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

Hanspeter WITSCHI 嵯峨井 勝

出版者

Japan Society for Atmospheric Environment

雑誌

大気汚染学会誌 (ISSN:03867064)

巻号頁・発行日

vol.24, no.1, pp.1-20, 1989-02-20 (Released:2011-11-08)

参考文献数

106

被引用文献数

1

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近年, 日本人のがんによる死亡率のうちで肺がんによる死亡率が著しく増加してきている。この増加の主な原因は喫煙や食品によるものと考えられているが, 都鄙間の比較や腺がんの割合の増加などから, 喫煙や食品だけでは説明が付かない点がある。そのようなことから, 大気汚染の影響を危惧する意見もあり, 例えば, ジーゼル排気ガス等の影響についてはある程度明らかになりつつある。ここでは, その化学的反応性の故に発がんに対する影響が危惧されているオゾン (O3) と二酸化窒素 (NO2) の2つのオキシダント様大気汚染ガスの肺がん発生に及ぼす影響に関する最近の知見とその問題点について科学的検討を加えた。

著者

嵯峨井 勝

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.74, pp.19004, 2019 (Released:2019-08-20)

参考文献数

83

被引用文献数

3 8

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Recently, the main air pollutant has been fine particulate matter (PM2.5), which is taken up by the whole body with severe adverse health effects. The main chemical components of PM2.5 are salts of sulfate (and nitrate) and carbons. However, it remains unknown which components are toxic. Here, the author reviewed the literatures to determine which components are toxic and the main mechanisms underlying their toxicity. Many epidemiological studies have shown that sulfate concentration is strongly related to mortality. However, there is no experimental evidence showing that sulfate at environmental concentrations of PM2.5 causes cardiovascular disease or other disease. On the other hand, carbon components such as elementary carbon (EC) produces high concentrations of reactive oxygen species (ROS) via its phagocytosis by macrophages, and organic carbon (OC) also produces high concentrations of ROS during its metabolic processes, and the ROS cause acute and chronic inflammation. They cause many diseases including cardiovascular disease, asthma and cancer. Furthermore, there are many lines of evidence showing that epigenetic changes such as DNA methylation or microRNA expression induced by particulate matters also induce the development of many diseases such as those mentioned above. It has been reported that carbon components are incorporated into the brain and produce ROS, and that the ROS cause damage to brain cells and Alzheimer’s disease and cognitive disorders in the elderly.From these lines of evidence, the author would like to emphasize that the main toxicity of PM2.5 is due to carbon components, and it is important to take countermeasures to decrease the concentration of carbon components in ambient air.

著者

佐藤 伸 向井 友花 嵯峨井 勝

雑誌

日本衞生學雜誌 (ISSN:00215082)

巻号頁・発行日

vol.63, no.2, 2008-03-01

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.