Neurotoxicity of traffic-related air pollution

被引:276
作者
Costa, Lucio G. [1 ,2 ]
Cole, Toby B. [1 ,3 ]
Coburn, Jacki [1 ]
Chang, Yu-Chi [1 ]
Dao, Khoi [1 ]
Roque, Pamela J. [1 ]
机构
[1] Univ Washington, Dept Environm & Occupat Hlth Sci, 4225 Roosevelt,Suite 100, Seattle, WA 98105 USA
[2] Univ Parma, Dept Neurosci, Parma, Italy
[3] Univ Washington, Ctr Human Dev & Disabil, Seattle, WA 98195 USA
关键词
Traffic-related air pollution; Diesel exhaust; Neurotoxicity; Oxidative stress; Neuro-inflammation; Neurodevelopmental disorders; Neurodegenerative diseases; AUTISM SPECTRUM DISORDERS; DIESEL EXHAUST PARTICLES; PARTICULATE MATTER; PARKINSONS-DISEASE; ALZHEIMERS-DISEASE; BRAIN INFLAMMATION; OXIDATIVE STRESS; ENGINE EXHAUST; YOUNG-ADULTS; NEURODEGENERATIVE DISEASE;
D O I
10.1016/j.neuro.2015.11.008
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The central nervous system is emerging as an important target for adverse health effects of air pollution, where it may contribute to neurodevelopmental and neurodegenerative disorders. Air pollution comprises several components, including particulate matter (PM) and ultrafine particulate matter (UFPM), gases, organic compounds, and metals. An important source of ambient PM and UFPM is represented by traffic-related air pollution, primarily diesel exhaust (DE). Human epidemiological studies and controlled animal studies have shown that exposure to air pollution, and to traffic-related air pollution or DE in particular, may lead to neurotoxicity. In particular, air pollution is emerging as a possible etiological factor in neurodevelopmental (e.g. autism spectrum disorders) and neurodegenerative (e.g. Alzheimer's disease) disorders. The most prominent effects caused by air pollution in both humans and animals are oxidative stress and neuro-inflammation. Studies in mice acutely exposed to DE (250-300 mu z/m(3) for 6 h) have shown microglia activation, increased lipid peroxidation, and neuroinflammation in various brain regions, particularly the hippocampus and the olfactory bulb. An impairment of adult neurogenesis was also found. In most cases, the effects of DE were more pronounced in male mice, possibly because of lower antioxidant abilities due to lower expression of paraoxonase 2. (C) 2015 Elsevier B.V. All rights reserved.
引用
收藏
页码:133 / 139
页数:7
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