Parkinson’s disease is the world’s fastest-growing neurological disorder. More than 6 million people worldwide live with it, and that number is expected to double by 2040. For most of the past century, Parkinson’s was framed as a disease of aging or genetics. But an important shift is now underway in the research community. The majority of people developing Parkinson’s disease today have no identifiable genetic cause, which means something in their environment is driving the disease.1 A growing body of research published now points to environmental toxins and pathogens as primary contributors to Parkinson’s rise.2
How Parkinson’s Disease Develops: The Biological Cascade
Understanding why so many different environmental exposures can lead to the same disease requires understanding the biological sequence that drives Parkinson’s. The core feature of Parkinson’s disease is the progressive damage of dopamine-producing neurons in a brain region called the substantia nigra. Without sufficient dopamine, the brain cannot properly coordinate movement, producing the hallmark tremors, rigidity, and slowness that define the disease. The biological fingerprint of this process is the accumulation of a misfolded protein called alpha-synuclein into toxic clumps known as Lewy bodies within surviving neurons.
The pathway leading there involves mitochondrial dysfunction and oxidative stress, impaired clearance of cellular debris, neuroinflammation driven by activated immune cells in the brain, and ultimately, irreversible neuronal loss.3 What is remarkable and clinically significant is that many different toxins can initiate this same cascade at different entry points. This is why such a diverse group of environmental exposures converges on a single disease.
Mitochondrial Dysfunction in Parkinson’s Disease
If you want to understand why so many different toxins, infections, and environmental insults can all lead to the same disease, mitochondria are the answer. Mitochondria are the cell’s energy producers, generating ATP through a four-complex respiratory chain in the inner mitochondrial membrane. In Parkinson’s disease (PD), the most consistent finding is a deficiency in mitochondrial Complex I.4
When Complex I is impaired, the electron transport chain becomes inefficient, ATP production drops, and reactive oxygen species (ROS) are generated in excess. This oxidative stress creates a damaging feedback loop. ROS damage lipids, proteins, and mitochondrial DNA, further impairing mitochondrial function, which generates more ROS, which causes more damage. You can see how this is a cycle that perpetuates itself unless it is corrected.
This is clinically significant because mitochondria sit at the intersection of every pathway relevant to environmental Parkinson’s disease risk.
Environmental toxins such as rotenone and MPTP directly inhibit Complex I. Heavy metals, solvents, and mycotoxins disrupt mitochondrial membranes and generate oxidative stress. Infections trigger neuroinflammation, imposing additional metabolic demands on already-stressed mitochondria. When mitochondria fail, the cellular garbage-disposal systems responsible for clearing misfolded alpha-synuclein also fail. The result is an accelerating cycle of protein aggregation, energy depletion, and cell death that eventually becomes irreversible. This is why I think of treatments for mitochondrial repair as a foundational strategy for patients dealing with any of the chronic environmental exposures discussed in this article.
Pesticides: The Clearest Environmental Link
Pesticides are the environmental toxicants with the most well-established relationship to Parkinson’s disease. In 1983, a group of young adults in California developed sudden, severe Parkinsonism after injecting a synthetic heroin contaminated with MPTP, a compound that destroys dopaminergic neurons through inhibition of mitochondrial Complex I. That discovery prompted researchers to look at the herbicide paraquat, which shares a structural resemblance to MPTP and has since been linked to a 150 percent increased risk of Parkinson’s disease.5 Paraquat has been banned in over 70 countries, yet its use in the United States has more than doubled in recent years.
Rotenone, a commonly used insecticide, is another potent inhibitor of Complex I. A 2025 study found that even low-level rotenone exposure triggers lasting epigenetic changes in the substantia nigra that persisted in rat brains weeks after exposure ended, suggesting that a single period of toxin exposure can prime the brain for disease years or decades later.6 A 2024 meta-analysis also identified organophosphates among the highest-risk pesticides, with odds ratios for Parkinson’s disease exceeding 5.0 among exposed individuals.7
Industrial Solvents and Parkinson’s Disease
Industrial solvents are widely used in metal degreasing, dry cleaning, paint thinners, and adhesives, yet they have historically received less research attention than pesticides despite overlapping mechanisms of harm. A systematic review examined the full body of toxicological and epidemiological evidence on solvents and Parkinson’s disease.8 The review found that case reports of Parkinsonism have been associated with several solvents, with trichloroethylene (TCE) emerging as the strongest candidate.
