Throughout the past 10 years, studies ranging in intensity have suggested a link between pesticide exposure and the development of Parkinson’s disease.1-3 An additional study has found a link between two solvents and Parkinson’s disease.4 This study was cited by Parrish and Gardner5, who suggested a potential risk for Parkinson’s disease by ambient pesticide exposure among those living downwind from a golf course. In 2013, Fields6 published an article that discussed these two reports. The issue has become a source of concern among those who play golf and live near a golf course and may result in patients turning to their primary care clinicians for up-to-date information and opinion. 

The following review will reveal the strengths and weaknesses surrounding the issue of pesticides, Parkinson’s disease, and golf and will provide information that a practitioner would need to evaluate past and future studies suggesting such risk to golfers and golf course residents. 

Background on Parkinson’s disease

Parkinson’s disease is a disorder of the substantia nigra (basal ganglia) section of the brain.2 Figures 1 and 2 represent a simplified version of normal basal ganglia and dopamine receptors. When neurons within the basal ganglia degenerate, they lose the ability to produce dopamine (dopaminergic neuron degeneration), resulting in abnormalities of movement. Parkinson’s symptoms develop when these neurons degrade from 550,000 to 100,000.7Figure 3 demonstrates this regression of dopamine levels within the neuron synapse. 

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The symptoms of Parkinson’s disease are listed in Table 1, and some of the available medications for treatment are included in Table 2. Figure 4 suggests the mechanism of action produced by these medications, which inhibit the oxidative breakdown of dopamine within the neuron. The diagnosis of Parkinson’s is made on the basis of physical and neurologic symptoms, as there are no serologic or diagnostic imaging tests available. The disease is confirmed when 2 of the 3 primary symptoms are present, one of which must be slow movement. Van Den Eeden et al8 estimates that Parkinson’s disease afflicts 17 of every 100,000 persons and is increasing worldwide with the expansion of an aging population. Most individuals afflicted by this disease are able to live without severe disability due to the slow degradation of dopamine-generating neurons and the number of treatment options available. It is the disabling symptoms that are of chief concern. 


The link between pesticides
and Parkinson’s disease

Pesticides have long been associated with the development of neurologic disorders. A Medline search using the terms “Parkinson’s” and “pesticides” yielded more than 1500 citations. Animal and human studies have connected the development of Parkinson’s with various groups and classifications of pesticides, which have been implicated in dopaminergic neuron degeneration. According to the CDC,9 the insecticide classes of organochlorine and organophosphorus compounds are thought to be specifically linked to Parkinson’s disease. Organochlorines are chlorinated hydrocarbons used extensively from 1940 to 1960. Parkinson’ disease symptoms differ from organophosphate poisoning, resulting in acute cholinergic toxicity (SLUDGE/BBB — Salivation, Lacrimation, Urination, Defecation, Gastric Emesis, Bronchorrhea, Bronchospasm, Bradycardia). According to the Colorado Environmental Pesticide Education Program,10 these two classes were the most frequently banned or severely restricted pesticides. Table 3 lists those pesticides banned or severely restricted in the U.S. The up-to-date list of restricted pesticides can be found in the Environmental Protection Agencies Restricted Use Products report.11

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In 2006, Ascherio et al1 found a 70% incidence of Parkinson’s among farm and non-farm workers exposed to pesticides. Although a diagnosis of Parkinson’s disease was made in these individuals based on movement disorders, pesticide use or exposure was only listed anecdotally by the respondents who did not report a specific pesticide.1 Despite evaluating a cohort of more than 140,000 individuals, Ascherio et al merely reinforced the connection between organochlorine pesticides and Parkinson’s. A specific pesticide link is required to make a connection to the development of Parkinson’s.

Wang et al2 recognized the need to make this connection between specific pesticides used and Parkinson’s disease. The researchers analyzed individuals working and living in the California Central Valley who were exposed to 3 specific pesticides (ziram, maneb, and paraquat). Contact occurred through air contamination at both the workplace and those residences within 500 meters of pesticide application.2 Wang and colleagues found an 80% increase in Parkinson’s disease development (especially among those younger at onset of symptoms) when exposed to a combination of 2 of the 3 pesticides. The risk was highest when ambient exposure occurred at both the residence and place of work, but it was lower (though not insignificant) among nonworking residents exposed through air contamination at home only. While this lower risk could be used to support a risk to golf course residents, the study further loses strength due to self-reporting. Wang et al also stated that a “derived poundage of active ingredient” could not be translated across pesticide classes equally. This would be needed to establish a connection to dopaminergic neuron toxicity and degradation. This has the effect of decreasing any association among golf course residents and would degrade any epidemiologic connection to golfers exposed to pesticides versus golf course workers. 

One year later, Van Maele-Fabry et al3 provided the best attempt at quantification of workplace exposure between pesticides and Parkinson’s through a meta-analysis approach. The researchers combined 12 prior analyses to increase the statistical power in their study. In addition, they expanded the selection of subjects internationally. The statistical method used evaluated homogeneity (similarities in comparability)2; the researchers also used statistical pooling to reduce publication bias (overstating conclusions). When high heterogeneity (diversity) was found, the evidence proved insufficient to demonstrate a causal relationship between pesticide exposure and Parkinson’s. While the results by Van Maele-Fabry et al showed a statistical increase in the risk of Parkinson’s disease, this increase was limited due to the documentation and diagnostic inconsistencies. Incidentally, Van Maele-Fabry et al also demonstrated a protective factor in cigarette use and caffeine intake. An inference can be made that these attributes are prevalent among golfers and may have provided some protection among older golfers who smoke.