Parkinson's profile

Why are certain races, regions hardest hit by the disease?

Parkinson's profile

The largest U.S. study of the epidemiology of Parkinson’s disease shows the highest prevalence (13,800 cases or more per 100,000 residents ages 65 and older) in red. Lower prevalence rates are progressively indicated by orange, yellow, light green and green. NEUROEPIDEMIOLOGY/S. KARGER AG

BY Michael Purdy

Washington University researchers are leading multiple pioneering efforts to study brain changes in Parkinson's disease and to identify factors in the environment that can cause or contribute to the disorder.

One such effort, led by Allison Wright Willis, MD, assistant professor of neurology, has used an unprecedented collection of data on 36 million Medicare patients to analyze how racial, economic and environmental factors affect Parkinson's risk.

Among other results, Wright Willis has shown that Parkinson's is twice as likely to strike whites and Hispanics as blacks and Asians and is more common in the Midwest and the Northeast.

"These are the two regions of the country most involved in metal processing and agriculture, and chemicals used in these fields are the strongest potential environmental risk factors for Parkinson's disease that we've identified so far," Wright Willis says.

Genetic factors explain only
a small percent of cases. Environmental factors are likely more common contributors.

By crossing her analysis of the Medicare data with EPA data on pollution, Wright Willis has also showed that high levels of manganese and copper pollution in urban areas are linked to increased risk of Parkinson’s disease.

Manganese is an important factor in efforts to understand the potential long-term risks of welding being led by Brad A. Racette, MD, professor of neurology. 

In a paper published in April 2011 in Neurology, Racette and his colleagues showed that workers exposed to the manganese in welding fumes may be at increased risk of damage to the same brain area harmed by Parkinson's disease.

"In the United States alone, there are over 1 million workers who perform welding as a part of their jobs," says Racette. "If further investigation of this potential link between neurotoxic effects and these fumes proves it is valid, it would have a substantial public health impact for the U.S. workforce and the economy."

The study involved 20 welders with no symptoms of Parkinson’s disease, 20 people with Parkinson’s disease who were not welders, and 20 people who were not welders and did not have Parkinson’s. The welders were recruited from two shipyards and one metal fabrication company, and each had an average of 30,000 hours of lifetime welding exposure.

All participants were given brain PET and MRI scans and motor skills tests. A neurologist who specializes in movement disorders also examined all participants. The welders' average blood manganese levels were found to be two times the upper limits of normal blood manganese levels established in prior studies of general populations.

In one area of the brain, PET scans indicated that welders had an average 11.7 percent reduction in a marker of the chemical dopamine compared to people who did not weld. Dopamine helps nerve cells communicate and is decreased in specific brain regions in people with Parkinson’s disease. The welders’ motor skills test scores also showed mild movement difficulties that were not as extensive as those found in the early Parkinson’s disease patients.

"We've done a lot of basic groundwork over the past five years, such as establishing scientific methods for assessing lifetime exposure to welding fumes, or ways to assess potential signs of damage or risk," Racette says. "Now that work is starting to pay off in terms of new insights into factors that may be contributing to Parkinson's."

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