16
Dec
Pesticides and Parkinson’s Disease: The Toxic Effects of Pesticides on the Brain
(Beyond Pesticides, December 16, 2021) A study by Shanghai Jiao Tong University, China, finds Parkinson’s Disease (PD) risk increases with elevated levels of organochlorine (OCP) and organophosphate (OP) pesticides in blood. Among patients with PD, specific organochlorine compounds have greater associations with cognitive impairments, including depression and brain function. Research finds exposure to chemical toxicants, like pesticides, can cause neurotoxic effects or exacerbate preexisting chemical damage to the nervous system. Although the mechanism by which pesticides induce disease development remains unclear, researchers suggest changes in protein enzyme composition and cellular dysfunction from pesticide exposure interrupt normal brain function.
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 individuals 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 10 to 15 percent of PD incidences are genetic, PD is quickly becoming the world’s fastest-growing brain disease. Therefore, research like this highlights the need to examine alternate risk factors for disease development, especially if disease triggers are overwhelmingly non-hereditary. The researcher notes, “Based on these findings, more stringent environmental regulations may need to be implemented to reduce PD risk in the population, especially in agricultural areas where communities may be exposed to unsafe pesticide levels.”
The study evaluates 90 patients with idiopathic or spontaneous (non-genetic) PD and their spouses, as well as 90 healthy control individuals. The patients included in the study adhere to specific criteria: “diagnosed as idiopathic [spontaneous] PD according to 2015 MDS clinical diagnostic criteria for PD; no family history of PD; no history of other significant neurological disorders (i.e., stroke, epilepsy, head trauma); and no familial history of behavioral abnormality.” Most PD patients are male, which is consistent with the PD diagnoses ratio among the general population. Researchers collected blood samples from PD patients and the control group after an overnight fasting period. Using gas chromatography/mass spectrometry (GC-MS), researchers analyze samples of 19 commonly used pesticides in the Shanghai, China region, including 16 OCP (α-hexachlorocyclohexane [HCH], β-HCH, γ-HCH, δ-HCH, propanil, vinclozolin, heptachlor, aldrin, dieldrin, endosulfan, hexachlorobenzene, quintozene, p,p’-DDE, p,p’-dichlorodiphenyldichloroethane [DDD], o,p’-dichlorodiphenyltrichloroethane [DDT], p,p’-DDT), and three OP (parathion-methyl, methidathion, and phosalone) pesticide compounds.
Concentrations of organochlorine pesticides (α-HCH, β-HCH, γ-HCH, δ-HCH, propanil, heptachlor, dieldrin, hexachlorobenzene, p,p’-DDT and o,p’-DDT) are higher among patients with PD compared to healthy patients. Of the organochlorines, α-HCH and propanil concentrations have the greatest association with PD risk through increasing reactive oxygen species (ROS) levels and decreasing mitochondrial membrane function in SH-SY5Y cells. However, only propanil induced accumulation of α-synuclein, a predominant protein in the brain tissue of PD patients. Lastly, using the Hamilton Depression Scale and Montreal Cognitive Assessment scores, researchers discover PD patients have higher depression scores and lower cognitive function.
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. Although organochlorine pesticides are been phased out in food production, these pesticides were ubiquitous, especially in the rural U.S., where pesticide exposure is nearly unavoidable due to drift and runoff. DDE, a breakdown product of DDT, is still widely found in the environment, including waterways and food. Moreover, occupational exposure poses a unique risk, as pesticide exposure is direct via handling and application. A 2017 study finds that occupational use of pesticides (i.e., fungicides, herbicides, or insecticides) increases PD risk by 110 to 211 percent. Even more concerning is that some personal protection equipment (PPE) may not adequately protect workers from chemical exposure during application. However, 90 percent of Americans have at least one pesticide compound in their body, primarily stemming from dietary exposure, like food and drinking water. These compounds have a global distribution, with evaporation and precipitation facilitating long-range atmospheric transport, deposition, and bioaccumulation of hazardous chemicals in the environment. Thus, exposure to these toxicants can cause several adverse environmental and biological health effects. With the increasing ubiquity of pesticides, current measures safeguarding against pesticide use must adequately detect and assess total chemical contaminants.
