著者

嵯峨井 勝 ウィンシュイ ティンティン

出版者

一般社団法人日本衛生学会

雑誌

日本衛生学雑誌 (ISSN:00215082)

巻号頁・発行日

vol.70, no.3, pp.220-229, 2015 (Released:2015-09-26)

参考文献数

47

被引用文献数

7 8

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Traffic-related air pollution is a major contributor to urban air pollution. Diesel exhaust (DE) is its most important component of near-road and urban air pollutions and is commonly used as a surrogate model of air pollution in health effects studies. In particular, diesel exhaust particles (DEPs) and nanoparticles in DEPs are the components considered hazardous for health. It is widely known that exposure to DEPs is associated with mortality caused by respiratory and cardiovascular diseases. Recently, evidence has been accumulating showing that DEPs and nanoparticles may cause neurodegenerative disorders. Here, we introduce evidence suggesting their association with these disorders. The chemical components and the translocation of DEPs and nanoparticles to the brain are described in part 1. In part 2, we introduce the mechanism of development of neurodegenerative diseases such as stroke, Alzheimer’s disease, and Parkinson’s disease via oxidative stress and inflammatory events. Furthermore, there are many lines of epidemiological evidence showing that the particulates impair cognitive function and ability of memory through oxidative and inflammatory events in the brain. These lines of evidences are supported by many animal experiments on neurological disorders.

著者

嵯峨井 勝 ウィンシュイ ティンティン

出版者

日本衛生学会

雑誌

日本衛生学雑誌 (ISSN:00215082)

巻号頁・発行日

vol.70, no.2, pp.127-133, 2015 (Released:2015-05-21)

参考文献数

37

被引用文献数

1

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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.