What do we know about the association between environmental toxicants and Parkinson disease?

Parkinson disease was first described by James Parkinson in 1817, but as of 2026, there is still no known cure for this neurodegenerative disease. Parkinson disease is one of the fastest growing neurological disorders in the world (1).

In a neurodegenerative disease such as Parkinson disease, there is a progressive loss and death of nerve cells, or neurons, as is also the case in Alzheimer disease.

Large-scale genetic research studies have led to the understanding that external or environmental factors are primarily responsible for causing Parkinson disease. Experts in the field now believe that Parkinson disease could be largely preventable (2).

The main symptoms of Parkinson disease include resting tremor (typically described as “pill-rolling” because the thumb and fingers appear to be rolling a pill between them), slowed movements (such as decreased hand dexterity and a shuffling walk), and rigidity (stiffness). Symptoms usually begin on one side of the body and later spread to involve both sides. Other symptoms may include a soft voice, masked facial expression, and smaller writing. Balance issues and memory problems generally occur later in the course of the disease.

What changes in the brain result in Parkinson disease?

In people with Parkinson disease, neurons in the part of the brain called substantia nigra, as well as other brain regions, degenerate progressively. These neurons produce the neurotransmitter dopamine, so as a result of the loss of the neurons, dopamine levels become depleted. This depletion accounts for the clinical symptoms we see in patients with Parkinson disease. The most commonly used drug for Parkinson disease, levodopa, acts by replenishing depleted dopamine in the brain, resulting in temporary improvement in symptoms, but no currently available drug for Parkinson disease can slow the progression of the disease or reverse the disease.

What precisely causes these neurons to degenerate and die is not yet clearly understood, but experts believe that interactions between a susceptible person’s genes and environmental factors play a role. Such interactions lead to oxidative stress, inflammation, mitochondrial dysfunction, abnormal protein processing, and other mechanisms culminating in the death of the neurons.

What is currently known is that an abnormal form of a protein called alpha-synuclein, abundant in the central nervous system, is found inside the neurons in people with Parkinson disease (3). These abnormal proteins form stubborn clumps and become a major component of Lewy bodies, which are abnormal structures residing in the neurons affected in a group of neurodegenerative diseases that include Parkinson disease and dementia with Lewy bodies (4). It is humbling to realize that the normal function of alpha-synuclein in the brain is not fully understood, but it seems to be involved in the signaling process from one neuron to another (5). Parkinson disease progresses because these abnormal proteins can somehow be spread from diseased neurons to healthy ones (6).

An intuitive response to solving this problem would be to say, “Can we somehow eliminate these abnormal proteins from the brain in order to cure Parkinson disease?” In fact, drugs in the form of antibodies targeting alpha-synuclein are being studied in clinical trials, but unfortunately, results have been disappointing so far (7).

Because of the current lack of effective drug treatments for Parkinson disease that can change the disease course, prevention is key. As part of a functional medicine and integrative medicine approach to Parkinson disease prevention, we ask the questions, “What lifestyle choices and environmental factors are associated with Parkinson disease, and what can we do to prevent the disease?”

Environmental toxicants and Parkinson disease

There are three categories of environmental toxicants that are most strongly implicated in causing Parkinson disease: pesticides, dry-cleaning and degreasing chemicals, and air pollution (2).

Pesticides, such as paraquat, rotenone, 2,4-dichlorophenoxyacetic acid, organochlorine pesticides, and organophosphate pesticides, are associated with Parkinson disease across lines of epidemiological and laboratory evidence (8). Paraquat is a weedkiller used on soybean, corn, and cotton fields, among other crops. Residents who lived or worked near where paraquat was sprayed was twice as likely to have Parkinson disease as people who did not (2). Rotenone was used as a botanical insecticide and remains a widely used fish poison. It is toxic to the mitochondria and produces Parkinson disease features in rats. The herbicide 2,4-dichlorophenoxyacetic acid is widely used to control weeds in crops and in home lawns and public parks.

Organochlorine pesticides (including DDT and heptachlor) were banned in most developed countries decades ago, but their presence in the environment is still widespread due to their chemical stability and persistence. Their blood concentrations are higher in people with Parkinson disease. In mouse studies, exposure to them in early life increases the risk of neurodegeneration later in life—a phenomenon known as silent neurotoxicity (2). Organophosphate pesticides are extensively used in agriculture, taking up about 40% of the share of commercially produced pesticides.

