UCLA Health study links pesticide exposure to higher Parkinson’s disease risk

Jeff M. Bronstein, MD, PhD, Movement Disorders Neurology
Jeff M. Bronstein, MD, PhD, Movement Disorders Neurology - UCLA Health
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A recent study from UCLA Health reports that long-term residential exposure to the pesticide chlorpyrifos is linked to more than a 2.5-fold increased risk of developing Parkinson’s disease. The findings, published in Molecular Neurodegeneration, combine human data with laboratory research to show how chlorpyrifos can harm dopamine-producing brain cells.

Parkinson’s disease affects nearly one million Americans and is characterized by tremors, stiffness, and movement difficulties. While genetics contribute to the disorder, environmental factors such as pesticide exposure are increasingly recognized as important. Chlorpyrifos has been widely used in agriculture for decades; its use in homes was banned in 2001 and agricultural restrictions were imposed in 2021, but it remains present on many crops both in the United States and abroad.

The study analyzed information from 829 people diagnosed with Parkinson’s disease and 824 without the condition, all part of UCLA’s ongoing Parkinson’s Environment and Genes project. Researchers used California pesticide use records along with participants’ home and work addresses to estimate individual exposures over time. Laboratory experiments exposed mice to aerosolized chlorpyrifos for 11 weeks using inhalation methods similar to typical human exposure, while zebrafish studies explored biological mechanisms.

Results showed that individuals with long-term residential exposure had more than double the risk of developing Parkinson’s compared to those without such exposure. Mice exposed to chlorpyrifos developed movement issues and lost dopamine-producing neurons—the same cells affected in humans with Parkinson’s. They also exhibited brain inflammation and abnormal accumulation of alpha-synuclein protein. Zebrafish studies indicated that chlorpyrifos disrupts autophagy, a cellular process responsible for clearing damaged proteins; restoring this process or removing synuclein protected neurons from damage.

Researchers suggest these findings highlight autophagy dysfunction as a potential target for future treatments aimed at protecting the brain from pesticide-related harm. Although chlorpyrifos use has declined recently in the U.S., past exposures remain relevant, and similar pesticides continue to be used worldwide. Further research may explore whether other pesticides cause comparable damage or if interventions supporting cellular cleanup could reduce Parkinson’s risk among those exposed.

“This study establishes chlorpyrifos as a specific environmental risk factor for Parkinson’s disease, not just pesticides as a general class,” said Dr. Jeff Bronstein, professor of Neurology at UCLA Health and senior author of the study. “By showing the biological mechanism in animal models, we’ve demonstrated that this association is likely causal. The discovery that autophagy dysfunction drives the neurotoxicity also points us toward potential therapeutic strategies to protect vulnerable brain cells.”

The University of California Los Angeles is a major public research institution known for its broad academic programs across various disciplines and commitment to societal progress through knowledge creation (official website). It attracts students and scholars globally while fostering diversity within its community.



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