Long-term exposure to the pesticide chlorpyrifos may increase the risk of developing Parkinson’s disease by more than 2.5 times, reported a study published in Molecular Neurodegeneration.
For the study, researchers examined data from 829 people with Parkinson’s disease and 824 people without the condition.
Ultimately, they found that people with prolonged residential exposure to the chemical had more than 2.5 times the risk of developing Parkinson’s disease compared with those without exposure.
The animals developed movement difficulties, lost dopamine-producing neurons and showed increased inflammation as well as accumulation of alpha-synuclein, a protein associated with Parkinson’s disease.
Although the human findings do not establish that chlorpyrifos causes Parkinson’s disease, the results offer further insight into how pesticide exposure may contribute to neurodegeneration.
Long-term exposure to the pesticide chlorpyrifos may increase the risk of developing Parkinson’s disease by more than 2.5 times, reported a study published in Molecular Neurodegeneration.
"This study establishes chlorpyrifos as a specific environmental risk factor for Parkinson's disease, not just pesticides as a general class," said senior author of the study, Dr. Jeff Bronstein, professor of Neurology at UCLA Health, in a press release.
"By showing the biological mechanism in animal models, we've demonstrated that this association is likely causal,” he added.
For the study, researchers examined data from 829 people with Parkinson’s disease and 824 people without the condition. They estimated participants’ long-term exposure to chlorpyrifos, an organophosphate pesticide used to control agricultural pests, by examining residential and workplace histories alongside records of pesticide applications in California.
Ultimately, they found that people with prolonged residential exposure to the chemical had more than 2.5 times the risk of developing Parkinson’s disease compared with those without exposure.
To investigate how chlorpyrifos might affect the brain, the researchers exposed mice to aerosolized forms of the pesticide for 11 weeks. The animals developed movement difficulties, lost dopamine-producing neurons and showed increased inflammation as well as accumulation of alpha-synuclein, a protein associated with Parkinson’s disease.
To understand how this neuronal damage occurs, they turned to zebrafish models, ultimately finding that chlorpyrifos disrupts autophagy, the cellular process responsible for clearing damaged proteins and other unwanted material. They also found that restoring autophagy or eliminating synuclein protein protected neurons from damage, suggesting that these pathways could represent potential therapeutic targets.
Although the human findings do not establish that chlorpyrifos causes Parkinson’s disease, the results offer further insight into how pesticide exposure may contribute to neurodegeneration. Further research is needed to determine whether targeting the same mechanisms could help protect against pesticide-related neurological damage.
Sources: Science Daily, Molecular Neurodegeneration
