Amy Lindberg spent 26 years in the Navy and she still walked like it—with intention, like her chin had someplace to be. But around 2017, her right foot stopped following orders. Lindberg and her husband Brad were five years into their retirement. After moving 10 times for Uncle Sam, they’d bought their dream house near the North Carolina coast. They had a backyard that spilled out onto wetlands. From the kitchen, you could see cranes hunting. They kept bees and played pickleball and watched their children grow.
But now Lindberg’s right foot was out of rhythm. She worked hard to ignore it, but she couldn’t disregard the tremors. And she’d started to misplace words and thoughts, especially when she got excited. Was this normal? She was 57, fit and clean-living. Could the culprit be menopause?
The diagnosis took all of five minutes. Lindberg had Parkinson’s disease, the neurologist said, with all the classic symptoms. PD—as the scientists she would meet call it—is a neurological disorder, and a life sentence. Sufferers gradually lose control of their muscles, their bowels, their esophagus. Doctors told Lindberg that there was no way to know what had caused it.
The daughter of a sailor, Lindberg had built her life around the military. She was commissioned in the Navy out of college and became an officer at 23. Her first posting was to Marine Corps Base Camp Lejeune in North Carolina, a city-sized training hub that supports more than 60,000 sailors and marines. There were murmurs even then—whispers of weird cancers and stillbirths—but Lejeune was one of the prettier pieces of land in the Navy’s property portfolio. The bachelor officers’ quarters were on a grassy thumb of shoreline called Paradise Point, where the New River meets the Atlantic.
“Lejeune was just picturesque,” Lindberg says. “We had a river right there, and the beach wasn’t far away, and you worked half a mile from where you lived.” She loved her job at the hospital and made lifelong friends. She met her husband—a photo on her desk shows a blond Lindberg beaming beneath her Navy cap while Brad smiles broadly in his dress blues. “It was really nice,” she says. “You’d never suspect the water.”
Parkinson’s is the second most common neurological disease in the United States, after Alzheimer’s; each year 90,000 Americans are diagnosed. For decades, Parkinson’s research has focused on genetics, on finding the rogue letters in our genome that cause this incurable misery. Today, published research on the genetics behind Parkinson’s outnumbers all other potential causes six to one. This is partially because one of the disease’s most generous benefactors, Google cofounder Sergey Brin, can tie Parkinson’s to his genetics. Some Parkinson’s patients diagnosed before age 50—as Michael J. Fox was—can trace the disease to their genes; Brin, whose mother has the disease, carries a mutation of the LRRK2 gene, which significantly increases the likelihood of him developing PD. Over the years, Fox’s foundation has raised billions for Parkinson’s research, and Brin has personally committed $1.8 billion to fighting the disorder. All told, more than half of Parkinson’s research dollars in the past two decades have flowed toward genetics.
But Parkinson’s rates in the US have doubled in the past 30 years. And studies suggest they will climb another 15 to 35 percent in each coming decade. This is not how an inherited genetic disease is supposed to behave.
Despite the avalanche of funding, the latest research suggests that only 10 to 15 percent of Parkinson’s cases can be fully explained by genetics. The other three-quarters are, functionally, a mystery. “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. “So, we’re moving to a new question: What else could it be?”
“The health you enjoy or don’t enjoy today is a function of your environment in the past,” says Ray Dorsey, a physician and professor of neurology at the University of Rochester. Your “environment” could be the refinery a town over, the lead in the paint of your mother’s home, the plastic sheath of the Hot Pocket you microwaved in 1996. It is air pollution and PFAS and pesticides and so much more.
And this environment of yours—the sum of all your exposures, from conception to the grave—could be making you sicker than you realize. In a study of half a million Britons, Oxford researchers determined that lifestyle and the environment is 10 times more likely to explain early death than genetics. But that also offers a tantalizing prospect. If Parkinson’s is an environmental disease, as Dorsey and a small band of researchers emphatically believe, then maybe we can end it.
