Study links high risk of Parkinson’s disease to living near a golf course: “Cases are exploding.”

Parkinson’s disease (PD) is a complex and progressive neurological disorder, affecting millions globally, with rising incidence rates that cannot be explained by genetics alone. Increasingly, research has pointed to environmental exposures—particularly pesticides—as key contributors to the disease’s development. While much of this attention has focused on agricultural settings, a new population-based study shifts the lens to a less obvious, but widely common, landscape: golf courses.

Golf courses are often seen as community cornerstones—spaces of leisure, prestige, and scenic beauty. Yet behind their immaculate fairways lies a heavy reliance on chemical treatments, including pesticides known to be neurotoxic. In the United States, golf courses are treated with some of the highest volumes of pesticides per acre, often exceeding usage levels permitted in many other countries. Until recently, little research had explored whether living near these manicured grounds could affect long-term health. A new study, however, offers compelling evidence that proximity to golf courses may significantly increase the risk of developing Parkinson’s disease, particularly for those living in vulnerable water regions or densely populated urban areas.

Proximity to Golf Courses and Parkinson’s Disease—What the Evidence Reveals

Emerging research has begun to spotlight the environmental factors that may contribute to the development of Parkinson’s disease (PD), a complex neurodegenerative condition. Among these factors, pesticide exposure has garnered increasing attention. A recent population-based case-control study leveraging data from the Rochester Epidemiology Project has now added a compelling dimension to this discussion: the proximity of residential homes to golf courses.

The study examined more than 5,500 individuals across a 27-county region spanning southern Minnesota and western Wisconsin between 1991 and 2015. Of these, 419 were newly diagnosed with PD. Using precise home address data and detailed mapping of 139 golf courses in the region, researchers found a notable trend: individuals living within 1 mile of a golf course had more than double the odds of developing Parkinson’s disease compared to those residing more than 6 miles away (adjusted odds ratio [aOR], 2.26; 95% CI, 1.09–4.70). The pattern persisted, with increased odds even at distances of 1–3 miles, though the risk tapered with greater distance.

This risk gradient aligns with what’s known about the heavy use of pesticides on U.S. golf courses, where application levels can be up to 15 times higher than in European counterparts. Pesticides commonly used on golf courses—including chlorpyrifos and 2,4-D—have been implicated in PD through mechanisms such as oxidative stress and mitochondrial dysfunction, both of which affect the dopamine-producing neurons critical in the disease’s progression.

Importantly, the association held even after controlling for a range of factors including age, sex, race, socioeconomic status, and urban versus rural location. This strengthens the argument that the relationship is not simply due to demographic or socioeconomic confounders.

These findings point to a potentially underrecognized source of environmental exposure to neurotoxic chemicals: the manicured greens and fairways that dot suburban and urban landscapes. While the precise pathways of exposure—whether through air, soil, or water—are complex and still under investigation, the data suggests that merely living near these recreational spaces could carry health risks that extend beyond what was previously understood.

Drinking Water as a Possible Pathway of Exposure

While living near a golf course was strongly associated with an increased risk of Parkinson’s disease (PD), the study also sheds light on a subtler, potentially more insidious pathway of exposure: contaminated drinking water. Specifically, the research investigated whether municipal water systems that draw from groundwater sources near golf courses might serve as a conduit for pesticide exposure.

The study found that individuals who received their tap water from groundwater-based service areas containing a golf course had nearly double the odds of developing PD compared with those living in similar areas without a golf course (aOR, 1.96; 95% CI, 1.20–3.23). When compared to individuals using private wells, the odds were still 49% higher (aOR, 1.49; 95% CI, 1.05–2.13).

These associations became even more striking in regions identified as having vulnerable groundwater—areas with coarse soils, shallow bedrock, or karst geology, where contaminants are more likely to infiltrate water supplies. Among residents in such areas, those living near a golf course had 82% higher odds of developing PD compared to residents in non-vulnerable areas (aOR, 1.82; 95% CI, 1.09–3.03).

Groundwater vulnerability is critical because many pesticides used on golf courses are known to leach into the soil and infiltrate aquifers. For example, chlorpyrifos and 2,4-D—both linked to PD in prior toxicological studies—have been detected in groundwater at levels far exceeding health-based guidelines. A notable case from Cape Cod, Massachusetts, found one pesticide in drinking water at concentrations more than 200 times the recommended safety threshold.

In this study, an overwhelming majority (77.3%) of participants lived in water service areas that relied on groundwater, including 86.6% of PD cases. The widespread dependence on these sources underscores how pesticide runoff from golf courses could affect entire communities through a shared water supply. Municipal water systems often treat and distribute groundwater uniformly, meaning a single contamination point can impact hundreds or thousands of residents.

