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Public Radio's Environmental News Magazine (follow us on Google News)

Discovering new causes of Parkinson’s

Air Date: Week of

Dr. Samuel Goldman of The Parkinson's Institute.

A new study suggests that exposure to the common industrial solvent TCE or trichloroethylene may lead to Parkinson’s disease. Host Steve Curwood speaks with Dr. Samuel Goldman of The Parkinson’s Institute in California about the disease and how his team identified potential environmental causes.


CURWOOD: Parkinson’s disease afflicts some 700,000 Americans. The disorder often causes tremors and an unsteady gait. And more than many other diseases, Parkinson’s is linked to environmental exposures. Now comes news that among the possible causes of the disease is a common workplace chemical. Joining me to talk with about the new research is Dr. Samuel Goldman, one of the authors. Welcome, Sir.

GOLDMAN: Thank you. Thanks for having me.

CURWOOD: My pleasure. Your study is really interesting. You looked at twins, and you looked at twins where one brother has Parkinson’s disease and one doesn’t. And you then reconstructed a detailed work history for them - any place they’d worked for more than six months since they were 10-years-old. What did you find?

GOLDMAN: We found that the twin who was exposed to a compound called trichloroethylene, or TCE, had a more than six-fold increased risk of having Parkinson’s disease than their unexposed co-twin. And there were also some other solvents that we looked at as well, including one called PERC, or perchloroethylene, which is the most common dry cleaning solvent, and that was also associated with a markedly increased risk of Parkinsons.

CURWOOD: What if they had been exposed to TCE or PERC?

GOLDMAN: Exposure to TCE or PERC was associated with a nearly nine-fold increased risk of Parkinson’s disease.

CURWOOD: That’s a startling number, isn’t it? You must have been pretty excited to see this.

GOLDMAN: Well, excited, dismayed… We’ve always believed that the vast majority of Parkinson’s disease is a consequence of environmental risk factors, but it’s important to recognize that this is a single study, so replication of our results is really important at this point before we can progress to being really certain that this is a causal link.

CURWOOD: Talk to me a bit about these chemicals. TCE, now that’s trichloroethylene, now what does it do?

GOLDMAN: TCE was extremely widely used - it still is, but not so much as 30 years ago. So it would be used, now, primarily for degreasing of metal parts in manufacturing. And in fact, it’s in a broad range of consumer products and it has been for decades. And actually, up and through the 1970s, TCE was used to de-caffeinate coffee. It has been used as a general anesthetic. It was in wide use during the 1940s and 1950s primarily as an obstetrical anesthetic, strangely.

CURWOOD: So, tell me a bit about how you did design this study. You got almost a hundred sets of twins?

GOLDMAN: Correct. Well, we’ve been following this cohort of twins since the early 90s, and then that’s a very powerful study design to be able to look at environmental risk associations with disease.


GOLDMAN: Because twins, if they’re identical twins, they are genetically identical. And if they are fraternal twins, they are at least genetically very similar. So we are able to remove the genetic background effect from the equation and focus specifically on differences in environmental exposures.

CURWOOD: Now, what were the most occupations for the people who got sick?

GOLDMAN: The most common occupational exposure settings for TCE and PERC were among electricians and dry cleaners as well as people who repaired industrial machinery and artists.

CURWOOD: Artists?

GOLDMAN: Artists use solvents commonly.

CURWOOD: Of course art is a career; it’s also a hobby. What hobbies were people most at risk of getting Parkinson’s from this toxic exposure?

GOLDMAN: The hobbies that we observed were people working in carpentry. Artists again, people who worked in photography in particular. But oftentimes it’s in the household settings where exposure levels can be exceedingly high because there is no one enforcing a regulatory maximum or protective equipment in the home.

CURWOOD: So, Dr. Goldman, if somebody came into your office today and said, ‘Gee, I read your study. I want you to know that I worked at an aircraft engine repair place and was up to my elbows everyday in TCE. I’m fine today.’ What would you tell him he could do to help keep from getting Parkinson’s?

GOLDMAN: I would love to be able to offer some advice, but currently there really is no way that we’re aware of, to delay or prevent Parkinson’s disease. I think the most important thing we can do right now is to replicate this observation and if it’s found to be a consistently observed link between exposure to these compounds and Parkinson’s, I would hope that the funding agencies would really get behind this work and help us move it forward.

CURWOOD: And what are we to make of the fact that so many environmental contaminants seem to be linked, or even perhaps cause, Parkinson’s disease - there are earlier studies that have shown that have shown that several pesticides cause it by destroying brain cells, and research also points to, what, some heavy metals like manganese?

GOLDMAN: To me, as an investigator, for many years in Parkinson’s disease, I am really shocked at the paucity of environmental factors that we’ve been able to identify.

CURWOOD: Paucity? Too few?

GOLDMAN: I would like to know what causes Parkinson’s disease. So I feel like we’ve really only begun to scratch the surface of identifying risk factors for Parkinson’s disease. What’s really interesting about Parkinson’s is that there are very few naturally occurring disease clusters.

When you find a cluster, it’s a good sign that there’s likely to be a shared environmental determinant in those people. But there are very few naturally occurring clusters of Parkinson’s disease. So that implies that the environmental factors that go into causing Parkinson’s disease are likely spread out over a very long period of time and maybe different in everyone.

So what we’ve been able to link so far is, as you pointed out, several pesticides have been linked, but only a couple - paraquat - an herbicide -, and rotenone - an insecticide. As someone who has worked in this field for many years, I’m somewhat discouraged at the small number of environmental compounds that have been definitively linked with Parkinson’s disease.

CURWOOD: What you’re saying to me is that Parkinson’s disease as a disorder might be akin to, if you’ll forgive me, a broken leg. In other words, you can break your leg skiing, it could be in a car crash, you could fall over in your garden, you could get hit by a door. That it’s the endpoint of any number of processes.

GOLDMAN: That’s absolutely right. I think that we’ll find that there are many environmental insults that ultimately coalesce to result in Parkinson’s disease. But that in any given individual, the route to get to that point is different.

CURWOOD: Sam Goldman, thanks so much for talking with us today.

GOLDMAN: Well, it’s been a real pleasure and thanks for your interest in our work.

CURWOOD: Sam Goldman is a physician and public health researcher with the Parkinson’s Institute in Sunnyvale, California. He was part of a team whose research appears in the Current issue of the Annals of Neurology.



Dr. Samuel Goldman, et al. Annals of Neurology, Nov. 2011

The Parkinson’s Institute

NIH on Parkinson’s


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