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Pesticides Linked to Parkinson’s Disease

Study after study finds all sorts of negative health effects from exposure to pesticides, including cancers, endocrine (hormone) disruption, and neurological effects.  Pesticide exposures can occur in the home, at work or school, in the air (drift), and in food and water. A recent study found that higher chronic pesticide exposure, such as occupational exposure (e.g. farm worker), is linked to developing Parkinson's disease.

University of California San Francisco (UCSF) researchers found the higher rates of Parkinson's disease both in people who have genetic susceptibility to developing the disease, and also in those who don't have a genetic susceptibility. Meaning everyone is at risk for developing Parkinson's disease with enough chronic exposure.

Studies find that chronic exposure to some pesticides has a higher risk for Parkinson's disease than others, and especially strong links are with the pesticides 2,4-D, chlorpyrifos, paraquat, glyphosate, and rotenone. Some countries, including in Europe and Canada, ban the use of some of these chemicals due to concerns about links to Parkinson’s, but the U.S. only restricts the use of some of them (e.g. paraquat).

Many pesticides are neurotoxins. Dr. Ray Dorsey (publisher of book: Ending Parkinson's Disease: A Prescription for Action ) said studies show a dose-response effect between chronic pesticide exposure and Parkinson's disease: "an almost perfect correlation between the amount of pesticides used in certain communities and the rates of PD. He points out that Parkinson's disease is the world's fastest growing brain disease with a lifetime risk of about 1 in 15. (That's high!)

Bottom line: Try to minimize your exposure to pesticides. Organic farms don't use the pesticides implicated in neurological harm - because organic standards don't allow it. Also, use organic or least-toxic Integrated Pest Management (IPM) for pest control in your home. Avoid using pesticides in your yard, especially the lawn. Stay away from recently pesticide treated areas. Eat organic foods as much as possible.

In the following article: sporadic Parkinson's disease means it happened spontaneously, which is different from someone having a genetic risk factor. From Beyond Pesticides: Pesticide Exposure Increases the Risk of Developing Gene-Specific and Sporadic Parkinson’s Disease Incidences

Research at the University of California San Francisco (UCSF) finds that pesticide exposure increases the risk of developing Parkinson’s disease (PD), regardless of whether disease onset is idiopathic (spontaneous) or genetic (GBA genetic risk variant). Although the exact etiology [cause] of PD remains unknown, epidemiological and toxicological research repeatedly identifies exposure to pesticides, as well as specific gene-pesticide interactions, as significant adverse risk factors that contribute to PD. Furthermore, this study, “Gene Variants May Affect PD Risk After Pesticide Exposure,” suggests that environmental triggers like occupational exposure to pesticides can prompt PD in individuals with or without the genetic precursor

This research demonstrates the importance of assessing disease etiology concerning occupational pesticide exposure, especially if disease triggers are overwhelmingly non-hereditary. Since not all individuals genetically predisposed to the disease develop PD, with only 10 to 15 percent of PD cases being genetic, government officials need to consider alternate etiological pathways that include environmental risk factors. Study researchers note, “‘Environmental exposures may have differential effects in different genotypes’ and may predispose people with PD to different symptom burden.”

Parkinson’s disease is the second most common neurodegenerative disease, with at least one million Americans living with PD and about 50,000 new diagnoses each year. The disease affects 50% more men than women and people with PD have a variety of symptoms, including loss of muscle control and trembling, anxiety and depression, constipation and urinary difficulties, dementia, and sleep disturbances. Over time, symptoms intensify, but there is no current cure for this fatal disease. While only a small percentage of PD incidences are genetic and PD is quickly becoming “the world’s fastest-growing brain disease,” research like this is vital for examining other potential risk factors for developing Parkinson’s disease.

Parkinson’s Disease occurs when there is damage to the dopaminergic nerve cells (i.e., those activated by or sensitive to dopamine) in the brain responsible for dopamine production, one of the primary neurotransmitters mediating motor function. Although the cause of dopaminergic cell damage remains unknown, evidence suggests that pesticide exposure, especially chronic exposure, may be the culprit. Pesticide use is ubiquitous, especially in the rural U.S., where pesticide exposure is nearly unavoidable due to drift and runoff. Moreover, occupational exposure poses a unique risk, as pesticide exposure is direct via handling and application.

2017 study finds that occupational use of pesticides (i.e., fungicides, herbicides, or insecticides) increases the risk for PD by 110 to 211 percent. Carbamate pesticides increase PD risk by 455 percent, with pesticide use for ten years or more doubling PD risk. Even more concerning is that some personal protection equipment (PPE) may not adequately protect workers from chemical exposure during application.

Nonoccupational (residential) pesticide exposure, such as proximity to pesticide-treated areas, presents a risk for PD development. A Louisiana State University study finds that residents living adjacent to a pesticide-treated pasture and forest from the agriculture and timber industry, respectively, have higher rates of PD incidence. Furthermore, pesticide residue in waterways and on produce present an alternate route for residential pesticide exposure to increase the risk for PD via ingestion.