Animal studies demonstrated that TCE has the potential to induce damage to the substantia nigra through the same pathways of oxidative stress, mitochondrial disruption, and impaired alpha-synuclein clearance seen with other neurotoxic exposures. TCE is the most common organic contaminant in U.S. groundwater, and exposure through drinking water, workplace contact, and off-gassing from contaminated soil affects millions of Americans.
Elevated Lead: A Lifelong Accumulating Risk
The role of lead in Parkinson’s disease is not about recent exposure. Lead is stored in tissues, especially bone, so the risk is the cumulative lifetime burden. Lead is known to disrupt dopaminergic function and induce oxidative stress, both of which are central mechanisms in Parkinson’s pathogenesis. The challenge with studying lead has always been measurement. Blood lead reflects only recent exposure, not accumulated exposure over decades.
A landmark case-control study from Harvard School of Public Health addressed this directly by measuring bone lead using an X-ray fluorescence technique that captures long-term biological accumulation. Among 330 Parkinson’s patients and 308 controls recruited from movement disorders clinics, those with the highest quartile of bone lead had over a three-fold increased odds of Parkinson’s disease compared to those in the lowest quartile.9
Lead was ubiquitous in gasoline, house paint, plumbing, and industrial emissions throughout most of the 20th century. Millions of Americans carry significant lead burdens from childhood and adulthood exposures that may be quietly increasing their neurological risk today.10
Mold, Mycotoxins, and Parkinson’s Disease
For those of us who work with patients suffering from mold-related illness, the connection between mycotoxin exposure and neurological disease is not surprising. Mycotoxins are toxic secondary metabolites produced by molds, and a growing body of evidence links them to neurological and neuropsychiatric symptoms, including movement difficulties, cognitive impairment, and disorders of balance and coordination.
A comprehensive review highlights that individuals with pre-existing immune dysregulation, including those with autoimmune disorders and chronic inflammatory conditions, are particularly vulnerable to mycotoxin-driven exacerbation of underlying pathophysiology. The combination of chronic inflammation from mold colonization and direct neurotoxin production is proposed as a mechanism of systemic neuronal damage, with a specific connection to Parkinson’s disease noted in the literature.11
The most detailed mycotoxin research in the context of Parkinson’s involves ochratoxin A (OTA), produced by Aspergillus and Penicillium molds. A 2025 systematic review analyzed 30 studies and mapped the findings against the Adverse Outcome Pathway for Parkinson’s disease. The evidence showed that OTA consistently causes mitochondrial dysfunction, increases alpha-synuclein half-life by 26%, and causes dopamine-producing neuron loss, alpha-synuclein aggregates, neuroinflammation, and Parkinsonian motor deficits across multiple animal models.12 The neurological effects were still detectable six months after OTA exposure had ended. OTA is thermally stable and has been measured in human blood and urine.
Parkinson’s Disease and Epstein-Barr Virus
EBV is a virus I write and think about frequently in the context of chronic illness, and its potential connection to Parkinson’s disease is something people with reactivated EBV should be aware of. One study measured serum antibody titers to six common pathogens — cytomegalovirus (CMV), Epstein-Barr virus (EBV), herpes simplex virus type-1 (HSV-1), Borrelia burgdorferi, Chlamydia pneumoniae, and Helicobacter pylori — in 131 PD patients and 141 controls. The study defined ‘infectious burden’ (IB) as a composite measure of serologic exposure to these pathogens. The findings were significant: blood results were positive for five or six of these pathogens in 35% of PD patients compared to only 15% of controls.13 Viral burden alone, bacterial burden alone, and combined infectious burden were each associated with Parkinson’s disease.