Trichloroethylene (TCE) and perchloroethylene (PCE) are industrial solvents used in dry cleaning and metal degreasing. TCE was the predominant dry cleaning solvent from the 1930s until the 1950s, when it was replaced by PCE, which remains the most commonly used dry-cleaning chemical in the U.S. TCE and PCE are present in up to one-third of U.S. drinking water supplies (9). Animal studies have shown that TCE causes key Parkinson disease features, including abnormal clumping of the alpha-synuclein protein in neurons, death of dopamine-producing neurons in brain regions affected in Parkinson disease, and mitochondrial dysfunction (9). (Mitochondria are known as the “powerhouses of the cell” because they convert nutrients into ATP, the main energy currency for the cell. The brain is an organ of high energy demand and therefore relies heavily on the proper function of the mitochondria.)

The strongest epidemiological evidence so far for the role of TCE in causing Parkinson disease came from a study that included personnel stationed at the Marine Corps Base Camp Lejeune in North Carolina, where the drinking water was contaminated with TCE, PCE, and other chemicals. In this large population-based study that included more than 340,000 Marine and Navy service members, the individuals stationed at Camp Lejeune had a 70% higher risk of developing Parkinson disease compared with those stationed at another base that did not have contaminated water (9).

A review article in the New England Journal of Medicine sums up the research evidence by pointing out that exposure to pesticides or industrial solvents is associated with a 40% or greater risk of Parkinson disease in most studies, and the higher the exposure to these chemicals, the higher the risk of Parkinson disease (8).

High dairy intake has been associated with a higher risk of Parkinson disease. In a study that combined the data from four large population-based studies, people with the highest consumption of dairy products had a 60% higher risk of Parkinson disease, compared with people with the lowest dairy consumption (10). Interestingly, when the data was examined separately for men and women, the risk with dairy consumption was 80% higher for men and 30% higher for women—suggesting that dairy consumption may increase the risk of Parkinson disease more so for men than women (though women who consumed dairy still had an increased risk). It is thought that the association between dairy intake and Parkinson disease is possibly due to toxicants bioconcentrated in milk (8, 11). On the other hand, diets high in vegetables, fruits, and grains are associated with a lower risk of Parkinson disease (11).

Air pollution is made up of chemicals and particles. Most air pollution studies related to Parkinson disease focus on particulate matter, which consists of tiny particles suspended in the air. The smallest particles are of the most serious concern because they can travel into the brain directly through nerves in the nose, often carrying with them toxicants such as heavy metals, which are elevated in the brains of people with Parkinson disease (2). PM_2.5, which is particulate matter with a diameter of 2.5 micrometers or smaller, has been associated with higher risks of Parkinson disease in epidemiologic studies across the world. Within the U.S., the incidence of Parkinson disease varies by a factor of at least 2 across geographic regions: Areas with higher incidence are more urban and industrialized and have more air pollution (2). Laboratory studies show that PM_2.5 causes abnormal clumping of the alpha-synuclein protein in cells (which we discussed above), mitochondrial dysfunction, oxidative stress, inflammation, and disrupted gut microbiome, all of which are associated with Parkinson disease (2).

Not everyone who is exposed to the environmental toxicants discussed above will develop Parkinson disease. It is possible that having certain genes makes a person more likely to be harmed by certain environmental toxicants. It is also possible that exposure to a combination of different toxicants, exposure at different times or places, or exposure for longer periods of time puts individuals at higher risks of developing Parkinson disease. Having “leaky gut” may predispose a person to higher absorption of pesticides and other toxicants through their digestive tract (2).

Other risk factors

While not a focus of this blog, other factors that increase the risk of Parkinson disease include lack of physical activity, amphetamine or methamphetamine, heavy metals, and traumatic brain injury (1). There is an observed association of a reduced risk of Parkinson disease in cigarette smokers, but the reason behind this association is not known. Taking up cigarette smoking would certainly be ill-advised given its many health harms. Coffee and tea drinking are associated with a lower risk of Parkinson disease, especially in men (11).

Taking protective actions

Based on a knowledge of the association of these environmental toxicants with Parkinson disease, there are actions we can take now to reduce the risk of Parkinson disease, according to experts in the field (2). We can minimize exposure to the environmental toxicants we have discussed in this blog. For example, we can choose organic foods, which have lower concentrations of pesticides. If you work with pesticides, use personal protective equipments such as chemically resistant gloves and respirators, and if possible, do not live near pesticide-treated fields.

