Parkinson’s disease (PD) has been described as the fastest-growing brain disease, affecting an estimated ten million people worldwide. There is now accumulating evidence to suggest that air pollutants could be a risk factor for PD, thus potentially further increasing the patient population.
GlobalData forecasts the number of PD patients in the 16 major markets (16MM: the US, France, Germany, Italy, Spain, the UK, Japan, Australia, Brazil, Canada, China, India, Mexico, Russia, South Africa and South Korea) will increase from 8,047,380 cases in 2021 to 8,732,690 cases in 2025, as shown in Figure 1. PD is 1.5 times more likely to develop in men than women, and the incidence increases with age. People with the condition have reduced dopamine levels due to the loss of nerve cells in an area of the mid-brain called the substantia nigra, which is what is responsible for many of the PD symptoms. The exact cause resulting in the loss of nerve cells in the brain is unclear, but medical experts speculate a combination of genetics and environmental factors are responsible, although not everyone who is genetically predisposed to PD develops the condition.
A 2021 study by Jo and colleagues published in JAMA Neurology found a statistically significant association between nitrogen dioxide (NO₂) exposure and PD risk. High exposure to pollutant NO₂ increases the chance of developing PD by 40% compared with low exposure. Other pollutants examined in the study were particulate matter (PM2.5), ozone (O₃), sulfur dioxide (SO₂) and carbon monoxide (CO), none of which were found to have a statistically significant association with PD risk.
NO₂ is commonly released from vehicles and power plants that rely on burning fossil fuels. NO₂’s end effect on the brain may begin from the olfactory nerve, which is anatomically predisposed to exposure to airborne pollutants. Inhaling NO₂ can potentially have a poisonous impact on the olfactory nerve, which is one possible explanation for the association between NO₂ exposure and the risk of PD identified in this study. Inhalation of NO₂ may also increase systemic pro-inflammatory cytokines possibly related to neuroinflammation in the brain, an important pathogenic mechanism of neurological diseases such as PD.
In 2016, Ritz and peers published a study in Environmental Health Perspectives that found ambient air pollution levels from traffic sources to be associated with risk of PD, with a 9% higher risk per interquartile range increase (2.97μg/m³) in modelled NO₂. The odds ratio for the risk of PD was greater for participants living in the capital city than those in provincial towns.
These studies are not stating a causative link between certain air pollutants and PD. They do, however, indicate that this is an area of research that warrants further investigation, especially if PD is, to an extent, a preventable condition. The level of exposure is also an essential factor to consider, as low exposure does not result in the same likelihood of PD risk as high exposure. Airborne pollutants are a public health concern in cities and developing nations undergoing intense industrialisation, and heightened air pollution may further increase the expected PD burden in the 16MM.