The specific mechanism through which air pollution affects the prognosis of ischemic stroke, or stroke caused by reduced blood supply to the brain, is uncertain. A group of researchers recently conducted a study to see whether increased inflammation in the brain, often referred to as neuroinflammation, is to blame.
The team published their findings in the February 16, 2023 issue of Particle and Fiber Toxicology. Rats treated internally in Beijing, China, urban aerosols for one week showed greater neuroinflammation and worse motor dysfunction after ischemic stroke than rats not exposed to air pollution.
Furthermore, this effect was not found in urban-aerosol-treated mice, which do not have a receptor for polycyclic aromatic hydrocarbons (PAHs), which are compounds derived from the combustion of fossil fuels, wood, waste and tobacco. This suggests that PAHs are implicated in both neuroinflammation and hypermobility in ischemic stroke caused by air pollution exposure.
“We designed this study to determine the effects of air pollution on disorders in the central nervous system,” said Yasuhiro Ishihara, senior author of the research paper and professor at the Graduate School of Integrated Sciences for Life at Hiroshima University. “Our narrow focus was to determine whether the prognosis of ischemic stroke was affected by air pollution,” Ishihara said.
The group went a step further by identifying specific components of air pollution that may directly contribute to the reduced prognosis in ischemic stroke.
They found evidence that intranasal exposure to air pollution from Beijing, China increased neuroinflammation after ischemic stroke in mice through activation of microglial cells, which are immune cells found in the brain. Movement disorders were also negatively affected in ischemic stroke rats exposed to the same air pollution.
A second set of experiments replacing Beijing air pollution with PM2.5 (small, aerosolized particles of air pollution that are 2.5 microbs or less in width) from Yokohama, Japan, demonstrated similar results, suggesting that the PM2.5 fraction of urban air pollution contains chemicals responsible for increased neuroinflammation and reduced ischemic stroke prognosis.
To identify the chemicals in air pollution responsible for the reduction in ischemic 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 whether Beijing is exposed to air pollution. Rats would have the same effect without working aryl hydrocarbon receptors.
Mice lacking the aryl hydrocarbon receptor exhibited less microglial cell activation and movement disorders than normal mice, suggesting that ischemic stroke mice exposed to PAH air pollution present in Beijing air pollution have at least some of these effects. Neuroinflammation and are responsible for the poor prognosis.