For regular golfers, their cherished pastime could be exposing them to a significantly heightened risk of a serious neurological condition. Groundbreaking research from the University of California Los Angeles (UCLA) indicates that prolonged exposure to a pesticide commonly applied to golf courses may more than double an individual's likelihood of developing Parkinson's disease.
The Pesticide in Question: Chlorpyrifos
The study, published in the journal Molecular Neurodegeneration, focused specifically on the pesticide chlorpyrifos. Introduced in 1965, this chemical has been widely used in agriculture, forestry, and on maintained grassy areas such as golf courses. Although the European Union banned its use in 2020 and the UK prohibited it in 2016, the research highlights that the disease's long latency period means many may have been exposed decades before these restrictions came into effect.
Parkinson's disease is a progressive neurological disorder affecting roughly 1 million Americans, with the Parkinson's Foundation estimating that 1.2 million Americans will be diagnosed by 2030. It is caused by the degeneration of nerve cells in the brain that produce dopamine, leading to symptoms like tremors, stiffness, balance problems, and speech difficulties that worsen over time.
Key Findings from Human and Animal Studies
The UCLA research team analysed data from 829 people with Parkinson's disease and 824 without it, all participants in a long-term environmental study. By cross-referencing California's pesticide use reports with participants' home and work addresses over at least 30 years, they calculated individual exposure levels.
The results were stark. Individuals with the highest exposure to chlorpyrifos faced a 2.5-fold increased risk of developing Parkinson's compared to those with the least exposure. Crucially, exposures occurring 10 to 20 years before disease onset showed a stronger link than exposures in the decade immediately prior, underscoring the condition's slow development.
To understand the biological mechanism, scientists conducted parallel experiments on mice and zebrafish. Mice exposed to aerosolised chlorpyrifos for 11 weeks developed movement issues and lost, on average, 26% of their dopamine-producing neurons. They also showed brain inflammation and a buildup of the protein alpha-synuclein, a hallmark of Parkinson's.
Disrupted Cellular Process Points to Potential Treatments
In zebrafish, which share about 70% of their genes with humans, the team discovered that chlorpyrifos causes damage by interrupting autophagy. This is the body's essential cellular recycling process, where old or damaged components are broken down to make way for new ones.
Dr Jeff Bronstein, senior study author and professor of neurology at UCLA Health, stated: 'This study establishes chlorpyrifos as a specific environmental risk factor for Parkinson's disease, not just pesticides as a general class. By showing the biological mechanism in animal models, we've demonstrated that this association is likely causal.'
He added that the discovery regarding autophagy dysfunction 'points us toward potential therapeutic strategies to protect vulnerable brain cells.' This insight opens new avenues for research into treatments that could mitigate pesticide-induced damage.
The study adds to a growing body of evidence linking environmental factors to the rising incidence of Parkinson's in the US and elsewhere. Other research has implicated pollutants like PM2.5 particulate matter and prolonged exposure to loud noise in worsening the disease's progression.
While there is no cure for Parkinson's, medications like Levodopa help manage symptoms by boosting dopamine levels in the brain. The new findings emphasise the importance of monitoring individuals with known historical exposure to chlorpyrifos and other pesticides for early signs of neurological conditions.
