Pesticides, Parkinson’s and golf

According to the previously mentioned studies, practitioners dealing with agricultural workers handling pesticides have reason for concern.1-3 Despite this suggested concern, a North American and European Medline search yields only 3 papers examining the estimated risk of pesticides to golfers. Murphy, Cooper, and Clark published a study evaluating the potential hazards of pesticide exposure via inhalation among golfers.12 The study looked at health risks from dermal exposure to 3 pesticides and extrapolated risk to measured air residues. Due to the suspected inhalation risk, the 3 specific pesticides were banned from golf course application (see Table 3).

Encouraged by this research, Murphy and Haith sought to establish an expanded pesticide list as an inhalation risk to golfers.13 These researchers took a broad geographical look at Parkinson’s risk by expanding the study group to 3 sites in the Northeast U.S., including Boston, Philadelphia, and Rochester. In addition, the researchers expanded the pesticides evaluated from their previous 3 to 15. The same study parameters were used in a search for the additional pesticides at risk. Despite a geographically broad and pesticide-specific search, Murphy and Haith’s study was without support for chronic inhalational health risks of current pesticides in use to golfers. The research team based their findings on possible regional variances, such as wind and temperature, in the application of the pesticides evaluated.

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One year later, Putnam, Doherty, and Clark14 published a paper on dermal pesticide exposure to golfers. This study looked at 2 pesticides (chlorpyrifos and carbaryl) and 2 methods of exposure (inhalation and dermal). The test subjects were evaluated after walking a simulated 4-hour round of golf 1 hour following full-course pesticide application. Dermal exposure, not inhalation, was determined to be the overriding method of contact post-insecticide application. Despite the short time interval between exposure and application, these dermal doses were found to be 19 to 68 times below the Environmental Protection Agency (EPA) standards.14

The link among pesticides, Parkinson’s disease, and golf was further degraded by 4 factors. First, the exposures were designed to represent a worst-case scenario, as the exposure was early and represented an unlikely pattern for the average, or even professional, golfer to repeat. Second, when pesticides are applied to turf grass, it is not daily and the applications degrade quickly over several days, further decreasing ambient exposure. The same protection was found to apply to greenskeepers as well. Third, these dermal doses correlate with EPA risk assessment. Last, Putnam et al found that if post-application exposure was delayed an additional hour, further dermal doses were reduced by an additional 30% (an 80% reduction in total dose).14

Putnam et al did note the presence of morning dew, which retards insecticide degradation, and an absence of solar radiation (in overnight application) as providing a lack of protection. Based on these data, Putnam et al suggested that turf grass application be adjusted to “half- or partial-course applications spaced over a day or two.” Putnam et al believed that this provided a best management practice that would further decrease the exposure risk to golfers; however, best management practice standards for pesticide use and application are established by the Occupational Safety and Health Administration (OSHA), as this agency has governmental oversight in this area. Despite having this oversight, as of 2011, U.S. public recording of specific pesticides used on golf courses are not required except in California.15

Golf course residency and Parkinson’s 

The concern to golf course residents is raised by Fields,6 who recommended that new purchasers of golf course residences consider buying upwind on a golf course. This suggestion is based on a letter to the editor citing chemical solvent exposure and the risk of Parkinson’s disease.5 As already established by Wang et al,2 there was demonstration of low risk to ambient pesticide exposure in the combination of pesticides within an active agricultural region. In 2012, Parrish et al performed a rudimentary, retrospective, randomized study that attempted to provide a connection between ambient pesticide exposure and golf course residents.5 This study looked at 26 cases of individuals living with Parkinson’s in a metropolitan area. Of those Parkinson’s cases, 19 lived within 2 miles of a golf course. From the 19 reported cases, 16 lived downwind of a golf course. Three of the total 26 cases were found to have been exposed to solvents, though they were not among the 19 reported living in the radius of concern. Thus, Parrish and Gardner’s thesis had several shortcomings. First, there was no evidence that any solvents were used on or near the golf courses in their study. Second, Parrish and Gardner’s study was very low in power, analyzing only 19 of 26 cases of individuals living with Parkinson’s disease within 2 miles of a golf course in a metropolitan area. Third, Parrish and Gardner’s conclusion was based only on an empirical connection between the 16 downwind cases.5

