Long-term exposure to the pesticide chlorpyrifos, which has been widely used in United States agriculture, has been associated with more than a 2.5-fold increase in the risk of developing Parkinson's disease, according to newly published research.
The results come from a large, community-based case–control study led by scientists at the University of California, Los Angeles (UCLA). Alongside the human data, the researchers also used animal models to pinpoint the specific types of brain injury that chlorpyrifos may trigger.
The work strengthens ongoing worries about links between pesticides and Parkinson's. However, proving long-term chemical exposure and disentangling it from other influences-such as genetics-has long been difficult.
“This study establishes chlorpyrifos as a specific environmental risk factor for Parkinson's disease, not just pesticides as a general class,” says neurologist Jeff Bronstein, from UCLA.
How the study estimated chlorpyrifos exposure and Parkinson's disease risk
To investigate the association, the team compared 829 people diagnosed with Parkinson's disease with 824 people without the condition.
They estimated each participant’s chlorpyrifos exposure by combining home and workplace address histories with California pesticide-use records going back to 1974.
People with the highest workplace exposure over the longest time periods showed 2.74 times higher odds of developing Parkinson's disease compared with those who had minimal or no exposure.
Importantly, the risk rose markedly when exposure dated back more than a decade, aligning with the long development timeline of Parkinson's disease, which frequently begins years before symptoms become noticeable.
Evidence from animal models: chlorpyrifos, dopamine-producing neurons, alpha-synuclein and autophagy
To explore whether the relationship might be causal rather than coincidental, the researchers carried out experiments in mice and zebrafish.
In mice exposed to chlorpyrifos, the team observed: - Signs of movement impairment - Loss of dopamine-producing neurons in the brain, a recognised hallmark of Parkinson's disease - Clumps of the alpha-synuclein protein, consistent with pathological markers seen in Parkinson's
In zebrafish, chlorpyrifos disrupted autophagy, a crucial cellular process that clears and recycles waste. When the scientists stimulated autophagy, neurons were more effectively protected from harm.
That connection between chlorpyrifos and autophagy is particularly notable because multiple previous studies suggest autophagy may be one of the biological pathways involved in Parkinson's-related brain damage-and chlorpyrifos may be acting through that same route.
“By showing the biological mechanism in animal models, we've demonstrated that this association is likely causal,” says Bronstein.
Regulation and wider context for pesticide exposure
Chlorpyrifos has previously been associated with brain abnormalities in children and is banned in the UK and the European Union. In the United States, its use has been partly restricted over recent decades, yet it continues to be applied to food crops in many states.
Even if chlorpyrifos increasingly appears to contribute to Parkinson's disease risk, it remains only one piece of a much larger puzzle. Although the exact origins of Parkinson's disease are still unclear, known risk factors include the genes a person is born with, poor quality sleep, and even living near a golf course-potentially reflecting pesticide exposure.
Practical implications for reducing chlorpyrifos and pesticide-related risk
While this study focuses on establishing risk and mechanism rather than offering personal medical guidance, it adds weight to the value of reducing avoidable pesticide exposure-particularly for people who work in or near treated areas. In occupational settings, that can include careful adherence to safety instructions, limiting time in recently treated zones, and using properly specified protective equipment when handling pesticides.
It also underlines the importance of accurate exposure records. Long-running pesticide-use databases, combined with address histories, helped this research estimate exposure over decades-an approach that could be strengthened further by consistent reporting, improved occupational histories, and, where feasible, environmental or biological monitoring.
What the researchers want to study next
Looking ahead, the researchers plan to examine other kinds of pesticides and their possible impacts on the brain. They also want to test whether treatments that prevent disruption of autophagy could shield neurons from damage caused by chlorpyrifos exposure and potentially slow Parkinson's progression.
“The discovery that autophagy dysfunction drives the neurotoxicity also points us toward potential therapeutic strategies to protect vulnerable brain cells,” says Bronstein.
The research has been published in Molecular Neurodegeneration.
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