A recent study published in the journal Particle and Fibre Toxicology has shed light on the potential mechanism through which air pollution affects the prognosis of ischemic stroke, a type of stroke caused by reduced blood supply to the brain. The study suggests that increased inflammation in the brain, known as neuroinflammation, may play a significant role in this association.
Researchers conducted experiments on mice, subjecting them to intranasal exposure of urban aerosols from Beijing, China for one week. They discovered that the mice exposed to air pollution exhibited greater neuroinflammation and experienced worsened mobility dysfunction following an ischemic stroke, compared to the control group of mice that were not exposed to air pollution. Interestingly, this impact was not observed in mice lacking a receptor for polycyclic aromatic hydrocarbons (PAHs), which are compounds released during the combustion of fossil fuels, wood, waste, and tobacco. This suggests that PAHs are implicated in both neuroinflammation and the aggravated mobility dysfunction seen in ischemic stroke caused by air pollution.
Lead author of the research paper, Professor Yasuhiro Ishihara from Hiroshima University, explained that the study aimed to investigate the effects of air pollution on disorders in the central nervous system, with a specific focus on the prognosis of ischemic stroke. The researchers went a step further by identifying specific components of air pollution that may directly contribute to the worsened prognosis in ischemic stroke.
Further experiments replaced the Beijing air pollution with PM2.5 particles (tiny aerosolized particles of air pollution that are 2.5 micrometers or smaller) from Yokohama, Japan. These experiments yielded similar results, suggesting that the PM2.5 fraction of urban air pollution contains the chemical responsible for increased neuroinflammation and decreased prognosis in ischemic stroke.
To pinpoint the chemicals in air pollution responsible for the negative effects on ischemic stroke prognosis, the researchers utilized mice lacking the aryl hydrocarbon receptor. The results showed that these mice exhibited lower activation of microglial cells (immune cells in the brain) and experienced reduced movement disorder compared to normal mice, indicating that the PAHs present in Beijing air pollution are at least partially responsible for the neuroinflammation and diminished prognosis seen in ischemic stroke mice exposed to air pollution.
These findings highlight the detrimental impact of air pollution, particularly PAHs, on ischemic stroke outcomes. Understanding the underlying mechanisms involved in the association between air pollution and stroke prognosis is crucial for developing effective preventive strategies and mitigating the adverse effects of pollution on human health.