Air pollution exacerbates movement disorders after stroke

Air pollution has been shown to have a negative effect on the prognosis of ischemic stroke, or stroke caused by reduced blood flow to the brain, but the exact mechanisms are unknown. A research team recently conducted a study to determine whether increased brain inflammation, also known as neuroinflammation, is the main cause.

The team published their findings in the February 16, 2023 issue Particle and Fiber Toxicology.

Mice exposed intranasally to urban aerosols from Beijing, China, for one week showed increased neuroinflammation and worsening movement disorders after ischemic stroke, compared with control mice not exposed to air pollution. In addition, this effect was not observed in aerosol-treated urban mice that lack receptors for chemicals released by burning fossil fuels, wood, garbage, and tobacco, called polycyclic aromatic hydrocarbons (PAHs). This suggests that PAHs are involved in neuroinflammation and increased movement disorders associated with air pollution exposure in ischemic stroke.

“We designed this study to determine the effects of air pollution on disorders of 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 narrower focus is to determine whether the ischemic stroke prognosis is affected by air pollution or not,” said Ishihara.

The group went a step further by identifying specific components of air pollution that may directly contribute to a lower prognosis in ischemic stroke.

They found evidence that exposure to intranasal 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 disorder also has a negative impact on ischemic stroke rats exposed to the same air pollution. A second series of experiments replacing Beijing air pollution with PM2.5 (small aerosol particles of air pollution with a width of 2.5 microbes or less) from Yokohama, Japan showed similar results, showing that the PM2.5 fraction of urban air pollution contains chemicals. responsible for increased neuroinflammation and decreased ischemic stroke prognosis.

To identify the chemicals in air pollution that are responsible for the reduced prognosis of ischemic stroke, the research team used mice lacking aryl hydrocarbon receptors, receptors that are activated by the presence of PAHs, to determine whether or not they were exposed to Beijing air pollution. would have the same effect in rats without working aryl hydrocarbon receptors. Mice lacking aryl hydrocarbon receptors displayed less microglial cell activation and movement disorders compared to normal mice, suggesting that PAHs present in Beijing air pollution are responsible for at least some neuroinflammation and the lower prognosis seen in ischemic stroke mice exposed to air pollution.

Ultimately, the research team’s goal is to better understand the mechanism by which PM2.5 causes neuroinflammation, because air pollution is first inhaled into the respiratory tract. “Can tiny particles travel from the nose to the brain? Does pulmonary or systemic inflammation affect the brain’s immune system?” said Ishihara.

##

Other contributors include Nami Ishihara and Ami Oguro of the Biomedical Sciences Program at the Graduate School of Integrated Sciences for Life at Hiroshima University in Higashi-Hiroshima, Japan; Miki Tanaka of the Biomedical Sciences Program at the Graduate School of Integrated Sciences for Life at Hiroshima University and the Laboratory of Pharmacotherapy and Experimental Neurology at the Kagawa School of Pharmaceutical Sciences at Tokushima Bunri University in Sanuki, Japan; Kouichi Itoh of the Laboratory of Pharmacotherapy and Experimental Neurology at the Kagawa School of Pharmaceutical Sciences at Tokushima Bunri University; Tomoaki Okuda of the Faculty of Science and Technology at Keio University in Yokohama, Japan; Yoshiaki Fujii-Kuriyama of the Medical Research Institute in Molecular Epidemiology at Tokyo Medical and Dental University in Tokyo, Japan; Yu Nabetani of the Department of Applied Chemistry at the Miyazaki University School of Engineering in Miyazaki, Japan; Megumi Yamamoto of the Department of Environment and Public Health at the National Institute of Minamata Disease in Minamata, Japan; Christoph FA Vogel of the Department of Environmental Toxicology and the Center for Health and the Environment at the University of California Davis in Davis, California.

This work was supported by Research Fellowship for Young Scientists (Grant Number 20J10103), KAKENHI Grant from the Japanese Society for the Promotion of Science (Grant Number 21K06702, 20H04341, 17H04714, 15KK0024), Environmental Technology Research and Development Fund of the Japan Environmental Restoration and Conservation Agency ( Grant Numbers JPMEERF20165051 and JPMEERF20205007) and the National Institute of Environmental Health Sciences (Grant Numbers R01ES029126 and R01ES032827).

About Hiroshima University

Since its establishment in 1949, Hiroshima University has strived to become one of the leading and most comprehensive universities in Japan for the promotion and development of scholarship and education. Comprising 12 undergraduate schools and 5 graduate schools, ranging from natural sciences to humanities and social sciences, the university has grown to become one of Japan’s leading comprehensive research universities. English website: https://www.hiroshima-u.ac.jp/en