat, a widely used herbicide structurally similar to the metabolite of MPTP responsible for its toxicity, was soon implicated. So was rotenone, another pesticide that is also toxic to mitochondria in dopamine-producing cells, causing Parkinson-like symptoms in laboratory animals. 

CHE’s consensus conference

In response to the growing interest in identifying environmental and other factors that could explain increases in the incidence and prevalence of Parkinson’s disease, the Collaborative for Health and Environment, along with Parkinson’s Action Network (now a part of the Michael J. Fox Foundation for Parkinson’s Research), convened a multidisciplinary group of experts in Sunnyvale, California in 2007 to assess what was then known about risk factors for the disease.

Following the meeting, the group published a consensus statement in which they identified behavioral and environmental factors known to be or plausibly associated with increased risk.  

Among environmental agents, the group agreed that exposure to several pesticides was likely to increase risk based on available epidemiologic and laboratory mechanistic data. They were unable to reach consensus on whether or not people living in rural areas and people drinking well water were at increased risk, as had been reported in some, but not all, studies. Because of few data then available, the group did not further consider potential roles of organic industrial solvents or air pollution. 

The Parkinson’s PLAN: A new path to prevention

Now, 19 years later, a new summary of current evidence is available in an engaging book by neurologists Dr. Ray Dorsey and Dr. Michael Okun, The Parkinson’s PLAN: A New Path to Prevention and Treatment (Public Affairs, 2025). Written in a highly accessible style, the authors make the case that Parkinson’s disease is largely due to exposure to environmental agents and that much of the disease burden is preventable. 

Although inherited susceptibility genes are now better understood, more than 85 percent of Americans with the disease do not carry mutations in either of the two most common of them, and not every carrier gets Parkinson’s disease. This suggests that even in people genetically susceptible, some other trigger is necessary to initiate the disease.   

The environmental agents for which the authors find the most compelling evidence of links to Parkinson’s disease risk are some pesticides, the solvents TCE and perchloroethylene (PCE), air pollution, and manganese. These agents can cause the disease through different mechanisms at the sub-cellular level, typically through mitochondrial toxicity, and symptoms can vary—suggesting that there are different pathways to Parkinson’s disease with many common features clinically and biologically. 

But, the authors note, despite the growing evidence of environmental causes, the published scientific literature still overwhelmingly focuses on genetic risk factors rather than environmental causes and opportunities for primary prevention. 

Many environmental drivers remain unaddressed  

Paraquat, rotenone, pyrethrins, pyrethroids, heptachlor (no longer widely used), chlorpyrifos, and some fungicides are among the pesticides that increase the risk of Parkinson’s disease after exposures. 

Although banned in many countries, paraquat remains one of the most heavily used herbicides in the United States, with 15 million pounds used in 2018 alone. It was re-authorized for continued use by the EPA in 2024, guaranteeing that exposures in farm workers and neighboring communities will continue.  

Although the US EPA scheduled most uses of the solvent TCE to be phased out by 2026, implementation of the ban was put on hold in March 2024 due to legal challenges, and the timeline remains uncertain. Meanwhile, because of widespread use over decades, groundwater in much of the United States is contaminated with TCE, leading to exposures in over 17 million people drinking water from private wells. 

TCE is one of the contaminants discovered in ground water sources of drinking water at Camp Lejeune, North Carolina in the 1980s, where military families had been exposed for many years. Studies by Drs. Caroline Tanner and Samuel Goldman showed a marked increase in Parkinson’s disease risk in veterans who had spent time at Camp Lejeune many years earlier compared to a similar group of veterans who served at Camp Pendleton in California. Based on their work, they were able to get Parkinson’s disease recognized as presumptively due to TCE exposures, making affected veterans eligible for disability benefits and compensation.  

Like TCE, the solvent PCE (used for dry cleaning) also contaminates soil and groundwater in many areas in the United States. PCE vaporizes into the air in and above dry-cleaning facilities, exposing workers and residents in apartments in the same buildings. Both solvents can also infiltrate through building foundations near contaminated soil and water into indoor air where residents are exposed.  

In their book, Drs. Dorsey and Okun also review the evidence linking air pollution to increased Parkinson’s disease risk. They describe the early autopsy studies of Dr. Lilian Calderón-Garcidueñas in Mexico City, where the air was badly fouled with vehicle exhaust. In the brains of 203 people who had died prematurely of unrelated causes (average age only 25 years), she found evidence of Parkinson’s pathology in about 25 percent and Alzheimer’s disease pathology in even more. These individuals were too young to have clinical manifestations of Parkinson’s disease at the time of their deaths, but her findings suggest that the impacts of air pollution on the brain begin early. Since then, a number of studies in the United States and other countries show an increased risk of Parkinson’s disease with exposure to higher levels of traffic-related air pollution.   

Prevention and improved treatment

The PLAN in the book’s title is an acronym for Prevent, Learn, Amplify, and Navigate. The authors set out an ambitious agenda to both prevent the disease and improve treatment for affected people. They advocate banning dangerous chemicals (including those linked to this disease), improved measurement of trends, and development and implementation of more patient-centered treatments by skilled practitioners.  

They lay out actions that individuals can take to lower their Parkinson’s disease risk, and make the important point that these actions will also lower the risk of other diseases as well. But, individual actions will not be sufficient. Policy changes, such as shifting some federal subsidies from pesticide-dependent conventional agriculture to organic production and creation of pesticide-free schools, are examples of community and societal interventions that could help reduce exposures and risk. Further reductions in air pollution and building homes and schools safer distances from freeways are additional measures that would reduce risk of Parkinson’s disease and a number of other disorders clearly linked to contaminated air.  

Drs. Dorsey and Okun persuasively make the case that much of Parkinson’s disease is preventable and that action is urgently needed. 

Ray Dorsey recently joined Kristin Schafer, director of the Collaborative for Health and Environment, and me for a conversation sponsored by CHE and the New School at Commonweal to discuss the book and some of its many implications. A recording of that conversation, CHE Café: Why Parkinson’s disease is preventable, is now available. 

Mo Banks