You can find out more about NPF's National Medical Director, Dr. Michael S. Okun, by also visiting the NPF Center of Excellence, University of Florida Center for Movement Disorders & Neurorestoration.
Pesticides, Agent Orange, and potential environmental risk factors for the development of Parkinson’s disease continue to make the news. Patients and families may be comforted by headlines on chemicals and Parkinson’s disease, most of which they may never be exposed to. The recent report by Goldman and colleagues from the Parkinson’s Institute, a National Parkinson Foundation Center of Excellence in Sunnyvale, CA, may open some eyes to environmental exposures and Parkinson’s disease risk.
Goldman and colleagues cleverly chose to study twins from the WWII Veterans Cohort. By utilizing twin pairs (half were identical twins) researchers limited the potential effects of genetics on the development of Parkinson’s disease. One person from each twin pair was required to have been diagnosed with Parkinson’s disease. A very careful occupational and hobby history was then extracted, with the chief weakness of this study lying in how the histories were obtained. First hand histories from patients were sparse with spouses and siblings providing second hand proxy histories in most cases. The main study weakness was somewhat balanced by the employment of an occupational hygienist. An occupational hygienist is a carefully trained professional that can independently determine exposures, hazards, or risks in a workplace environment. The hygienist and the researchers examined six solvents, and determined that only trichloroethylene (TCE) was associated with an increased risk (6.1X) of developing Parkinson’s disease in men. Additionally men exposed to TCE or to another chemical called PERC (tetrachloroethylene) had an 8.9 times increased risk of developing Parkinson’s disease. Interestingly n-hexane, xylene, and toluene, which have all been thought to be potentially associated with the development of Parkinson’s disease, did not show an increased risk in this cohort. All of the studies of environmental exposures should be interpreted with caution, and patients and families should look for common themes among multiple research reports, as the potential for error in these types of population based studies can be high. TCE exposure will therefore require more study, and also study within the female population of Parkinson’s disease patients.
The next question a patient or family member should ask about TCE is what kind of work might lead to an exposure. The following is a list of potential places one might come in contact with TCE:
- Grease remover
- Typewriter fluid
- Paints and strippers
- Carpet cleaners and spot removers
- Computer part cleaners
- Decaffeinated coffees
- Textile plants
- Anaesthetics in an operating room setting
The following is a list of the highest risk of occupations associated with TCE exposure:
- Dry cleaners
- Industrial machinists and repair crews
- Health care workers
Patients and families should appreciate that there is a difference between acute TCE exposure and chronic TCE exposure. Acute high dose exposure seems to depress the central nervous system, and may lead to breathing problems, heart arrhythmias, coma, and a host of other problems. Acute TCE may also prove to be a nasty skin irritant. When we talk about TCE exposure and Parkinson’s disease, we are referring to chronic long-term exposure. Chronic exposure has also been associated with unsteadiness, dizziness, headaches, memory loss and many other symptoms. The current study presented at the American Academy of Neurology by Goldman and colleagues suggests that Parkinson’s disease risk may need to be added to the potential sequalae of chronic TCE exposure.
Patients and families should be aware that the risk factors for Parkinson’s disease seem to now be extending beyond genetics, and may be inclusive of environmental exposures. Hancock and colleagues recently reported that insecticides and herbicides, especially organochlorines and organophosphorus compounds, increased the risk of Parkinson’s disease even in those without a family history. Pesticides and environmental risk factors therefore have emerged as important considerations in the development of Parkinson’s disease. Patients, families and physicians should all be aware of these chemicals, and should assess their risks for exposure.
Additionally, we are pleased to announce the launch of the new National Parkinson Foundation Helpline! People with Parkinson's, their families, friends and health care providers are invited to call 1-800-4PD-INFO (473-4636) to receive current and up-to-date information about Parkinson's disease generally, emotional support, and referrals to health professionals and community resources.
Goldman SM. Trichloroethylene and Parkinson's disease: dissolving the puzzle. Expert Rev Neurother. 2010 Jun;10(6):835-7.
Frigerio R, Sanft KR, Grossardt BR, Peterson BJ, Elbaz A, Bower JH, Ahlskog JE, de Andrade M, Maraganore DM, Rocca WA. Chemical exposures and Parkinson's disease: a population-based case-control study. Mov Disord. 2006 Oct;21(10):1688-92. PubMed PMID: 16773614.
Gash DM, Rutland K, Hudson NL, Sullivan PG, Bing G, Cass WA, Pandya JD, Liu M, Choi DY, Hunter RL, Gerhardt GA, Smith CD, Slevin JT, Prince TS. Trichloroethylene: Parkinsonism and complex 1 mitochondrial neurotoxicity. Ann Neurol. 2008 Feb;63(2):184-92.
Kochen W, Kohlmüller D, De Biasi P, Ramsay R. The endogeneous formation of highly chlorinated tetrahydro-beta-carbolines as a possible causative mechanism
in idiopathic Parkinson's disease. Adv Exp Med Biol. 2003;527:253-63.
Guehl D, Bezard E, Dovero S, Boraud T, Bioulac B, Gross C. Trichloroethylene and parkinsonism: a human and experimental observation. Eur J Neurol. 1999
Huber F. [Clinical aspects and neuropathology of trichloroethylene poisoning]. Z Unfallmed Berufskr. 1969;62(4):226-67. German.
Hancock DB, Martin ER, Mayhew GM, Stajich JM, Jewett R, Stacy MA, Scott BL, Vance JM, Scott WK. Pesticide exposure and risk of Parkinson's disease: a family-based case-control study. BMC Neurol. 2008 Mar 28;8:6.