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The Environmental Root of Parkinson’s: How a Decades-Long Genetic Obsession Hid a Toxic Truth

After 26 years of service in the U.S. Navy, Amy Lindberg still carried herself like a service member—every step intentional, her chin held high with clear purpose. But around 2017, her right foot began to defy that lifelong discipline.

By that point, Lindberg and her husband Brad had been retired for five years. Following 10 cross-country moves for military assignments, they’d settled into their dream home along the North Carolina coast. Their backyard opened onto sprawling wetlands; from the kitchen window, they could watch cranes wade and hunt. They kept beehives, played pickleball, and watched their children build lives of their own.

But that year, Lindberg’s right foot fell out of step. She tried hard to brush off the odd stiffness, but persistent tremors were impossible to ignore. She also started fumbling for words and losing her train of thought, especially when she got excited. At 57, she was active, healthy, and lived a clean lifestyle—was this just normal aging? Could it be menopause?

It took just five minutes for a neurologist to deliver the answer: Lindberg had Parkinson’s disease, and she presented every classic symptom. Parkinson’s, or PD as researchers call it, is a progressive neurological disorder with no cure. Over time, patients slowly lose control of their muscles, digestive function, and ability to swallow safely. Doctors told Lindberg they had no way to know what triggered her case.

Born to a sailor, Lindberg built her entire career around the military. She was commissioned right out of college and earned her officer rank at 23. Her first posting was Marine Corps Base Camp Lejeune in North Carolina, a massive training facility the size of a small city that supports more than 60,000 sailors and Marines. Even back then, quiet rumors swirled around the base: unexplained cancers, higher rates of stillbirth. But Lejeune was also one of the most scenic posts in the military portfolio. Bachelor officer quarters sat on a grassy, jutting stretch of shoreline called Paradise Point, where the New River flows into the Atlantic.

“Lejeune was just beautiful,” Lindberg recalls. “We had the river right there, the beach wasn’t far, and I worked just half a mile from where I lived.” She loved her work at the base hospital, made friends she still has today, and met her husband—a photo on her desk shows a young blonde Lindberg grinning under her Navy cap, Brad beaming beside him in his dress blues. “It was such a nice time,” she says. “You’d never have guessed anything was wrong with the water.”


Parkinson’s is the second most common neurodegenerative disease in the U.S., after Alzheimer’s, with 90,000 new diagnoses every year. For decades, the bulk of Parkinson’s research has fixated on genetics, hunting for the rogue gene sequences that cause this incurable condition. Today, published studies on the genetic origins of Parkinson’s outnumber research into all other potential causes by six to one.

That bias is partially driven by funding: one of the disease’s biggest donors, Google co-founder Sergey Brin, has a known genetic link to Parkinson’s. Brin carries a mutation in the LRRK2 gene, which drastically raises his risk of developing PD, and his mother lives with the disease. Michael J. Fox, who was diagnosed before age 50, also has a genetic form of the condition. Fox’s foundation has raised billions for PD research, and Brin has personally committed $1.8 billion to the fight. All in all, more than half of all Parkinson’s research funding over the past 20 years has gone to genetic studies.

But PD rates in the U.S. have doubled in the last 30 years, and studies project they will rise another 15 to 35 percent each coming decade. That pattern does not fit a purely inherited genetic disease.

Even with all that genetic research funding, recent studies show only 10 to 15 percent of Parkinson’s cases can be fully explained by genetics. That leaves roughly 75 percent of cases functionally unexplained. “More than two-thirds of people with PD don’t have any clear genetic link,” says Briana De Miranda, a researcher at the University of Alabama at Birmingham. “That’s led us to a new question: What else is causing this?”

“The health you have today, for better or worse, is shaped by the environments you’ve been in in the past,” says Ray Dorsey, a neurologist and professor at the University of Rochester. That “environment” can be anything: a nearby oil refinery, lead in the paint of your childhood home, the plastic packaging of a microwave meal you ate in the 1990s. It includes air pollution, PFAS, pesticides, and hundreds of other untested compounds.