In another study, people with a higher infectious burden had significantly elevated serum alpha-synuclein levels and higher concentrations of the pro-inflammatory cytokines IL-1beta and IL-6.14 This directly links cumulative infection exposure to the two pathological features of Parkinson’s disease – alpha-synuclein accumulation and neuroinflammation. EBV is known to infect neurons directly, induce neuroinflammation, and generate antibodies that cross-react with alpha-synuclein via molecular mimicry.15
Up to 95 percent of the adult population has been exposed to EBV, and in many individuals it remains latent, but periods of reactivation driven by immune suppression, co-infections, or environmental toxin burden may be the trigger that tips the balance in vulnerable individuals toward neurodegeneration.
Lyme Disease: The Great Imitator and a Plausible Contributor
In my practice, I regularly see patients with both chronic Lyme disease and neurological symptoms, and I have seen cases where a Parkinson’s diagnosis was made before the discovery of Lyme disease. Lyme disease is caused by Borrelia burgdorferi, and it is well-established that it can generate chronic neuroinflammation, the same inflammatory environment that drives dopaminergic neurodegeneration in PD. Lyme disease has long been known as the ‘great imitator’ because it can mimic over 300 other conditions, including Parkinson’s disease, MS, and ALS.
The first autopsy-confirmed case of Lyme-associated Parkinson’s pathology was published in 2003, documenting striatonigral degeneration — a form of multiple system atrophy — in a patient with confirmed Borrelia infection in the blood and cerebrospinal fluid.16
Subsequent case reports have described reversible Parkinsonism due to Lyme basal ganglia lesions, with full resolution following Lyme treatment. The Lyme-Parkinson connection is clinically documented and likely has a similar mechanism of injury through oxidative damage.
COVID and Parkinson’s Disease
The relationship between SARS-CoV-2 and Parkinson’s disease is complex, bidirectional, and still unfolding, but the mechanistic evidence is compelling enough that it cannot be ignored. A detailed review frames this as a two-way relationship: COVID-19 may increase the risk of developing Parkinson’s disease, and conversely, pre-existing Parkinson’s disease significantly worsens COVID-19 outcomes.17 The review invokes the dual hit hypothesis, noting that both COVID and early Parkinson’s disease affect the same anatomical structures, the olfactory bulb and gastrointestinal tract, producing overlapping early symptoms including loss of smell and GI dysfunction. The SARS-CoV-2 virus enters through both these routes, potentially seeding or accelerating the same process.
At the cellular level, SARS-CoV-2 infection and its spike protein appear to directly activate the pathological cascade in Parkinson’s disease. Research demonstrated that the virus infects human dopaminergic neurons and significantly worsens neurodegeneration induced by alpha-synuclein fibrils.18 Mice infected via nasal delivery showed neuroinflammation persisting more than 60 days after the virus was no longer detectable in the brain. Alpha-synuclein itself plays a role in immune antiviral defense, and its upregulation during SARS-CoV-2 infection may be protective acutely, but sustained or repeated infections may lead to pathological misfolding over time. A 2023 retrospective study found an increased risk of developing Parkinson’s disease in the first year following COVID-19 infection.19 Given that Parkinson’s typically develops over decades, the full neurological toll of this pandemic may not be apparent for another 10 to 20 years.
The Common Thread: Cumulative Environmental Burden
What connects all of these exposures is a single biological cascade — mitochondrial damage, oxidative stress, alpha-synuclein accumulation, neuroinflammation, and dopaminergic neuron death. No single toxin causes Parkinson’s disease in isolation for most people. What we are looking at is a model of cumulative exposure, in which each insult adds to the total burden until a threshold is crossed. Genetic susceptibility adjusts where that threshold sits. But for most patients, the environmental load is what tips the balance.
Parkinson’s disease is increasingly understood as a largely preventable condition, driven by identifiable exposures that can be reduced, treated, and in some cases reversed before irreversible neuron loss occurs. In my practice, I think about this every time I work with a patient who has Lyme disease, Epstein-Barr virus, mold illness, or a history of significant environmental exposures. Successfully treating these exposures isn’t just about treating the immediate symptoms; it’s also about recognizing that we may be preventing something more significant in the future. For those who have developed Parkinson’s, there is hope when the underlying causes are discovered, successfully treated, and cellular damage is repaired.