In 1982, two years before Lindberg was stationed at Camp Lejeune, a 42-year-old heroin addict named George Carillo was wheeled into the Santa Clara Valley Medical Center in San Jose, California. A few days earlier, Carillo had been perfectly able-bodied. Now he was mute and unable to move. Baffled, the neurologists on call came to an impossible diagnosis: The patient, over a long weekend, had developed Parkinson’s disease.
Carillo would probably have spent the rest of his short life in a psych ward had a pioneering young neurologist named Bill Langston not intervened. The way Parkinson’s takes over the body is distinct, Langston told me. The disease attacks the neurons in a region of the brain called the substantia nigra, a small dark structure that stands out amid the squirms of beige. The neurons here release dopamine, which sends signals to other neurons that help the body to move smoothly and effectively. In Parkinson’s these neurons die off; by the time a patient is diagnosed, they have often lost 60 to 80 percent of them. The process usually takes years, Langston says. But in the case of Carillo, all the neurons had disappeared almost overnight.
Over the summer of 1982, Langston found five more “frozen addicts” across the Bay Area. Through gumshoe detective work, he discovered they had all injected a batch of what they believed to be a designer drug called MPPP, cooked in a Morgan Hill basement. But the chemistry had gone awry. Instead of 1-methyl-4-phenyl-4-propionoxypiperidine, a potent opioid with morphine-like effects, the dime-bag chemist had accidentally made 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, or MPTP, a pharmacological slipup that would rewrite neurology textbooks.
When Langston and colleagues secured a batch of MPTP and tested it on primates, they knew they had uncorked a revolution. “Any neurologist could see these monkeys and immediately know that’s Parkinson’s,” Langston says—which was especially compelling, since monkeys do not get Parkinson’s in the wild. In a first, Langston showed that MPTP killed the dopamine-producing neurons in monkeys’ substantia nigra. The discovery made him the most famous Parkinson’s researcher in the country and, Langston wrote at the time, promised to “turn the entire field of Parkinson’s disease upside down.” Parkinson’s, it appeared, could be caused by a chemical.
Amy Lindberg settled quickly into life at Lejeune. She played tennis and ran on her lunch breaks, flitting through sprinklers in the turgid Carolina summers. But something dark was lurking beneath her feet.
Sometime before 1953, a massive plume of trichlorethylene, or TCE, had entered the groundwater beneath Camp Lejeune. TCE is a highly effective solvent—one of those midcentury wonder chemicals—that vaporizes quickly and dissolves whatever grease it touches. The spill’s source is debated, but grunts on base used TCE to maintain machinery, and the dry cleaner sprayed it on dress blues. It was ubiquitous at Lejeune and all over America.
And TCE appeared benign, too—you could rub it on your hands or huff its fumes and feel no immediate effects. It plays a longer game. For approximately 35 years, Marines and sailors who lived at Lejeune unknowingly breathed in vaporized TCE whenever they turned on their tap. The Navy, which oversees the Marine Corps, first denied the toxic plume’s existence, then refused to admit it could affect Marines’ health. But as Lejeune’s vets aged, cancers and unexplained illness began stalking them at staggering rates. Marines stationed on base had a 35 percent higher risk of developing kidney cancer, a 47 percent higher risk of Hodgkin’s lymphoma, a 68 percent higher risk of multiple myeloma. At the local cemetery, the section reserved for infants had to be expanded.
Meanwhile, Langston had spent the remainder of the 1980s setting up the California Parkinson’s Foundation (later renamed the Parkinson’s Institute), a lab and treatment facility equipped with everything needed to finally reveal the cause of the disease. “We thought we were going to solve it,” Langston told me. Researchers affiliated with the institute created the first animal model for Parkinson’s, identified a pesticide called Paraquat as a near chemical match to MPTP, and proved that farm workers who sprayed Paraquat developed Parkinson’s at exceedingly high rates. Then they showed that identical twins developed Parkinson’s at the same rate as fraternal twins—something that wouldn’t make sense if the disease were purely genetic, since identical twins share DNA and fraternal twins do not. They even noted TCE as a potential cause of the disease, Langston says. Each revelation, the team thought, represented another nail in the coffin of the genetic theory of Parkinson’s.
