Exposure to Pesticides May Speed Symptom Progression
Both motor and non-motor symptoms may progress faster, study finds
People with Parkinson’s disease who are exposed to a high level of certain pesticides may see their motor and non-motor symptoms progress faster compared with those who are not as exposed, a U.S. study found.
Among the 10 pesticides whose high exposure was found to be associated with faster disease progression, copper sulfate pentahydrate and MCPA (dimethylamine salt) were the only ones linked to faster progression of all evaluated symptoms: motor, cognitive, and depressive.
The study, “Proximity to residential and workplace pesticides application and the risk of progression of Parkinson’s diseases in Central California,” was published in the journal Science of the Total Environment.
It is thought that Parkinson’s arises from a combination of genetic and environmental factors, and that breathing polluted air may place people at a higher risk of developing the neurodegenerative disease.
Nearly anyone can get exposed to some level of pesticides in a variety of places, including at home or at work. Pesticides can enter the body through contaminated air, water, food, and via direct contact with the skin.
The health risks of being exposed to pesticides depend on how dangerous they are and how they enter the body. The amount a person is exposed to, and for how long, also matters.
Pesticides such as paraquat (a herbicide) and rotenone (an insecticide) may increase the risk of developing Parkinson’s. But how fast Parkinson’s symptoms progress under exposure to pesticides remains unclear.
Data from California
To know more, a team of researchers in the U.S. analyzed demographic and clinical data from Parkinson’s patients who lived or worked next to crop fields in California, where farmers often use pesticides to protect crops and other plants from pests.
The researchers drew on data from California’s pesticide-use reports to determine the levels of pesticides patients might have been exposed to from 1974 to the date of their Parkinson’s diagnosis. They focused on the 53 pesticides that their previous work suggested were linked to the development of Parkinson’s.
A total of 501 people with idiopathic (unknown cause) Parkinson’s, who lived for at least five years in three central California counties — Fresno, Tulare, and Kern — were included in the analysis.
They were recruited as part of the Parkinson’s Environment and Genes study in 2001–2007 (242 people followed for an average of five years) and 2011–2017 (259 people followed on average for 2.7 years).
Most patients (62%) were men, of European ancestry (77%), and never smokers (57%). Their mean age at diagnosis was 66 years
Changes in motor symptoms were monitored using the Unified Parkinson’s Disease Rating Scale, part three. Changes in cognitive and depressive symptoms, two common non-motor symptoms, were monitored using the Mini-Mental State Examination and the Geriatric Depression Scale, respectively.
Results showed that 10 (19%) of the 53 pesticides analyzed “were associated with faster time to symptom progression,” the researchers wrote.
These included copper sulfate pentahydrate, MCPA dimethylamine salt, tribufos, sodium cacodylate, methamidophos, ethephon, propargite, bromoxynil octanoate, monosodium methanearsonate, and dicamba.
Six of them were associated significantly with faster motor symptom progression, eight were linked to faster cognitive decline, and five to faster progression of depressive symptoms.
Copper’s culpability
Notably, living or working closer to areas where a high level of copper sulfate pentahydrate or MCPA was recorded was linked to a faster progression of all three types of symptoms: motor, cognitive, and depressive symptoms.
Copper sulfate pentahydrate is used as a fungicide, herbicide, root killer, and antimicrobial in both agriculture and non-agricultural settings.
“Workplace exposure to copper has been implicated in [Parkinson’s development] before and our results both corroborate these results and implicate copper sulfate (pentahydrate) exposure in symptom progression and severity across multiple domains,” the researchers wrote.
MCPA, a chemical that breaks down in the environment to form a herbicide, also has been linked to Parkinson’s onset in a previous Dutch study, but “there is little experimental research connecting MCPA exposure to neurotoxicity,” they added.
“We also observed that exposure to several highly correlated pesticides mostly applied on cotton (sodium cacodylate, tribufos, propargite, and ethephon) was associated with faster cognitive decline and depression,” the team wrote.
The researchers also searched for a link between different exposure periods (more distant or more recent) and progression of symptoms.
However, exposure was “generally moderately to highly correlated over time due to widespread and consistent commercial application,” which “made it almost impossible to determine the most sensitive periods of exposure,” the researchers wrote.
“Our study has implicated individual pesticides in Parkinson’s disease progression in several domains,” the team wrote, adding that “further investigation should target both these individual pesticides and the cumulative risk of their mixtures to tease out potential [combinational] effects.”
“Identifying modifiable risk factors for disease progression may help identify new targets for research, perhaps leading to mechanistic insights important for medication development, and importantly help revise public health policy, aiming to reduce exposure to disease-modifying agents,” the researchers concluded.
The study was supported in part by the Michael J. Fox Foundation for Parkinson’s Research and the U.S. National Institute of Environmental Health Sciences.
About the Author
