In a study published in Particle and Fibre Toxicology, researchers have uncovered evidence linking air pollution to worsened outcomes for ischemic stroke patients, suggesting neuroinflammation might be the key culprit.
The study conducted by a team led by Yasuhiro Ishihara, a professor in the Graduate School of Integrated Sciences for Life at Hiroshima University, exposed mice to urban aerosols from Beijing, China, for one week.
The results showed increased neuroinflammation and worsening movement disorder following ischemic stroke, in contrast to control mice that were not exposed to air pollution.
A Key Chemical Culprit
Intriguingly, these detrimental effects were not observed in mice treated with urban aerosols but lacked a receptor for polycyclic aromatic hydrocarbons (PAHs).
These chemicals are released from the burning of fossil fuels, wood, garbage, and tobacco.
This finding suggests that PAHs may play a significant role in neuroinflammation and the heightened movement disorder associated with air pollution exposure in the aftermath of an ischemic stroke.
Probing Further
The research team also identified specific components of air pollution that might directly lower the prognosis of ischemic stroke.
They discovered that intranasal exposure to Beijing’s air pollution heightened neuroinflammation post-ischemic stroke in mice through the activation of microglial cells—immune cells in the brain.
Further experiments replacing Beijing air pollution with PM2.5 (tiny, aerosolized particles 2.5 micrometers or less in width) from Yokohama, Japan, yielded similar results.
This suggests that the PM2.5 fraction of urban air pollution contains the chemical responsible for increased neuroinflammation and decreased ischemic stroke prognosis.
Focusing on PAHs
To pinpoint the chemicals in air pollution accountable for the decreased prognosis in ischemic stroke, the team used mice lacking the aryl hydrocarbon receptor, activated by PAHs.
Mice without working aryl hydrocarbon receptors demonstrated lower microglial cell activation and movement disorder compared to normal mice.
This suggests that PAHs present in Beijing air pollution might be partially responsible for the observed neuroinflammation and lower prognosis in ischemic stroke mice exposed to air pollution.
Future Research Directions
Understanding the mechanism by which PM2.5 causes neuroinflammation is the primary aim of this research, as these particles first enter the body through inhalation.
“Can small particles move from the nose to the brain? Does lung or systemic inflammation affect the brain immune system?” Ishihara questioned.
Further research in this direction will be crucial to understanding and addressing the negative health impacts of air pollution.
If you care about stroke, please read studies that diets high in flavonoids could help reduce stroke risk, and MIND diet could slow down cognitive decline after stroke.
For more information about health, please see recent studies about a common food that may strongly increase heart disease risk, and results showing Vitamin K2 could help reduce heart disease risk.
The study was published in Particle and Fibre Toxicology.
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