This study is one of four to investigate disparities between pesticide blood serum levels among PD patients and healthy controls. Additionally, this study is the first to find a correlation between specific pesticide compounds in blood samples and PD in the population, focusing on mechanisms of cellular dysfunction of α-HCH and propanil. Organochlorine pesticides (OCPs) can persist in the environment decades after use stops as OCPs have higher chemical stability and gradual attenuation. Thus, these compounds tend to bioaccumulate in the ecosystem and within the bodies of most species from high lipophilicity (chemical uptake by fats). Organophosphate insecticides originate from the same compounds as World War II nerve agents, producing adverse effects on the nervous system. Chemical exposure can cause a buildup of acetylcholine (a chemical neurotransmitter responsible for brain and muscle function) can lead to acute impacts, such as uncontrolled, rapid twitching of some muscles, paralyzed breathing, convulsions, and, in extreme cases, death. The compromise of nerve impulse transmission can have broad systemic impacts on the function of multiple body systems. Regarding mental health disorders, pesticides, including organophosphates (OPs), have associations with a higher prevalence of minor psychiatric disorders. Moreover, OPs are one of the leading causes of intentional poisoning globally as pesticide toxicity makes them potentially lethal substances.
Although many countries ban most organochlorine compounds, these chemicals remain in soils, water (solid and liquid), and the surrounding air at levels exceeding U.S. Environmental Protection Agency (EPA) standards. Moreover, several studies identify various current-use pesticides involved in the pathology of PD. These include the insecticides rotenone and chlorpyrifos, herbicides 2,4-D, glyphosate and paraquat, carbamate compounds, and fungicides maneb and mancozeb. 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, is a risk factor for PD. The highest risks occur in areas where chemicals quickly percolate into drinking water sources. Similar to the organochlorines in the study, acute and chronic exposure to rotenone can inhibit mitochondrial brain function responsible for cell regeneration and induce oxidative stress. Carbamate pesticides increase PD risk by 455 percent, with risk doubling for individuals with ten or more years of chemical use. 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. While PD risk increases with pesticide exposure periods, researchers indicate there is still a need for further research on the chemical threshold for harm to the brain.
Although the exact cause of PD remains unknown, studies continuously identify exposure to pesticides and specific gene-pesticide interactions as significant adverse risk factors. Environmental triggers like occupational exposure to pesticides can prompt PD in individuals with or without the genetic precursor. However, PD can develop regardless of whether an individual is a carrier of GBA gene mutation or not.
This study adds to the large body of scientific studies strongly implicating pesticide’s involvement in Parkinson’s disease development. In addition to this research, several studies demonstrate autism, mood disorders (e.g., depression), and degenerative neurological conditions (e.g., ALS, Alzheimer’s, Parkinson’s) among aquatic and terrestrial animals, including humans, exposed to pesticides. Pesticides themselves, mixtures of chemicals such as Agent Orange or dioxins, and therapeutic hormones or pharmaceutical products can possess the ability to disrupt neurological function. Therefore, the impacts of pesticides on the nervous system, including the brain, are hazardous, especially for chronically exposed individuals (e.g., farm workers) or during critical windows of vulnerability and development (e.g., childhood, pregnancy). Considering health officials expect Parkinson’s disease diagnosis to double over the next 20 years, it is essential to mitigate preventable exposure from disease-inducing pesticides.
The scientific literature demonstrates pesticides’ long history of severe adverse effects on human health (i.e., endocrine disruption, cancer, reproductive/birth problems, neurotoxicity, loss of biodiversity, etc.) and wildlife and biodiversity. However, there are several limitations in defining real-world poisoning as captured by epidemiologic studies in Beyond Pesticides’ Pesticide-Induced Diseases Database. The adverse health effects of pesticides, exposure, and the aggregate risk of pesticides showcase a need for more extensive research on occupational and nonoccupational pesticide exposure, especially in agriculture. For more information on the effects of pesticide exposure on neurological health, see PIDD pages on Parkinson’s disease, dementia-like diseases, such as Alzheimer’s, and other impacts on cognitive function.
Parkinson’s disease may have no cure, but prevention practices like organics can eliminate exposure to toxic PD-inducing pesticides. Organic agriculture represents a safer, healthier approach to crop production that does not necessitate toxic pesticide use. Beyond Pesticides encourages farmers to embrace regenerative, organic practices. A compliment to buying organic is contacting various organic farming organizations to learn more about what you can do. Those impacted by pesticide drift can refer to Beyond Pesticides’ webpage on What to Do in a Pesticide Emergency and contact the organization for additional information. Furthermore, see Beyond Pesticides’ Parkinson’s Disease article from the Spring 2008 issue of Pesticides and You.
All unattributed positions and opinions in this piece are those of Beyond Pesticides.
Ty my niece akayla Bracey for the information.
December 16th, 2021 at 12:21 pm