Pesticide contamination in waterways is historically commonplace and widespread in U.S. rivers and streams, with over almost 90 percent of water samples containing at least five or more different pesticides. These pesticides further contaminate groundwater and drinking water sources. Similarly, the U.S. Department of Agriculture (USDA) finds detectable levels of pesticide residue on 57.5 percent of product samples in the Pesticide Data Program(PDP) analysis. Although the residue levels are within the U.S. Environmental Protection Agency’s tolerances, the assertion that any level of pesticide within EPA tolerances in the U.S. food supply does not pose safety concerns has been challenged by numerous independent scientific studies.

Pesticide exposure can cause severe health problems even at low residue levels, including endocrine disruptioncancersreproductive dysfunctionrespiratory problems (e.g., asthma, bronchitis), neurological impacts (e.g., developmental effects and Parkinson’s), among others. Nevertheless, both direct occupational and indirect nonoccupational exposure to pesticides can increase the risk of PD.

Several studies identify various pesticides as involved in the pathology of PD, including the insecticides rotenone and chlorpyrifos, and herbicides 2,4-Dglyphosate, and paraquat. A Washington State University study determined that residents living near areas treated with glyphosate—the most widely used herbicides in the U.S.—are one-third more likely to die prematurely from Parkinson’s disease.

In the Louisiana State University study, exposure to 2,4-D, chlorpyrifos, and paraquat from pasture land, forestry, or woodland operations, as prominent risk factors for PD, with the highest risk in areas where chemicals quickly percolate into drinking water sources. Overall, research finds exposure to pesticides increases the risk of developing PD from 33 percent to 80 percent, with some pesticides prompting a higher risk than others.

One of the most notorious pesticides associated with PD development are rotenone and paraquat, as PD pathology indicates the involvement of these two chemicals. Scientific literature comprehensively documents the neurotoxicant properties of paraquat and rotenone as laboratory experiments reproduce features of Parkinson’s in the brain of animals. Another study finds a 2.5-fold increase in PD risk among users of each chemical in comparison to non-users. Acute and chronic exposure to rotenone can inhibit the mitochondrial brain function responsible for cell regeneration and induce oxidative stress. Paraquat exposure can increase the production of specific proteins in the brain that damage cells producing dopamine, causing motor problems and muscle tremors.

Although many countries, including Europe and Canada, ban the use of both chemicals due to concerns about links to Parkinson’s, the U.S. merely restricts use. In the U.S., although EPA permits the use of rotenone to kill invasive fish species, the agency only restricts paraquat application to certified applicators, allowing chemical-use to rise over the decade, with 2018 seeing a 100 percent increase in paraquat use in wildlife refuges.

Parkinson’s disease has a multitude of epidemiologic research demonstrating several risk factors, including specific genetic mutations and external/environmental triggers (i.e., pesticide use, pollutant exposure, etc.). This research adds to the many that associate pesticide exposure with PD. Furthermore, this study demonstrates that PD can develop regardless of whether an individual is a carrier of GBA gene mutation or not.

This study is not the first to demonstrate a relationship between pesticide exposure and gene variation as a 2010 study finds individuals with specific gene variants (i.e., GBA mutation) are three and a half times more likely to develop Parkinson’s than those with the more common version of the gene. Furthermore, a 2013 study reveals that individuals with a PD-associated genetic mutation are more likely to develop the neurodegenerative disease upon exposure to pesticides. 

Excerpts from Medscape: Gene Variants May Affect PD Risk After Pesticide Exposure

The likelihood of developing Parkinson's disease (PD) is associated with prior exposure to occupational pesticides, both with regard to sporadic cases of PD and among patients who have a GBA genetic risk variant for PD, a new study suggests. This association was not as strong for the LRRK2 risk variant for PD. Pesticide exposure was also associated with cognitive decline, especially for carriers of the GBA variant, the researchers noted.

Ray Dorsey, MD, professor of neurology at the University of Rochester, in Rochester, New York, commented to Medscape Medical News that Caroline Tanner, MD, PhD, and Samuel Goldman, MD, MPH, leaders of the UCSF group, have been prominent in defining the role of pesticides in the development of PD.

"Many pesticides are neurotoxins, many are fat soluble, many target the same parts of cells, mitochondria, that we know are damaged in Parkinson's disease, and many laboratory animals when exposed to these develop the behavioral and pathological hallmarks of Parkinson's disease," Dorsey summarized.

For environmental risk factors, one generally looks to find a dose-response relationship. In the present study, "the fact that individuals who presumably had higher doses were more likely to develop disease actually supports the finding," he said. Furthermore, "we know there are genetic-environmental interactions, and this study provides some additional information regarding those interactions."

Dorsey is a coauthor of the recently published book Ending Parkinson's Disease: A Prescription for Action (from which all proceeds go to efforts to end PD). The book makes the case that environmental factors are of major importance in the development of PD, "the world's fastest growing brain disease." The lifetime risk is about 1 in 15; by comparison, the risk of dying in a car accident is about 1 in 100, he said.

Besides Tanner and Goldman, he said Alexis Elbaz, MD, PhD, at INSERM in Paris, France, and others have shown an almost perfect correlation between the amount of pesticides used in certain communities and the rates of PD.

Many of these substances have been banned in other countries, but use of some of these is increasing in the United States. Dorsey suggests developing safer alternatives as well as using organic growing methods when appropriate.

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