Nitrogen dioxide (NO2) is significantly associated with a higher risk of developing Parkinson’s disease, according to a recent study from Korea. This finding strengthens previous research showing a potential link between air pollution and Parkinson’s disease.
The findings also prompted researchers to suggest that better regulation of air pollution could reduce the incidence of neurodegenerative disorder.
The study, “Association of exposure to NO2 and other air pollution with the risk of Parkinson’s diseaseWas recently published in JAMA Neurology.
Recent research has linked long-term exposure to ingested and inhaled environmental pollutants with the onset of neurodegenerative disorders such as Parkinson’s disease. How this could happen, however, remains unclear.
A hypothesis states that the toxic alpha-synuclein clusters that characterize Parkinson’s disease at the molecular level first form in the olfactory bulb of the brain and in the intestine, before spreading throughout the nervous system. This implication supports the environmental exposure link by being directly related to what we inhale and consume, respectively.
Epidemiological studies seeking to confirm the relationship between pollution and Parkinson’s disease, however, have yielded inconsistent results. Some studies have found associations between the cloudiness and various airborne molecules, including ozone (O3), small particles (PM2.5), and NO2.
A team of researchers from Ulsan University College of Medicine in Seoul, South Korea, pointed out that most of the earlier studies had been conducted in North America and Europe, leaving little Asian data from from which to draw.
In an attempt to fill this gap, the group used records from Korea’s National Health Insurance Service (NHIS) to look for associations between the onset of Parkinson’s disease and six common ambient air pollutants: PM2.5, PM10 (slightly larger fine particles), NO2, O3, sulfur dioxide (SO2) and carbon monoxide (CO).
NHIS records include around 97% of Korean residents.
Investigators compared health records to air pollution records, which are tracked by the Seoul Research Institute of Public Health and the Environment.
They identified 78,830 adults over 40 (mean age 54.4 years, 52.1% female), not suffering from Parkinson’s disease, and who lived in Seoul from January 2002 to December 2006. They then followed the files of this group each year from January 2007 to December 2015.
A total of 338 people developed Parkinson’s disease during the study period, and among the pollutants analyzed, only exposure to high amounts of NO2 was linked to a statistically significant increase in Parkinson’s risk.
The association between NO2 and Parkinson’s disease remained strong, even after adjusting for age, gender, insurance type, and other medical conditions.
Researchers have observed that NO2 exposure is often linked to traffic emissions and that some studies suggest that it exerts toxic effects on the brain. These include worsening beta-amyloid buildup, which can trigger alpha-synuclein clusters, causing difficulty in nerve signaling and increased markers of inflammation.
“In conclusion,” the scientists wrote, “we identified a statistically significant association between the risk of [Parkinson’s] and exposure to NO2 in the previous 5 years, especially at high exposure levels. We found no evidence of an association between the risk of PD and exposure to PM2.5, PM10, O3, SO2 or CO. “
“These findings,” they added, “suggest that regulating air pollutants could reduce the impact of air pollutants. [Parkinson’s]. “