People living near a steel factory or another source of high manganese emissions are at higher risk of developing Parkinson’s disease, suggests a new study.
As many as one million Americans live with the degenerative disease, according to the Parkinson’s Disease Foundation. Pesticides from farms have long been suspected of upping the chances of developing Parkinson’s, but much less is known about the influences of city living.
“Environmental risk factors for Parkinson’s disease have been relatively under-studied, especially in urban areas where the overwhelming majority of Parkinson’s disease patients reside,” Dr. Brad A. Racette of the Washington University School of Medicine in St. Louis, Missouri, told Reuters Health in an e-mail.
Parkinson's disease
Earlier research had tied heavy metals to Parkinson-like brain damage, but it wasn’t clear if they could also play a role in people who aren’t exposed to the metals as part of their job.
So Racette and his colleagues analyzed data on about five million Medicare beneficiaries who hadn’t moved between counties from 1995 to 2003. Then they compared Parkinson’s rates to industry emissions of copper, lead and manganese obtained from the Environmental Protection Agency.
By 2003, less than one percent of people in urban areas developed Parkinson’s disease. In counties with little or no release of the metals, 274 out of every 100,000 people had the disease, compared to 489 in counties with high manganese levels.
Parkinson's disease
The risk remained increased even after accounting for differences in age, sex and race, report the researchers in the American Journal of Epidemiology.
Areas with high copper emissions also saw more cases of Parkinson’s, but the increase was so slight it could have been due to chance.
The researchers say they don’t know whether manganese actually caused more people to get Parkinson’s disease. It’s possible that other risk factors in counties with lots of manganese emissions could be to blame.
Parkinson's disease
“Although the findings related to manganese are very compelling, future studies investigating individual patient exposures and risk of Parkinson’s disease will be required to confirm our study,” said Racette.
“Understanding community level exposures to environmental toxins will be critical to determining the causes of most cases of Parkinson’s disease,” he added. “If our findings are confirmed, our data would suggest that reducing industrial metal emissions may result in a substantial reduction in the number of new cases.”
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Northwestern Medicine scientists have discovered that dopamine-releasing neurons in a region of the brain called the substantia nigra lead a lifestyle that requires lots of energy, creating stress that could lead to the neurons’ premature death, which causes Parkinson’s disease.
“Why this small group of neurons dies in Parkinson”s disease is the core question we struggled with,” said lead author D. James Surmeier.
“Our research provides a potential answer by showing this small group of neurons uses a metabolically expensive strategy to do its job. This ”lifestyle” choice stresses the neurons” mitochondria and elevates the production of superoxide and free radicals – molecules closely linked to aging, cellular dysfunction and death,” Surmeier said.
The good news is preclinical research shows this stress can be controlled with a drug already approved for human use.
By preventing calcium entry, the drug isradipine reduced the mitochondrial stress in dopamine-releasing neurons to the levels seen in neurons not affected by the disease.
Researchers are currently conducting a clinical trial to find out if isradipine can be used safely and is tolerated by patients with Parkinson”s.
Isradipine is already approved by the Food and Drug Administration for treatment of high blood pressure.
The symptoms of Parkinson”s disease include rigidity, slowness of movement and tremors. No treatment currently is known to prevent or slow the progression of Parkinson”s disease.