Airborne particulate matter is produced artificially or naturally from boilers, incineration plants, depository sites, automobiles, cigarettes, soil and volcanic eruptions, and causes air pollution. Inhalation of particulate matter is known to exacerbate respiratory allergic disorders such as bronchial asthma. On the other hand, recent studies suggest that inhaled particulate matter reaches the brain through the nasal epithelial layer, and in addition epidemiological studies show that exposure to particulate matter induces extension of hospitalization period and high case fatality rates after onset of ischemic stroke, suggesting that the brain is an important target of inhaled particulate matter.
Cerebral edema is one of significant factors to determine the prognosis of cerebral ischemic stroke. We reported that polycyclic aromatic hydrocarbons, which are components of airborne particulate matter, activate immune cells and cause inflammation. Furthermore, inflammation in the central nervous system (CNS) reportedly induce rupture of blood-brain barrier, leading to vasogenic edema. Based on these findings, we have investigated the relationship between exposure to airborne particulate matter and the prognosis of ischemic stroke focusing on neuroinflammation and cerebral edema. In this symposium, we will report the effects of particulate matter collected in Beijing on pathophysiology of photothrombosis mouse models and would like to discuss the action of airborne particulate matter in the CNS.