Interestingly, the study found no significant association between PD risk and municipal wells located directly on golf courses or wells that were classified as “shallow” (less than 100 feet deep). This suggests that while the general presence of a golf course in a water service area matters, the complexity of municipal water infrastructure—such as depth, flow, and treatment—could mediate exposure levels in ways not captured by well location or depth alone.

The Role of Airborne Pesticide Exposure and Urban Density

While groundwater contamination presents a clear pathway for pesticide exposure, the potential role of airborne transmission—particularly in urban and suburban areas—adds a compelling layer to the environmental risk landscape for Parkinson’s disease. In this study, researchers found that the association between living near a golf course and PD risk was notably stronger in urban areas, suggesting that inhalation of airborne pesticides may be a significant, though less visible, route of exposure. Golf courses are routinely treated with a variety of pesticides, many of which are volatile and capable of becoming airborne, especially when applied via spraying. These airborne chemicals can travel beyond the course boundaries, drifting into nearby neighborhoods, settling on lawns, entering homes through ventilation systems, and exposing residents—often unknowingly—to neurotoxic substances over extended periods.

Volatile compounds such as chlorpyrifos, a pesticide long used on golf courses and associated with neurodevelopmental and neurodegenerative risks, have been shown to persist in the air and travel considerable distances from their application sites. In urban areas, where homes are densely packed and green space buffers are minimal, the risk of exposure via air increases. This may explain why the study observed consistent risk of PD within a 3-mile radius of golf courses but found that risk decreased only beyond this distance—suggesting a possible “ceiling effect” at closer ranges, where exposure is already saturated regardless of exact proximity. Importantly, 90% of individuals living within 3 miles of a golf course were also located in groundwater-based water service areas, meaning many residents were likely exposed via multiple routes, further complicating the picture and potentially amplifying cumulative risk.

The study’s urban-suburban-rural stratification, based on Rural-Urban Commuting Area (RUCA) codes, supports this hypothesis. In urban settings, pesticide drift is more likely to affect a larger number of people due to higher population density and smaller lot sizes, which reduce the distance between homes and treated turf. Unlike in rural areas where land tracts are larger and vegetation may serve as a partial barrier, urban residents have limited protection from pesticide particles moving through the air. The increased density of buildings and infrastructure may even trap airborne pollutants in localized zones, potentially intensifying exposure. Furthermore, these areas may also have less regulatory oversight or community awareness about the frequency and type of pesticide applications occurring on nearby recreational grounds.

Understanding the Biological Plausibility—How Pesticides May Trigger Parkinson’s Disease

To appreciate the significance of the association between golf course proximity and Parkinson’s disease (PD), it’s essential to understand the biological mechanisms through which pesticides may influence the development of this neurodegenerative disorder. PD is characterized by the progressive loss of dopaminergic neurons in the substantia nigra, a region of the brain responsible for movement control. Decades of research have pointed to both genetic predisposition and environmental exposures as key contributors to this neuronal loss, with pesticide exposure being one of the most consistently implicated environmental risks. Substances commonly used on golf courses—including organophosphates like chlorpyrifos and herbicides such as 2,4-dichlorophenoxyacetic acid (2,4-D)—have been shown in laboratory studies to induce neurodegenerative changes similar to those seen in PD patients.

Pesticides such as paraquat and rotenone are particularly well-studied for their Parkinson’s-related effects. These chemicals can cross the blood-brain barrier and trigger oxidative stress, disrupt mitochondrial function, and initiate apoptotic pathways that ultimately lead to the death of dopamine-producing neurons. The convergence of these processes mirrors the pathological hallmarks of Parkinson’s disease. Experimental models in animals have repeatedly demonstrated that chronic low-dose exposure to these compounds can result in motor deficits and neuroinflammation, lending strong biological credibility to the observed epidemiological associations. Importantly, while paraquat and rotenone are better known in agricultural contexts, their presence on golf courses—though less documented—is plausible given the broad spectrum of turf management chemicals used in the industry.

Moreover, pesticides are not uniform in their toxicity or persistence. Some degrade quickly in sunlight or water, while others linger in soil, air, and groundwater for extended periods. This persistence can lead to prolonged exposure windows for residents living near treated landscapes, especially if these substances accumulate in household dust, drinking water, or even local produce. The risk may be compounded over time, particularly in populations with long-term residential stability, as was observed in the study cohort, many of whom had lived at the same address for years or even decades. Given that PD has a long prodromal phase—often spanning 10 to 20 years before the onset of clinical symptoms—early, repeated exposure to neurotoxic pesticides may set in motion the slow degeneration of neural systems without immediate warning signs.

While no single pesticide has been definitively proven to cause Parkinson’s disease in humans, the convergence of toxicological evidence, mechanistic plausibility, and consistent epidemiological signals presents a compelling case for concern. The study’s findings fit within this broader scientific narrative, suggesting that living near a golf course—a setting often treated with multiple pesticide formulations—may act as a proxy for cumulative environmental exposure to neurotoxic agents.

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