But there was a problem. The Human Genome Project had launched in 1990, promising to usher in a new era of personalized medicine. The project’s goal, to identify all of the genes in man, was radical, and by the time it was completed in 2000, frothy comparisons to the moon landing were frequent. Unraveling our genome would “revolutionize the diagnosis, prevention, and treatment of most, if not all, human diseases,” then president Bill Clinton said.
But for Langston and his colleagues, the Human Genome Project sucked the air out of the environmental health space. Genetics became the “800-pound gorilla,” as one scientist put it. “All the research dollars went toward genetics,” says Sam Goldman, who worked with Langston on the twin study. “It’s just a lot sexier than epidemiology. It’s the latest gadget, the bigger rocket.” A generation of young scientists were being trained to think of genetics and genomics as the default place to look for answers. “I characterize science as a bunch of 5-year-olds playing soccer,” says another researcher. “They all go where the ball is, running around the field in a herd.” And the ball was decidedly not environmental health. “Donors want a cure,” Langston says. “And they want it now.”
In 1997, researchers found a family in Italy that had passed along Parkinson’s disease for generations. Although the gene in question would later be shown to cause just a fraction of Parkinson’s cases, the damage was done. The Parkinson’s Institute faced stronger economic headwinds and difficulties with administration, and Langston eventually chose to shut it down. The environmental theory of Parkinson’s went back on the shelf.
No one knows exactly how much of the world’s drinking water is laced with TCE. The US Centers for Disease Control and Prevention reckons that the water supply of between 4 and 18 percent of Americans is contaminated, although not always at dangerous concentrations; the Environmental Working Group figures 17 million Americans drink the stuff. In Silicon Valley, where TCE was integral to the manufacturing of early transistors, a necklace of underground plumes have been identified along Highway 101 from Palo Alto to San Jose. Santa Clara County has more toxic Superfund sites, at 23, than any other county in the country. (Several tech giants have offices near or on top of these sites; in 2013, workers at a Google office were subjected to unhealthy levels of TCE for months after a ventilation system failed.)
And while TCE’s connection to cancer is well studied, what it does to our brain is more mysterious. That’s because good data on exposure is devilishly hard to come by. The US, with its fractious health care system, has few national databases, and chemical exposures are rarely tracked.
In 2017, Sam Goldman realized that Camp Lejeune offered the perfect opportunity to change this. Goldman—an epidemiologist and a doctor—has made a career out of teasing apart data: finding unusual case reports, looking for patterns, interviewing patients in the clinic about what chemicals they handled at old jobs and what exposures they faced in their childhood. In the case of Lejeune, Goldman could examine VA medical records to find Parkinson’s diagnoses and compare them to service records. But Goldman’s genius wasn’t finding this Lejeune cohort—it was realizing he had a control group, too.
Camp Pendleton, in Southern California, is the Marine Corps’ West Coast equivalent to Lejeune. Thousands of young, healthy Marines shuffle through its barbed-wired gates each year. But Pendleton has one thing Lejeune does not: uncontaminated drinking water.
When Goldman compared both populations, the results were shocking: Marines exposed to TCE at Lejeune were 70 percent more likely to have Parkinson’s than those stationed at Pendleton. And in a follow-up study last year, he showed that disease progression in Lejeune vets with the highest exposure to TCE was faster than those with low or no exposure, too. In the world of Parkinson’s research, Goldman’s study was a blockbuster.
But to really prove a link, you need more than just correlation. So, on the third floor of a drab university building in Birmingham, Alabama, Briana De Miranda has re-created Camp Lejeune in her lab, but for mice.
