Oxidative stress derived from airborne fine and ultrafine particles and the effects on brain-nervous system: part 1.

Traffic-related air pollution is a major contributor to urban air pollution. Diesel exhaust (DE) is the most important component of near-road and urban air pollution and is commonly used as a surrogate model of air pollution in health effects studies. In particular, diesel exhaust particles (DEP) and the nanoparticles in DEP are considered hazardous components on health effects. It is widely known that exposure to DEP is associated with mortality due to respiratory and cardiovascular diseases. Recently, there has been accumulating evidence that DEP and the nanoparticles in DEP may be causes of neurodegenerative disorders. Here, we introduce the evidence suggesting their association with such disorders. First, we describe the chemical components and the translocation of DEP and nanoparticles to the brain, and then introduce the evidence and a mechanism by which reactive oxygen species (ROS) and any inflammatory mediators can be produced by DEP phagocytosis of macrophages, microglia and astrocyte cells in the brain. There are many lines of evidence showing that the neurodegenerative disorders are profoundly associated with enhanced oxidative and inflammatory events. Second, we describe a mechanism by which neurodegenerative diseases, such as stroke, Alzheimer's disease and Parkinson's disease, are induced via oxidative stress and inflammatory events.