Ozone air pollution exposure may increase Parkinson’s risk: Study
Finnish health register data tracks air quality across decades
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- Long-term exposure to ozone air pollution may increase the risk of developing Parkinson’s disease.
- Animal studies suggest ozone exposure can trigger brain damage similar to Parkinson's pathology.
- Further research using reliable methodologies is needed to confirm the association.
Long-term exposure to ozone, a form of air pollution, may increase the risk of developing Parkinson’s disease, according to a new study from Finland.
“In this nationwide register study of long-term exposure to gaseous air pollutants and [Parkinson’s] risk, we observed a borderline statistically significant increased risk for [Parkinson’s] after long-term exposure to [ozone],” researchers wrote.
The study, “Long-term exposure to six gaseous air pollutants and risk of Parkinson’s Disease,” was published in npj Parkinson’s Disease.
Parkinson’s risk elevated among those with higher ozone exposure
The causes of Parkinson’s are not fully understood. the disease’s development may be influenced by many different risk factors. An emerging body of evidence suggests that some types of air pollution may increase Parkinson’s risk, but these associations have not been proven definitively.
Ozone is a type of air pollution that forms as a result of reactions between chemicals made from industry and fossil fuel combustion. In previous studies, ozone has been identified as one of the main air pollutants that may influence the risk of Parkinson’s disease.
In this study, researchers examined the relationship between long-term exposure to ozone and several other air pollutants using data collected from health registries in Finland between 1996 and 2015. The analysis included more than 20,000 people who developed Parkinson’s, as well as more than 130,000 people who did not but were similar in terms of demographic factors. Using statistical analyses, the researchers examined whether individuals who developed Parkinson’s had significantly greater exposure to pollution in the years before their diagnosis.
Results showed that the risk of Parkinson’s was significantly elevated by about 3% among individuals with higher ozone exposure six to 16 years before diagnosis.
A few other types of air pollution showed negative associations with Parkinson’s risk; in other words, higher levels of these pollutants were associated with lower Parkinson’s risk. However, the researchers said these associations are likely tied to ozone because high levels of these other pollutants can lead to lower levels of ozone in the atmosphere.
The team noted that animal studies have suggested that ozone exposure can trigger brain damage similar to what happens in Parkinson’s, further supporting the idea that these disease risk associations are mainly driven by ozone.
The scientists noted that this analysis is limited by its reliance on registry data, underscoring the need for additional studies to further explore the association between Parkinson’s risk and air pollution.
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