Parkinson’s Rates Are Surging. Is Exposure to Poisons to Blame?

To Caroline “Carlie” Tanner, MD, PhD, a neurologist and epidemiologist specializing in movement disorders, it’s no surprise that Parkinson’s disease was first referenced in England in 1817, at the height of the Industrial Revolution when cities were cloaked in smoke and soot.

Today, smoke and soot have given way to more insidious, less visible toxicants. Research shows that exposure to toxicants destroys neurons, including those that produce dopamine, a neurotransmitter that facilitates smooth, balanced movement. Years later, patients developed Parkinson’s symptoms, including tremors that evolve into immobility, cognitive and mood changes, and difficulty swallowing.

Tanner’s groundbreaking population studies have quantified the risks of these toxicants and have highlighted the role of environmental triggers. Her research was instrumental in the Paraquat Prevention Act introduced in the U.S. House of Representatives in June 2026 and the phasing out or banning of other toxicants.

We asked Tanner about the upsurge.

How much have Parkinson’s cases increased in recent years and why?

From 1990 to 2021, global Parkinson’s disease cases have increased from approximately 3 million to nearly 12 million.

There’s no doubt that toxicants are contributing to the upswing. True, some portion of the increase can be explained by improved diagnostics and disease recognition. Also, people are living longer and reaching the age when they are most vulnerable to Parkinson’s disease — over 50, with peak diagnosis between 60 to 69.

It’s important to note that these are estimates. We don’t have a good system for reporting Parkinson’s disease in most countries and we lack long-term data.

What role do toxicants play in Parkinson’s?

Years ago, genetics and aging were believed to be the underlying causes of Parkinson’s disease. The impact of toxicants became clear in 1983 when a group of drug users rapidly developed Parkinson’s after injecting themselves with a synthetic heroin, biologically similar to paraquat, an herbicide, now proven to increase Parkinson’s disease risk. Today, Parkinson’s disease is believed to be the combined effects of toxicants, age, genetic makeup, and behaviors like diet and exercise.

Our 1989 study in China, when the country was rapidly developing, found that residents who lived in areas where they were exposed to toxicants like weedkillers, pesticides, and industrial solvents, had a higher rate of Parkinson’s than those in rural villages who grew wheat and raised pigs.

What role do genes play in Parkinson’s?

Our 1999 study of fraternal and identical twins, in which one or both of each pair had Parkinson’s disease, found that genes were not a risk factor in Parkinson’s disease occurring after age 50, but they matter more in early-onset Parkinson’s disease occurring before 50, about 4% to 10% of cases.

We also found in a 2012 study that about 20% of the population are born with a reduced ability to detoxify certain toxicants. This raises their risk by 1,000% if they are exposed to them.

Which toxicants have been closely linked to Parkinson’s?

Another 2012 study of twins, in which one was exposed to the solvent TCE, a metal degreaser, and the other was not, showed inflated Parkinson’s disease risk of 500% for the former. A more recent study showed that vets exposed to drinking water contaminated by TCE at Camp Lejeune, N.C., faced a 70% increased risk.

We also studied the effects of paraquat and the insecticide rotenone and found that farmers regularly exposed to each were 2.5 times more likely to develop Parkinson’s.

Nicotine is a toxicant, but smoking is said to be protective against Parkinson’s. How so?

In our 2002 twins study, in which one twin was a smoker and the other was not, we found that nonsmokers had a higher lifetime likelihood of developing Parkinson’s. The reasons are unknown, but I would never advise using tobacco to reduce Parkinson’s disease risk.

Are there other factors that influence Parkinson’s risk?

It’s known that traumatic brain injury (TBI) sets off a cascade of biological damage that targets neurons associated with Parkinson’s disease.  We found that it can increase risk by 44%. A diet high in saturated fats and excess fat contributes to Parkinson’s disease risk. Fat can trigger a chronic inflammatory response that can affect the brain, prompting immune cells to create an environment that damages the neurons associated with Parkinson’s disease.

There are no treatments to halt Parkinson’s progression. What’s one action that recently diagnosed patients can take to optimize their health?

Regular exercise. It helps preserve motor function and it may even prevent Parkinson’s. UCSF is involved in a phase 3, multisite trial in which patients with early Parkinson’s disease will undergo a moderate or high-intensity exercise regimen to see if this delays progression.