The sum of all these exposures, from conception until death, may be making you far sicker than you realize. A study of half a million people in the U.K. led by Oxford University researchers found that lifestyle and environmental factors are 10 times more likely to cause early death than genetics. That finding also opens up a hopeful possibility: if Parkinson’s is primarily an environmentally caused disease, as Dorsey and a small group of researchers argue, then we may be able to eliminate it entirely.


Back in 1982, two years before Lindberg was stationed at Camp Lejeune, a 42-year-old heroin addict named George Carillo was admitted to Santa Clara Valley Medical Center in San Jose, California. Just a few days earlier, Carillo had been fully able-bodied. Now he was unable to speak or move. Stumped doctors arrived at an almost unthinkable diagnosis: Carillo had developed full-blown Parkinson’s disease in the span of a long weekend.

Carillo would likely have spent the rest of his short life in a psychiatric ward if a pioneering young neurologist named Bill Langston hadn’t stepped in. Langston explained that Parkinson’s progression follows a very specific pattern. The disease attacks dopamine-producing neurons in a small, dark region of the brain called the substantia nigra. Dopamine sends signals that coordinate smooth, controlled movement. In Parkinson’s patients, these neurons die off; by the time someone is diagnosed, they have already lost 60 to 80 percent of their dopamine-producing cells in this region. This process usually takes years, Langston says. But in Carillo’s case, nearly all of those neurons died overnight.

By the end of that summer, Langston had identified five more similarly “frozen” addicts across the San Francisco Bay Area. Through old-fashioned detective work, he found all of them had injected a batch of what they thought was a synthetic opioid called MPPP, cooked in a homemade lab in Morgan Hill. But the chemist’s reaction went wrong. Instead of making the intended opioid, he accidentally created 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, better known as MPTP—a mistake that would upend everything the field thought it knew about Parkinson’s.

When Langston and his team tested MPTP on primates, they immediately knew they had made a revolutionary discovery. “Any neurologist looking at those monkeys would instantly recognize they had Parkinson’s,” Langston says. That was particularly remarkable, because monkeys don’t develop Parkinson’s naturally in the wild. For the first time, Langston proved MPTP kills the dopamine-producing neurons in the substantia nigra, just like Parkinson’s does. The discovery made him one of the most famous Parkinson’s researchers in the country, and Langston wrote at the time that it promised to “turn the entire field of Parkinson’s disease upside down.” It proved, for the first time, that Parkinson’s could be caused by an external chemical.


Lindberg settled into life at Camp Lejeune easily. She played tennis and ran during her lunch breaks, cooling off under sprinklers in the thick, humid North Carolina summers. But a toxic secret was already lurking in the groundwater under her feet.

Sometime before 1953, a large plume of trichlorethylene, or TCE, seeped into the base’s aquifer. TCE was a midcentury “wonder chemical”: a super effective solvent that vaporizes quickly and cuts through any grease. The exact source of the Lejeune spill is still debated, but base personnel used TCE to maintain machinery, and the base dry cleaner used it to clean dress uniforms. The chemical was everywhere at Lejeune, and across the United States.

At the time, TCE was thought to be harmless: you could rub it on your hands or breathe its fumes and feel no immediate effects. But it causes damage slowly over time. For roughly 35 years, Marines and sailors living at Lejeune unknowingly breathed in vaporized TCE every time they turned on a tap. The Navy, which oversees the Marine Corps, first denied the toxic plume even existed, then refused to acknowledge it could harm service members’ health. But as Lejeune’s veterans aged, unexplained cancers and chronic illnesses began to appear at staggeringly high rates. Marines stationed on base had a 35 percent higher risk of kidney cancer, 47 percent higher risk of Hodgkin’s lymphoma, and 68 percent higher risk of multiple myeloma. The local cemetery even had to expand the section reserved for infant burials.