De Miranda is a toxicologist, not a neurologist, which is an unusual CV for a cutting-edge Parkinson’s researcher. When I visit her in October 2024, she shows me the plexiglass chamber where a few dozen mice doze in a pile. They’ve been spending their days in this chamber for months, inhaling a small amount of TCE almost every day. This experiment is the first to re-create the exposure someone like Lindberg experienced over years at Camp Lejeune.
De Miranda walks into a dark annex of her lab and asks a tech to pull up some imagery. “These are dopamine neurons in the brain,” De Miranda says, pointing to a scan of the control mice. In unexposed mice the substantia nigra looks like a nighttime satellite image of Manhattan—thousands of neurons sending dopamine across the mice’s brains to orchestrate fluid scurrying and sniffing and munching. Then the tech pulls up the brain scans of mice who have been exposed to TCE. Suddenly we’re in West Virginia. It’s not pitch black, but most of the lights are off and the ones that remain have been dimmed. The dopamine neurons have died, De Miranda explains. And she’s seeing the physical effects in the mice too. “We see minor motion defects; we see it in their gait, and we are seeing cognitive effects,” De Miranda says.
De Miranda’s studies, the first ever on inhaled TCE toxicity and Parkinson’s, are compelling, her colleagues agree, and well designed. And although there is more work to be done, the results wrap a bow on Goldman’s epidemiological work and the Parkinson’s Institute’s years of research. TCE is a neurotoxin, and generations of Americans have been exposed. In December 2024, the Environmental Protection Agency finally moved to ban TCE in the United States.
“I think TCE is the most important cause of Parkinson’s in the US,” says Ray Dorsey, the Parkinson’s expert at the University of Rochester. In 2021, Dorsey, who frequently collaborates with De Miranda, Goldman, and a core group of like-minded scientists, published Ending Parkinson’s Disease. The book’s central thesis: Parkinson’s is a growing pandemic, and up to 90 percent of cases are caused by chemicals in our environment. Cut exposures like TCE and pesticides, and we can “end Parkinson’s” as we know it. “The full effect of the Parkinson’s pandemic,” Dorsey writes, “is not inevitable but, to a large extent, preventable.”
Since the 1990s, the number of Americans with chronic disease has ballooned to more than 75 percent of adults, per the CDC. Autism, insulin resistance, and autoimmune diagnoses have reached epidemic proportions. The incidence of cancer in people under the age of 50 has hit an all-time high. If Parkinson’s disease is—as Ray Dorsey believes—a pandemic that’s being caused by our environment, it’s probably not the only one.
After a century of putting genetics on a pedestal, the geneticists have some surprising news for us: The vast majority of chronic disease isn’t caused by our genes. “The Human Genome Project was a $3 billion investment, and what did we find out?” says Thomas Hartung, a toxicologist at Johns Hopkins. “Five percent of all disease is purely genetic. Less than 40 percent of diseases even have a genetic component.”
Most of the conditions we worry about, instead, stem from a complex interaction between our genes and our environment. Genetics loads the gun, as former National Institutes of Health head Francis Collins put it, but the environment pulls the trigger. Rather than revealing the genetic origins of disease, genomics has done the opposite. Only 10 percent of breast cancer cases are purely genetic. Chronic obstructive pulmonary disease? Rheumatoid arthritis? Coronary heart disease? All hover around 20 percent. The primary driver of disease is considerably more terrestrial: It’s the environment, stupid.
Yet only 1 percent of the roughly 350,000 chemicals in use in the United States have ever been tested for safety. In its 55-year history, the EPA has banned or restricted about a dozen (by contrast, the EU has banned more than 2,000). Paraquat, the pesticide that appears to cause Parkinson’s in farmworkers, has been banned in Europe and China but remains available in the US. And in January, a month after the EPA’s ban on TCE was finalized, the Trump administration moved to undo it, even as new evidence emerged of Parkinson’s clusters in the rust belt, where exposure to trichloroethylene is high.
It’s easy to mock the MAHAs and the TikTok trad moms making their own food coloring, but the chemical regulatory system in America does not inspire confidence. No one really knows what the chemicals we’re interacting with every day are doing to our bodies.