We can choose alternatives to the dry-cleaning chemical perchloroethylene (PCE). We can choose to minimize exposure to persistent organochlorine pesticides, which are lipophilic (fat-soluble) and accumulate in animals’ fatty tissues and milk. We can use water filtration systems to eliminate TCE and PCE from the watery supply in the home. We can use air purifiers with HEPA filters to remove PM_2.5 (fine particulate matter) from the air.

Though not a focus of this  blog, physical activity and exercise are associated with a significantly reduced risk of developing Parkinson disease (12). While greater amounts and intensity of exercise are associated with greater risk reduction, even modest exercise levels reduce the risk of Parkinson disease (11). Adopting a healthy diet that can promote an optimal gut microbiome is also prudent, since disruption of the gut microbiome is associated with Parkinson disease. Finally, when avoidance of environmental exposures is not possible or limited, there are natural compounds from foods or through supplementation that have demonstrated anti-oxidant, anti-inflammatory, and mitochondrial-protective mechanisms, which can be utilized in a mindful functional medicine and integrative medicine approach to health.

Too little research on prevention

Most medical research focuses on treating disease rather than preventing disease. This is not hard to understand when we realize that almost 60% of research funding in the U.S. comes from pharmaceutical companies, medical device companies, and biotechnology companies (2). Prevention only occupies 2% of research funding for Parkinson disease in the U.S. Even experts in the field, writing for the prestigious medical journal Lancet Neurology, recognize that “many stakeholders, from pharmaceutical companies to medical centres, might benefit financially from more individuals having a disease, especially if it is treatable.” (2)

In this context, the power of a functional medicine and integrative medicine approach to the prevention of Parkinson disease in real-world communities is even more valuable and much needed. The skillful integrative medicine doctor or functional medicine doctor will incorporate the latest scientific research evidence into individualized clinical care for people in the community.

As physician experts writing for the New England Journal of Medicine powerfully articulated, “Prevention of Parkinson’s disease remains an important focus of research. Attempts to address [various socioeconomic disparities]…, combined with a global effort to reduce exposure to environmental toxicants and improve lifestyle behaviors, will be needed.” (8)

References

1. Schiess N, Cataldi R, Okun MS, Fothergill-Misbah N, Dorsey ER, Bloem BR, et al. Six Action Steps to Address Global Disparities in Parkinson Disease: A World Health Organization Priority. JAMA Neurol. 2022;79(9):929-36.

2. Dorsey ER, De Miranda BR, Hussain S, Bloem BR, Elbaz A, Llibre-Guerra J, et al. Environmental toxicants and Parkinson's disease: recent evidence, risks, and prevention opportunities. Lancet Neurol. 2025;24(11):976-86.

3. Spillantini MG, Schmidt ML, Lee VM, Trojanowski JQ, Jakes R, Goedert M. Alpha-synuclein in Lewy bodies. Nature. 1997;388(6645):839-40.

4. Galvin JE, Lee VM, Trojanowski JQ. Synucleinopathies: clinical and pathological implications. Arch Neurol. 2001;58(2):186-90.

5. Calo L, Wegrzynowicz M, Santivanez-Perez J, Grazia Spillantini M. Synaptic failure and alpha-synuclein. Mov Disord. 2016;31(2):169-77.

6. Dehay B, Vila M, Bezard E, Brundin P, Kordower JH. Alpha-synuclein propagation: New insights from animal models. Mov Disord. 2016;31(2):161-8.

7. Alfaidi M, Barker RA, Kuan WL. An update on immune-based alpha-synuclein trials in Parkinson's disease. J Neurol. 2024;272(1):21.

8. Tanner CM, Ostrem JL. Parkinson's Disease. N Engl J Med. 2024;391(5):442-52.

9. Goldman SM, Weaver FM, Stroupe KT, Cao L, Gonzalez B, Colletta K, et al. Risk of Parkinson Disease Among Service Members at Marine Corps Base Camp Lejeune. JAMA Neurol. 2023;80(7):673-81.

10. Chen H, O'Reilly E, McCullough ML, Rodriguez C, Schwarzschild MA, Calle EE, et al. Consumption of dairy products and risk of Parkinson's disease. Am J Epidemiol. 2007;165(9):998-1006.

11. Ben-Shlomo Y, Darweesh S, Llibre-Guerra J, Marras C, San Luciano M, Tanner C. The epidemiology of Parkinson's disease. Lancet. 2024;403(10423):283-92.

12. Jiang Y, Zhang S, Chen Y, Wang H, He X, Bin C, et al. Physical activity and risk of Parkinson's disease: an updated systematic review and meta-analysis. J Neurol. 2024;271(12):7434-59.