For the rest of the 1980s, Langston worked to build the California Parkinson’s Foundation (later renamed the Parkinson’s Institute), a lab and treatment center designed to finally uncover the root cause of PD. “We thought we were going to solve it,” Langston told me. Researchers affiliated with the institute created the first animal model of Parkinson’s, identified the common pesticide Paraquat as having a near-identical chemical structure to MPTP, and proved that farm workers who sprayed Paraquat developed PD at extremely high rates. Then they showed that identical twins develop Parkinson’s at the same rate as fraternal twins—a finding that makes no sense if the disease is purely genetic, since identical twins share all their DNA while fraternal twins do not. Langston says they even flagged TCE as a potential cause of PD. The team thought each new finding was another step toward disproving the dominant genetic theory of PD.

But then the Human Genome Project launched in 1990, promising a new era of personalized medicine. The project’s goal—mapping every human gene—was seen as revolutionary, and by the time it was completed in 2000, it was widely compared to the moon landing. Unlocking the human genome would “revolutionize the diagnosis, prevention, and treatment of most, if not all, human diseases,” then-President Bill Clinton said at the time.

But for Langston and his colleagues, the Human Genome Project crowded out funding for environmental health research. Genetics became the “800-pound gorilla” in the field, as one researcher put it. “All the research money went to genetics,” says Sam Goldman, who worked with Langston on the twin study. “It’s just seen as sexier than epidemiology. It’s the new gadget, the bigger rocket.” A generation of young scientists were trained to look to genetics first for answers. “I compare science to a group of 5-year-olds playing soccer,” another researcher told me. “They all run after the ball as a herd, no matter where it goes.” And at that point, the ball was definitely not environmental health. “Donors want a cure,” Langston says. “And they want it now.”

In 1997, researchers identified a multi-generational Italian family that passed Parkinson’s down through generations. While that specific gene was later found to cause only a tiny fraction of all PD cases, the hype around the discovery cemented genetics’ hold on funding. The Parkinson’s Institute faced growing financial pressure and administrative challenges, and Langston eventually chose to close it. The environmental theory of Parkinson’s was put back on the shelf for decades.


No one knows exactly how much of the world’s drinking water is contaminated with TCE. The U.S. Centers for Disease Control and Prevention estimates that between 4 and 18 percent of Americans get their drinking water from contaminated sources, though not always at dangerous levels. The Environmental Working Group puts that number at 17 million Americans.

In Silicon Valley, where TCE was critical to manufacturing early semiconductors, a chain of underground toxic plumes has been found along Highway 101 from Palo Alto to San Jose. Santa Clara County has 23 toxic Superfund sites, more than any other county in the U.S. Several major tech companies have offices near or on top of these sites; in 2013, workers at a Google office were exposed to unsafe levels of TCE for months after a ventilation system failed.

While TCE’s link to cancer is well documented, its impact on the brain has remained far less studied. Good data on long-term low-level exposure is notoriously hard to collect. The fragmented U.S. healthcare system has few national databases tracking chemical exposures, so researchers have little large-scale data to work with.

In 2017, Sam Goldman realized Camp Lejeune offered the perfect opportunity to fill that gap. Goldman, an epidemiologist and physician, has spent his career untangling data: digging up unusual case reports, looking for patterns, and asking patients in clinic about what chemicals they handled at old jobs and what exposures they faced as children.

For Lejeune, he could access VA medical records to count Parkinson’s diagnoses, then cross-reference them with service records to confirm how long each veteran had been stationed on base. What made the study unique was that Goldman had a perfect control group.

Camp Pendleton, the Marine Corps’ large West Coast base, is the equivalent of Lejeune—thousands of young, healthy Marines pass through its gates every year. But Camp Pendleton has one key difference from Lejeune: its drinking water was never contaminated with TCE.

When Goldman compared the two populations, the results were staggering: Marines exposed to TCE at Camp Lejeune were 70 percent more likely to develop Parkinson’s than Marines stationed at Camp Pendleton. In a follow-up study published last year, he also found that PD progressed faster in Lejeune veterans with the highest TCE exposure, compared to those with low or no exposure. Goldman’s study was a blockbuster in the Parkinson’s research world.


