Exposure to air pollution may increase the risk of inflammation of the brain, and worsen movement disorder after stroke, a study conducted in mice suggests.
Air pollution has been shown to have a negative impact on the prognosis, or likely course, of ischemic stroke, or stroke caused by reduced blood flow to the brain, but the exact mechanism is unknown.
The study, published in the journal Particle and Fibre Toxicology, analysed whether or not increased inflammation of the brain, also known as neuroinflammation, is the main culprit.
It found that mice exposed to urban aerosols from Beijing, China, for one week demonstrated increased neuroinflammation and worsening movement disorder after ischemic stroke, compared to control mice that were not exposed to air pollution.
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), the researchers said.
This suggests that PAHs are involved in both neuroinflammation and increased movement disorder associated with air pollution exposure in ischemic stroke, they said.
”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, and professor at Hiroshima University, Japan.
”Our narrower focus was to determine whether or not the prognosis of ischemic stroke was affected by air pollution,” Ishihara said in a statement.
The team also identified specific components of air pollution that may directly contribute to lower prognoses or the likely course, of ischemic stroke.
They found evidence that intranasal exposure to air pollution from Beijing increased neuroinflammation after ischemic stroke in mice through activation of microglial cells, which are immune cells found in the brain.
Movement disorder was also negatively impacted in ischemic stroke mice exposed to the same air pollution, according to the researchers.
A second experiment replacing Beijing air pollution with PM2.5 — tiny, aerosolised particles of air pollution that are 2.5 microgrammes in width or less — from Yokohama, Japan, demonstrated similar results.
The study also suggests that the PM2.5 fraction of urban air pollution contains the chemical responsible for increased neuroinflammation and decreased ischemic stroke prognosis.
In order to identify chemicals in air pollution responsible for decreased ischemic stroke prognosis, the team used a mouse that lacked the aryl hydrocarbon receptor, that is activated by the presence of PAHs. They did so to determine whether or not exposure to the Beijing air pollution would have a similar effect on mice without working aryl hydrocarbon receptors.
The resaerchers found that mice lacking the aryl hydrocarbon receptor demonstrated lower microglial cell activation and movement disorder compared to normal mice. This suggests that the PAHs present in Beijing air pollution are responsible for at least some of the neuroinflammation and lower prognosis seen in ischemic stroke mice exposed to air pollution.
