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Parkinson's disease strikes 60,000 people each year in the U.S. More than a million Americans are living with the disease at any one time. [1] More people suffer from Parkinson's than from multiple sclerosis, muscular dystrophy and amyotrophic lateral sclerosis (Lou Gehrig's disease) combined.

Parkinson's is a progressive brain disorder that is almost always fatal, but the suffering can go on for years. The disease usually strikes people over age 60, but a few people get it before they reach 40.

Parkinson's begins when a certain class of brain cells begins to die, cells that produce a chemical called dopamine, which your body needs. Dopamine serves as a chemical messenger helping to control muscle activities. Loss of dopamine leads to the pro- gressive loss of muscular control, giving rise to a variety of symptoms: stiffness, tremor, slow movement, difficulty with balance, difficulty walking, a stooped-over, shuffling gait. As the disease progresses, the patient may develop difficulty speaking, symptoms of senility (dementia) similar to Alz- heimer's, and severe depression.

In recent years, an effective medication, levodopa (known as L-dopa), has relieved many of the symptoms of Parkinson's for many patients, at least for a period of time. In addition, transplanting dopamine- producing brain cells from dead fetuses into the brains of Parkinson's sufferers has delayed the progression of the disease in some cases. Nevertheless, Parkinson's remains a common but poorly-understood terminal disease.

The causes of Parkinson's disease have been debated for 150 years, with no resolution.

A breakthrough occurred in the early 1980s when a group of young people developed the symptoms of Parkinson's disease after taking an illegal drug called MPTP, which is similar to the narcotic pain killer meperidine (which is sold under the trade name Demerol).[2] MPTP is also similar in chemical structure to several pesticides and herbicides.

Subsequently, symptoms of Parkinson's were induced in monkeys by feeding them MPTP.[3] This led the medical community to begin thinking of Parkinson's as a disease caused by chemical exposures. Early studies began to show a pattern: many people with Parkinson's have a history of exposure to pesticides, especially insecticides and herbicides.[4-7]

However in the early 1990s, Parkinson's was linked to a gene in a few Italian and Greek families,[8] and this sent researchers down the genetic trail in search of the cause of Parkinson's. Genetic causes of disease are very fashionable at the moment and it is easier to find research funds to study genes than it is to find research funds to study the effects of pesticides.

This week the likelihood of a genetic cause for most Parkinson's disease was effectively ruled out by the publication of a study of nearly 20,000 twins.[9] The study cohort, made up of white male twins who served in World War II, was developed by the National Academy of Sciences 35 years ago. Most of the members of the study cohort are now in their mid-60s, so they have reached the age when Parkinson's begins to appear. Of the 20,000 twins studied, 193 individuals were confirmed to have Parkinson's. The study showed that identical twins do not get Parkinson's any more often than two unrelated individuals. If the disease had a genetic origin, then identical twins, who share every gene, would both be expected to get the disease. This does not happen, the new study shows.

The researchers reported that, "No genetic component is evident when the disease begins after age 50 years. However, genetic factors appear to be important when [Parkinson's] disease begins at or before age 50." Thus fewer then 10% of Parkinson's cases -- only those that begin relatively early in life -- have a genetic component.

That leaves environmental chemicals as the culprit for the vast majority of Parkinson's, according to the researchers who conducted the twin study. In announcing their results, they specifically pointed out that the search for causes of Parkinson's should now re-focus on environmental chemicals such as pesticides and herbicides.[10]

The twin study should provide comfort to family members of Parkinson's victims who have been fearful about their own future based on their genetic relationship to the victim.

However, the new study provides cause for concern among farmers, pesticide applicators, and people who live in farming communities where regular exposure to pesticides is unavoidable. Since the late 1980s, a steady stream of studies from around the world has shown again and again that a common thread among victims of Parkinson's is a history of exposure to insecticides and herbicides.[4-7,11-15] Most recently a study showed that exposure to industrial solvents is linked to Parkinson's.[16]

--Peter Montague (National Writers Union, UAW Local 1981/AFL-CIO)

1] See

[2] J.W. Langston and others, "Chronic Parkinsonism in humans due to a product of meperidine-analog synthesis," SCIENCE Vol. 219, No. 4587 (February 25, 1983), pgs. 979-980.

[3] R.S. Burns and others, "The neurotoxicity of 1-methyl-4-phenyl- 1,2,3,6-tetrahydropyridine in the monkey and man," CANADIAN JOURNAL OF NEUROLOGICAL SCIENCE Vol. 11 (Supplement 1) (February 1984), pgs. 166- 168. And see J.W. Langston and P.A. Ballard, Jr., "Parkinson's disease in a chemist working with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyri- dine," NEW ENGLAND JOURNAL OF MEDICINE Vol. 309, No. 5 (August 4, 1984), pg. 310.

[4] S.C. Ho and others, "Epidemiologic study of Parkinson's disease in Hong Kong," NEUROLOGY Vol. 39, No. 10 (October 1989), pgs. 1314-1318.

[5] C. Hertzman and others, "Parkinson's disease: a case-control study of occupational and environmental risk factors," AMERICAN JOURNAL OF INDUSTRIAL MEDICINE Vol. 17, No. 3 (1990), pgs. 349-355.

[6] G.P. Sechi, "Acute and persistent parkinsonism after use of diquat," NEUROLOGY Vol. 42, No. 1 (January 1992), pgs. 261-263.

[7] K.M. Semchuk and others, "Parkinson's disease and exposure to agricultural work and pesticide chemicals," NEUROLOGY Vol. 42, No. 7 (July 1992), pgs. 1328-1335.

[8] Mihael H. Polymeropoulos and others, "Mutation in the alpha- Synuclein Gene Identified in Families with Parkinson's Disease," Science Vol. 276, No. 5321 (June 27, 1997), pgs. 2045-2047.

[9] Caroline M. Tanner and others, "Parkinson's Disease in Twins," JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION Vol. 281, No. 4 (January 27, 1999), pgs. 341-346.

[10] Thomas H. Maugh II, "Chemicals Called Main Cause of Parkinson's," LOS ANGELES TIMES January 27, 1999, pg. unknown. See

[11] K.M. Semchuk and others, "Parkinson's Disease: a test of the multifactorial etiologic hypothesis," NEUROLOGY Vol. 43, No. 6 (June 1993), pgs. 1173-1180.

[12] J.P. Hubble, "Risk Factors for Parkinson's Disease," NEUROLOGY Vol. 43, No. 9 (September 1993), pgs. 1693-1697.

[13] A. Seidler and others, "Possible environmental, occupational and other etiologic factors for Parkinson's disease: a case-control study in germany," NEUROLOGY Vol. 46, No. 5 (May 1996), pgs. 1275-1284.

[14] H.H. Liou and others, "Environmental risk factors and Parkinson's disease: a case-control study in Taiwan," NEUROLOGY Vol. 48, No. 6 (June 1997), pgs. 1583-1588.

[15] J.M. Gorell, "The risk of Parkinson's disease with exposure to pesticides, farming, well water, and rural living," NEUROLOGY Vol. 50, No. 5 (May 1998), pgs. 1346-1350.

[16] A. Smargiassi and others, "A case-control study of occupational and environmental risk factors for Parkinson's disease in the Emilia- Romagna region of Italy," NEUROTOXICOLOGY Vol. 19, Nos. 4-5 (August- October 1998), pgs. 709-712



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