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New Study Strengthens the Link Between Pesticide Exposure and Parkinsonís Disease

A new study provides strong evidence of an association between exposure to the insecticide rotenone and Parkinson’s disease (PD).  The research appears in the January 26 online edition of Environmental Health Perspectives.

Researchers who want to understand whether pesticide exposure is a cause of Parkinson’s disease can do laboratory work to find out whether specific pesticides cause PD in animals like mice and to understand the molecular mechanisms that lead to brain cell death.  They can also interview groups of people exposed to pesticides — farmers, for example — to find out whether this exposure correlates with the development of PD.  But there is no way to directly test whether pesticides cause PD in people. 

In an attempt to link these two types of studies, Caroline M. Tanner, M.D., Ph.D., at the Parkinson’s Institute in Sunnyvale, CA, and her colleagues based their investigations upon previous laboratory studies that had implicated two molecular pathways in the development of PD.  In one of these the cell’s mitochondria, the structures that convert nutrients into energy, are impaired.  In another, there is oxidative stress, a condition that can cause a cell to self-destruct. 

So Dr. Tanner and her colleagues investigated whether pesticides known to cause mitochondrial dysfunction (including rotenone) or oxidative stress (paraquat, among others) were linked to the development of PD.

The scientists relied on data collected through the Agricultural Health Study, a National Institutes of Health study of nearly 90,000 farmers and others who have used pesticides in their work.  They identified a subgroup of participants – 110 people with PD and 358 healthy study participants of similar age and gender – known to have been exposed to rotenone, paraquat and similar pesticides.  Then, using statistical methods, they investigated whether pesticide exposure was associated with PD.


  • Parkinson’s was found 2.5 times as often in people who had used rotenone compared to people who were never exposed to this chemical.
  • Study participants with PD had similar symptoms, regardless of whether they had been exposed to rotenone, paraquat or pesticides not linked to the mitochondrial or oxidative stress pathways.
  • PD was diagnosed at an earlier age (age 59) in people exposed to chemicals associated with oxidative stress than in those exposed to other pesticides (age 64).


What Does it Mean?

The significant association of PD with the use of groups of pesticides that disrupt mitochondria directly (Complex 1 inhibitors such as rotenone) or indirectly by causing oxidative stressors, supports decades of experimental work. 

The research also may have public health implications.  In recent years rotenone, for the most part, has been discontinued, but many people may have been exposed to it.  Other agents that disrupt the same molecular pathway, including permethrin, are still in use.  The herbicide paraquat is widely used worldwide. 

While this study does not demonstrate that pesticides directly cause Parkinson’s, it does help to connect the dots between basic research and the development of Parkinson’s in people living with the disease. 

Learn More

What else do we know about why Parkinson's develops? Read about the causes of PD on PDF's website.

Source Date: Mar 08 2011