Bret Stetka, MD; Caroline M. Tanner, MD, PhD

Disclosures

July 02, 2012

In This Article

Should You Be Screening Farmers?

Medscape: You presented some interesting exposure data at yesterday's session.[4] What specific environmental exposures have been linked to PD?

Dr. Tanner: The chemical MPTP -- one of the most extensively studied compounds known to induce parkinsonism in humans -- is a very rare cause of parkinsonism. In the laboratory, MPTP causes oxidative stress and impairs mitochondrial function. Paraquat, a commonly used herbicide, is similar in structure to MPTP. In the laboratory, paraquat also causes oxidative stress and a Parkinson-like condition in animal models. This prompted several people to look at whether or not pesticide exposure and agricultural work might be associated with PD risk.

Big exposure categories, such as pesticide use, began to be identified, but getting details on specific chemicals was difficult because it required getting the life histories on the subjects. This was a bit of an impasse, because there are many different types of pesticides with very different biological effects. It seemed unlikely that all pesticides would be associated with PD.

That's why we started taking detailed occupational histories to collect pesticide exposures. And we did find paraquat to be associated with risk for PD in several different populations. One was an occupational case/control study where there were relatively few exposed people, but those who were exposed had a 2.5 times greater risk. Then we went to the farming population, because we knew they had to keep good records on what chemicals they've used. Again, we found paraquat to be associated with PD. So this association is becoming fairly convincing.[5]

The other thing in our recent paper was the finding of an increased risk for PD associated with rotenone. Rotenone has been used in research to block mitochondrial complex 1 in the laboratory for years. It's a naturally occurring compound in numerous plants, and native people had recognized it to be poisonous; they would grind up rotenone-containing plants and put them in the water to stun fish. It's been used in a wide range of pesticide products over the years -- including household products, such as flea powders; insecticides for houseplants or gardens; and home pest removal, as well as commercial products -- so it's hard to answer the question, "Were you exposed to rotenone?" But by studying farmers and their spouses, who actually had records on whether or not and when they used it, we were able to find a specific association with PD.

A third compound that I didn't talk about yesterday is 2,4-D (2,4-dichlorophenoxyacetic acid), which is also an herbicide and is a component in Agent Orange. As we were reporting an association between occupational exposure to 2,4-D and PD, the Veterans Administration reported that veterans exposed to Agent Orange were entitled to disability benefits for PD. Their determination was based on other information, not on our work, and they didn't make specific reference to 2,4-D exposure of course, but it's interesting that we came to the same conclusion through studying 2 different types of exposure to the same chemical.

I should say that our other study did not show an association with 2,4-D despite some of the farmers having used the agent, so these findings still need replication. Also, it is essential for basic scientists to study the effects of these chemicals associated with PD in humans in the laboratory, because there's no incentive for the pesticide manufacturing industry to identify new adverse health effects of pesticides. Their interest is in figuring out whether or not a compound kills the pest. And unless they're told to, they're probably not going to be doing studies on adverse health effects. So, we need scientists to be looking at these chemicals in the laboratory.

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