According to, the null hypothesis is a proposal used in statistical evaluation that states when there is no difference between study variables or that a single variable is essentially 0 that the study outcome “is presumed to be true until statistical evidence nullifies it for an alternative hypothesis”16 (para. 1). The assumption is that any difference is chance. As the breakdown of these prior studies suggests, the evidence to connect pesticides and Parkinson’s is soft at best. Armed with this information, a practitioner could feel justified in assigning the null hypothesis to the Fields’6 article. The practitioner would then consider pesticide exposure, golf, and golf course residency as historical information only. 


For the present, there is insufficient evidence to link ambient exposure to pesticides among golfers and the development of Parkinson’s disease. Previously published studies have based their conclusions on flawed case-controlled epidemiologic study methods. Further evaluations are needed to answer this question conclusively. A larger, more controlled evaluation of active pesticides in use is needed to determine conclusively that golfers are at risk of Parkinson’s disease due to frequent pesticide exposure.

Thomas Massing, MS, PA-C, FAPACVS, is a physician assistant at CompHealth in Woodstock, Ga. 


  1. Ascherio A, Chen H, Weisskopf MG, et al. Pesticide exposure and risk for Parkinson’s disease. Ann Neurol. 2006;60(2):197-203.

  2. Wang A, Costello S, Cockburn M, et al. Parkinson’s disease risk from ambient exposure to pesticides. Eur J Epidemiol. 2011;26:547-55. 

  3. Van Maele-Fabry G, Hoet P, Vilain F, Lison D. Occupational exposure to pesticides and Parkinson’s disease: A systematic review and meta-analysis of cohort studies. Environ Int. 2012;46:30-43.

  4. Goldman S, Quinlan P, Ross W, et al. Solvent exposures and Parkinson disease risk in twins. Ann Neurol. 2012;71(6):776-784.

  5. Parrish ML, Gardner RE. Is living downwind of a golf course a risk factor for parkinsonism? Ann Neurol. 2012;72(6):983-984.

  6. Fields D. Golf links to Parkinson’s disease? Huffpost Healthy Living. 2013. Retrieved from:

  7. Pakkenberg B, Møller A, Gundersen H, et al. The absolute number of nerve cells in substantia nigra in normal subjects and in patients with Parkinson’s disease estimated with an unbiased stereological method. 
J Neurol Neurosurg Psychiatry. 1991;54(1):30-33.

  8. Van Den Eeden S, Tanner C, Bernstein A, et al. Incidence of Parkinson’s disease: Variation by age, gender, and race/ethnicity. Am J Epidem. 2003;157(11):1015-1022.

  9. Centers for Disease Control and Prevention. Fourth national report on human exposure to environmental chemicals. 2009. Retrieved from:

  10. Colorado Environmental Pesticide Education Program. Banned and severely restricted Pesticides. 2006. Retrieved from:

  11. Environmental Protection Agency. Restricted use products. 2013. Retrieved from: http://www.epa./opprd001/rup/rupreport.pdf

  12. Murphy K, Cooper R, Clark J. Volatile and dislodgeable residues following trichlorfon and isazofos application to turfgrass and implications for human exposure. Crop Science. 1996;36:1446-1454.

  13. Murphy R, Haith D. Inhalation health risk to golfers from turfgrass pesticides at three northeastern U.S. sites. Environ Sci Technol. 2007;41(3):1038-1043.

  14. Putnam R, Doherty J, Clark J. Golfer exposure to chlorpyrifos and carbaryl following application to turfgrass. J Agric Food Chem. 2008;56(15):6616-6622.

  15. Arcury-Quandt A, Gentry A, Marin A. Hazardous materials on golf courses: Experience and knowledge of golf course superintendents and grounds maintenance workers from seven states. Am J Ind Med. 2001;54(6):474-485.

  16. Null hypothesis. 2013. Retrieved from: