期刊
CELLULAR AND ENVIRONMENTAL STRESSORS IN BIOLOGY AND MEDICINE
卷 1340, 期 -, 页码 84-94出版社
BLACKWELL SCIENCE PUBL
DOI: 10.1111/nyas.12720
关键词
air pollution; particulate matter; oxidative stress; inflammation
资金
- MRC [MR/L01341X/1] Funding Source: UKRI
- Medical Research Council [MR/L01341X/1] Funding Source: Medline
Exposure to combustion-related particulate matter (PM), at concentrations experienced by populations throughout the world, contributes to pulmonary and cardiac disease through multiple mechanistic pathways that are complex and interdependent. Current evidence supports an interactive chain of events linking pollution-induced pulmonary and systemic oxidative stress, inflammatory events, and translocation of particle constituents with an associated risk of vascular dysfunction, atherosclerosis, altered cardiac autonomic function, and ischemic cardiovascular and obstructive pulmonary diseases. Because oxidative stress is believed to play such an instrumental role in these pathways, the capacity of particulate pollution to cause damaging oxidative reactions (the oxidative potential) has been used as an effective exposure metric, identifying toxic components and sources within diverse ambient PM mixes that vast populations are subjected to-from traffic emissions on busy roads in urban areas to biomass smoke that fills homes in rural areas of the developing world.
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