But correlation isn’t causation. To prove TCE actually causes Parkinson’s, researchers needed lab evidence. That’s what Briana De Miranda is working on, on the third floor of a nondescript university building in Birmingham, Alabama. She has essentially recreated Camp Lejeune’s TCE exposure in her lab, using mice.

De Miranda is a toxicologist, not a neurologist—an unusual background for a leading Parkinson’s researcher. When I visited her lab in October 2024, she showed me a plexiglass chamber where dozens of mice rest. For months, the mice have breathed small amounts of TCE nearly every day, replicating the years of low-level exposure people like Lindberg experienced at Camp Lejeune. It’s the first experiment of its kind.

De Miranda walked into a dark back room of her lab and asked a technician to pull up brain scan images. “These are the dopamine neurons in the substantia nigra,” she said, pointing to a scan from the control group of unexposed mice. In healthy mice, the region looks like a nighttime satellite image of Manhattan: thousands of bright neurons sending dopamine across the brain to coordinate smooth movement, feeding, and exploration. Then the technician pulled up scans from TCE-exposed mice. Suddenly the image looked like a rural night in Appalachia: most of the lights were out, and the remaining ones were dimmed. The dopamine neurons had died, De Miranda explained. Her team has also seen physical and cognitive effects in the exposed mice. “We see minor movement defects, changes in their gait, and measurable cognitive impacts,” she says.

De Miranda’s study, the first ever to look at inhaled TCE toxicity and Parkinson’s, is widely regarded as well-designed and compelling by her colleagues. While more work remains, the results confirm Goldman’s epidemiological findings and decades of research from the old Parkinson’s Institute. TCE is a neurotoxin, and generations of Americans have been exposed to it. In December 2024, the U.S. Environmental Protection Agency finally moved to ban TCE nationwide.

“I think TCE is the most important cause of Parkinson’s in the U.S.,” says Ray Dorsey, the University of Rochester Parkinson’s expert who collaborates regularly with De Miranda, Goldman, and their core group of researchers. In 2021, Dorsey published Ending Parkinson’s Disease, which argues that PD is a growing pandemic, and up to 90 percent of cases are caused by environmental chemicals. If we cut exposures to toxic chemicals like TCE and Paraquat, we can “end Parkinson’s” as we know it. “The full impact of the Parkinson’s pandemic,” Dorsey writes, “is not inevitable but, to a large extent, preventable.”


Since the 1990s, the CDC reports that more than 75 percent of U.S. adults now live with at least one chronic disease. Diagnoses of autism, insulin resistance, and autoimmune disease have reached epidemic levels. Cancer rates for people under 50 are at an all-time high. If Parkinson’s is an environmentally caused pandemic, as Dorsey believes, it’s almost certainly not the only one.

After a century of centering genetics as the root of most disease, even genetic researchers are now acknowledging that the vast majority of chronic illness isn’t written into our DNA. “The Human Genome Project was a $3 billion investment, and what did we find out?” says Thomas Hartung, a toxicologist at Johns Hopkins University. “Five percent of all disease is purely genetic. Less than 40 percent of diseases even have a genetic component.”

Most common conditions, instead, stem from a complex interaction between our genes and our environment. As former National Institutes of Health director Francis Collins once put it: genetics loads the gun, but the environment pulls the trigger. Far from proving most disease is genetic, the Human Genome Project actually proved the opposite. Only 10 percent of breast cancer cases are purely genetic. Chronic obstructive pulmonary disease? Rheumatoid arthritis? Coronary heart disease? All have purely genetic causes in only around 20 percent of cases. The primary driver of most disease is far more mundane: it’s the environment, stupid.

Yet only 1 percent of the roughly 350,000 chemicals in commercial use in the U.S. have ever been fully tested for human safety. In its 55-year history, the EPA has banned or restricted only about a dozen toxic chemicals. By comparison, the European Union has banned more than 2,000. Paraquat, the pesticide linked to Parkinson’s in farm workers, is banned in Europe and China but still legal to use in the U.S. And in January 2025, just a month after the EPA’s TCE ban was finalized, the second Trump administration moved to reverse the ban—even as new research confirms clusters of Parkinson

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