Parkinson's disease, the most common neurodegenerative movement disorder caused by aging, can also be caused by pesticides and other neurotoxins. A new study found strong evidence that trichloroethylene (TCE) is a risk factor for parkinsonism, a group of nervous disorders with symptoms similar to Parkinson's disease. TCE is a chemical widely used in industry that is also found in drinking water, surface water and soil due to runoff from manufacturing sites where it is used. The study was published in the October 2007 issue of Annals of Neurology (http://www.
Led by Don M. Gash and John T Slevin, of the University of Kentucky in Lexington, KY, researchers conducting a clinical trial of 10 Parkinson's disease patients came across a patient who described long-term exposure to TCE, which he suspected to be a risk factor in his disease. TCE has been identified as an environmental contaminant in almost 60 percent of the Superfund priority sites listed by the Environmental Protection Agency and there has been increasing concern about its long term effects. The patient noted that some of his co-workers had also developed Parkinson's disease, which led to the current study of this patient and two of his co-workers diagnosed with Parkinson's disease who underwent neurological evaluations to assess motor function. All of these individuals had at least a 25 year history of occupational exposure to TCE, which included both inhalation and exposure to it from submerging their unprotected arms and forearms in a TCE vat or touching parts that had been cleaned in it. In addition, questionnaires about experiencing signs of Parkinson's disease, such as slowness of voluntary movement, stooped posture and trouble with balance, were mailed to 134 former workers. The researchers also conducted studies in rats to determine how TCE affects the brain.
The results showed that 14 former employees who reported three or more parkinsonian signs worked close to the TCE source, were found to exhibit signs of parkinsonism when they were examined and were significantly (up to 250 percent) slower in fine motor hand movements than age-matched controls. Clinical exams of 13 patients who reported no signs of parkinsonism revealed that they worked in the same areas as the symptomatic workers or further from the TCE vat, they exhibited some mild features of the condition and their fine motor movements were also significantly slower than controls, although they were faster than the group with symptoms. The rat studies showed that TCE exposure inhibited mitochondrial function (which in humans is associated with a wide range of degenerative diseases) in the substantia nigra, an area in the brain that produces dopamine and whose destruction is associated with Parkinson's disease. Specifically, Complex 1, an enzyme important in energy production, was significantly reduced in the substantia nigra. Dopamine neurons in this area also showed degenerative changes following TCE administration.
The authors acknowledge that while the study was not a large scale epidemiological investigation, the results demonstrate a strong potential link between chronic TCE exposure and parkinsonism. "It will be important to follow the progression of movement disorders in this cohort over the next decade to fully assess the long-term health risks from trichloroethylene exposure," they state. Although previous studies identified pesticides as a risk factor for Parkinson's disease, the drug MPTP was previously the only mitochrondrial neurotoxin linked to the disease. The authors conclude: "Trichloroethylene is implicated as a principal risk factor for parkinsonism based on its dopaminergic neurotoxicity in animal models, the high levels of chronic dermal and inhalation exposure to trichloroethylene by the three workers with Parkinson's disease, the motor slowing and clinical manifestations of parkinsonism in co-workers clustered around the trichloroethylene source, and the mounting evidence of neurotoxic effects in other reports of chronic trichloroethylene exposure."
Article: "Trichloroethylene: Parkinsonism and Complex 1 Mitochondrial Neurotoxicity," Don M. Gash, Kathryn Rutland, Naomi L. Hudson, Patrick G. Sullivan, Guoying Bing, Wayne A. Cass, Jignesh D. Pandya, Mei Liu, Dong-Yong Choi, Randy L. Hunter, Greg A. Gerhardt, Charlie D. Smith, John T. Slevin, T. Scott Prince, Annals of Neurology, December 2007.