New research focusing on the relationship between stroke and air pollution has uncovered what effects air pollution has on our brain health.
Air pollution has previously been shown to have a negative effect on the prognosis of ischemic stroke, or stroke caused by reduced blood flow to the brain, however, the exact mechanism has remained unknown.
A team of researchers have recently conducted a study to determine whether or not neuroinflammation is the main culprit.
They found that mice placed in an environment exposed to urban aerosols for one week demonstrated increased neuroinflammation, as well as worsening movement disorder after ischaemic stroke, compared to the control group who were not exposed to air pollution.
Furthermore, this effect was not observed in urban-aerosol treated mice lacking a receptor for chemicals released by the burning of fossil fuels, wood, garbage and tobacco, called polycyclic aromatic hydrocarbons (PAH).
Thus suggesting that PAHs are involved in both neuroinflammation and increased movement disorder associated with air pollution exposure in ischaemic stroke.
Yashuhiro Ishihara, senior author of the study, says: “We designed this study to determine the effects of air pollution on disorders in the central nervous system.
“Our narrower focus was to determine whether or not the prognosis of ischaemic stroke was affected by air pollution.”
The research team also identified specific components of air pollution that may directly contribute to lower prognoses in ischaemic stroke.
They believe they have discovered evidence that intranasal exposure to air pollution increased neuroinflammation after ischemic stroke in mice through activation of microglial cells, which are immune cells found in the brain. Additionally, movement disorder was also negatively impacted in ischaemic stroke mice exposed to the same air pollution.
A second set of experiments replacing the air pollution from the original environment with PM2.5 (tiny, aerosolised particles of air pollution that are 2.5 microbes in width or less) demonstrated similar results, thus suggesting the PM2.5 fraction of urban air pollution contains the chemical responsible for increased neuroinflammation and decreased ischaemic stroke prognosis.
In order to identify chemicals in air pollution responsible for decreased ischaemic stroke prognosis, the research team used a mouse that lacked the aryl hydrocarbon receptor, a receptor that is activated by the presence of PAHs, to determine whether or not exposure to air pollution in the first environment would have the similar effect on mice without working aryl hydrocarbon receptors.
Mice lacking the aryl hydrocarbon receptor demonstrated lower microglial cell activation and movement disorder compared to normal mice, suggesting that the PAHs present in the air pollution of the first environment are responsible for at least some of the neuroinflammation and lower prognosis seen in ischaemic stroke mice exposed to air pollution.
Ultimately, the goal of the research team is to better understand the mechanism by which PM2.5 causes neuroinflammation, since air pollution is inhaled first into the respiratory tract.
Ishihara, says: “Can small particles move from the nose to the brain? Does lung or systemic inflammation affect the brain immune system?”