That’s why, earlier this year, slices of brain from Briana De Miranda’s TCE-addled mice ended up with Gary Miller, a professor at Columbia University. Miller is the country’s leading proponent of a brand-new field called exposomics. Your “exposome” is the sum of your own personal environmental exposures, from the womb to the casket. Many exposures, like TCE, disappear from the bloodstream quickly; people who came into contact with a chemical in the past will never be able to prove it. The exposome is a way to potentially answer the question, “Just what the hell have I been exposed to?”
Miller began his career in the ’90s as a Parkinson’s researcher studying environmental exposures. But he grew tired of the “whack-a-mole approach” of modern toxicology: identifying one of the 350,000 chemicals on the market as a potential toxicant, looking for the exposure in the environment, looking for correlations, looking for toxicity in mice’s brains, rinse, repeat.
He wanted a shotgun approach, an answer to the way genome sequencing identifies all the genes in the body. What Miller wants is a Human Exposome Project. “We realized that this wasn’t just about Parkinson’s,” he says. “There were so many disease states we could look at.” Quantify our exposomes, Miller hopes, and we can know what ails us.
“We have the tools to put the big puzzle together,” says Rima Habre, an environmental health and exposomics expert at the University of Southern California. Through blood draws and metabolomic studies, the exposomics advocates want to measure the vast mixture of chemicals and pollutants in the body and figure out how they impact health. Take air pollution, Habre’s specialty. An ever-changing mélange of small molecules, from tailpipe emissions to tire bits to dust, it has been linked to obesity, endocrine disruption, heart attacks, and more. But if we can figure out what specifically in this toxic cloud is doing the damage, Habre says, we can work to quickly reduce it in our environment, the way we removed lead from gasoline.
Or autism. Autism diagnoses have exploded from 1 in 10,000 in the ’70s to 1 in 36 today, a rate that genetics and screening can’t explain, says Johns Hopkins’ Thomas Hartung. Hartung, another Human Exposome Project proponent, is growing clusters of neurons in the lab and subjecting them to flame-retardant chemicals—which are applied to couches and car seats across America—to see what happens. Already, the associations trouble him. The goal of all this, Hartung says, is a world where toxicologists like Briana De Miranda don’t have to spend money creating a mouse gas chamber, expose mice for three months, then wait several more months for results.
Miller’s goal with mice brains is to figure out what exactly about TCE is killing dopamine-producing neurons and leading to Parkinson’s—to unravel and define the interaction between our environment and our genetics in a way never before possible.
The parallels to the Human Genome Project—in both promise and froth—are clear. But there is a sense of empowerment in knowing that our health is not predetermined. Nearly every scientist interviewed for this story does a few simple things. They filter their water, they run an air purifier, they don’t microwave plastic. They don’t freak out about their daily exposures, but they do things like opt for fragrance-free products, avoid eating out of plastic when they can, and buy organic produce. Our exposures, while not always in our control, can be limited.
About two hours south of Lejeune in Wilmington, North Carolina, Amy Lindberg is having lunch with her husband, Brad, on a pier overlooking the Atlantic. Although Goldman, De Miranda, and Dorsey have unveiled the likely origins of her Parkinson’s, the random nature of it gnaws at her. “When I was diagnosed, it was just like, where’s everyone else?” Lindberg says. “I felt like, if I have it, what about my coworkers?” She nods to Brad, who also spent years drinking Lejeune’s water. “He suffered no ill consequences,” she says. She worries about her kids, one of whom was born on base.
She still exercises constantly, playing pickleball, boxing, and hopping on the elliptical. She’s found that movement, especially high-intensity exercise, reduces her symptoms. A recent Yale study confirmed as much, showing that interval training increases dopaminergic signals in the brains of Parkinson’s patients, suggesting that exercise slows disease progression and even improves neuron function. The environment may have caused Lindberg’s disease, but she can use it to fight back too.
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