Worldwide, an estimated 10 million people have Parkinson’s disease– a progressive, neurological condition that can lead to slowed, rigid movements, tremors and, in some cases, cognitive decline.
There is no cure for Parkinson’s, which primarily impacts those over the age of 65. While certain genetic and environmental risk factors have been identified, it remains unknown why some older individuals end up with the disease and others do not.
However, two new studies, published in the journals Environmental Research and Neurology, may help to untangle the role that pollution plays in determining who has an increased likelihood of developing the disease. By investigating the prevalence of Parkinson’s in central California and across the U.S., respectively, researchers at UCLA and the Barrow Institute of Neurological Research found that Parkinson’s is more likely to impact those working or residing in regions with increased levels of air pollution.
These publications “add to the increasing, if not overwhelming, evidence that environmental factors are likely important causes of Parkinson’s disease,” Ray Dorsey, professor of Neurology at the University of Rochester, told Environmental Health News (EHN).
Dorsey, who was not involved in the studies, is a co-author of the book “Ending Parkinson’s Disease,” which highlights the impact of ecological disruptions on diseases. He adds that the new research “represents an enormous contribution to the field.”
PM2.5 and Parkinson’s
Results from both studies indicate that Parkinson’s disease diagnoses are more common among individuals regularly exposed to pollutant particles of less than 2.5 micrometers in diameter, also known as “fine particulate matter” or PM2.5. In the Neurology magazine study, researchers found higher than average rates of Parkinson’s disease coupled with high levels of PM2.5 in South Texas, the Mississippi-Ohio River Valley and other locations. They also found that people living in neighborhoods with the median levels of air pollution had a 56% greater risk of Parkinson’s disease when compared to those living in neighborhoods with the lowest levels, which were found, predominantly, in the Western U.S.
The components of fine particulate matter are for the most part byproducts of diesel, gasoline, oil or wood combustion (waste emissions from power plants and industrial facilities) or are formed through chemical reactions that take place once gases, such as sulfur dioxide and nitrogen oxide, have been released into the air. According to the United States Environmental Protection Agency (EPA), PM2.5 poses serious health risks because the microscopic particles are easily inhaled and absorbed into the bloodstream.
These publications “add to the increasing, if not overwhelming, evidence that environmental factors are likely important causes of Parkinson’s disease.” – Ray Dorsey, University of Rochester
Given their minute size, some ultrafine particles of less than 100 nanometers in diameter (about 800 times thinner than a human hair) are able to travel across the blood brain barrier, a protective membrane that separates the invaluable contents of the central nervous system from the rest of the body. Once they reach the brain and spinal cord, prior research has shown, toxic pollutants can provoke oxidative stress and inflammation, which may eventually lead to neuronal death and neurodegenerative disease.
“Although we cannot conclude that the relationship between particulate matter and Parkinson’s disease is causal, we see a strong association when using a large nationwide dataset and high-resolution air pollution information,” Brittany Krzyzanowski, lead author on the Neurology study, told EHN. She added that, while policies are unlikely to change in the short-term, “vulnerable communities might use this information to find ways to mitigate their exposure by being vigilant of air quality alerts in their area and limiting time outdoors when advised.”
Carbon monoxide and Parkinson’s
The Environmental Research study, published this month, looked at the relationship between Parkinson’s disease and atmospheric levels of carbon monoxide, which was used as a marker of traffic-related pollution, as motor vehicles currently contribute more than 50% of total carbon monoxide emissions in the U.S. Study investigators recruited participants with and without Parkinson’s disease from three counties in central California and found a strong correlation between exposure to carbon monoxide over a 10-year period that preceded symptom onset and the development of Parkinson’s.
High levels of PM2.5, carbon monoxide and other pollutants have been previously linked to a wide range of health concerns including asthma, cardiovascular disease, stroke, cancer, dementia and poor pregnancy outcomes. As the prevalence of Parkinson’s disease continues to rise, experts emphasize that an improved understanding of how our environment contributes to disease development will be critical to discovering new ways to combat it.
“Ultimately, the air we breathe is a function of societal decisions,” Dorsey said. “Do we want to live longer, healthier lives free of stroke, dementia and Parkinson’s disease or do we want to breathe polluted air?”