Korean Study Ties Air Pollution to Developing Parkinson’s

Nitrogen dioxide (NO2) is associated significantly with a higher risk for developing Parkinson’s disease, according to a recent study from Korea. The finding reinforces previous research showing a potential link between air pollution and Parkinson’s.

The results also prompted researchers to suggest that better air pollution regulations might lower incidence of the neurodegenerative disorder.

The study, “Association of NO2 and Other Air Pollution Exposures With the Risk of Parkinson Disease,” was published recently in JAMA Neurology.

Recent research has linked long-term exposure to ingested and inhaled environmental pollutants with the occurrence of neurodegenerative disorders such as Parkinson’s. How this might happen remains unclear, however.

One hypothesis states that the toxic clumps of alpha-synuclein that characterize Parkinson’s on a molecular level first form in the brain’s olfactory bulb and in the gut, before spreading throughout the nervous system. This involvement supports the environmental exposure connection by being directly linked to what we inhale and consume, respectively.

Epidemiological studies seeking to confirm the relationship between pollution and Parkinson’s have delivered inconsistent results, however. Some studies have found associations between the disorder and various airborne molecules, including ozone (O3), small particulate matter (PM2.5), and NO2.

A team of researchers from the University of Ulsan College of Medicine, in Seoul, South Korea, pointed out that most past studies have been carried out in North America and Europe, leaving little Asian data from which to draw.

To attempt to fill this gap, the group used Korea’s National Health Insurance Service (NHIS) records to look for associations between Parkinson’s occurrence and six common ambient air pollutants: PM2.5, PM10 (slightly larger small particulate matter), NO2, O3, sulfur dioxide (SO2), and carbon monoxide (CO).

NHIS records include approximately 97% of Korean residents.

The investigators compared health records to those of air pollution, which are tracked by the Seoul Research Institute of Public Health and Environment.

They identified 78,830 adults older than 40 (mean age 54.4, 52.1% female), without Parkinson’s, and who lived in Seoul from January 2002 to December 2006. They then followed this group’s records annually from January 2007 to December 2015.

A total of 338 individuals developed Parkinson’s over the study period, and from among the analyzed pollutants, only exposure to high amounts of NO2 were linked to a statistically significant increase in Parkinson’s risk.

The association between NO2 and Parkinson’s remained strong, even after adjusting for age, sex, type of insurance, and other medical conditions.

The researchers observed that NO2 exposure often is related to traffic emissions and that some studies have suggested that it exerts toxic effects on the brain. These include worsening the buildup of amyloid-beta, which can trigger the formation of alpha-synuclein clumps, causing nerve signaling difficulties and increasing markers of inflammation.

“In conclusion,” the scientists wrote, “we identified a statistically significant association between the risk of [Parkinson’s] and exposure to NO2 for the previous 5 years, especially at high exposure levels. We found no evidence for the association between the risk of PD and exposure to PM2.5, PM10, O3, SO2, or CO.”

“These findings,” they added, “suggest that regulation of air pollutants might reduce the incidence of [Parkinson’s].”