Abstract
While the health effects of air pollution have been an international public health concern since at least the 1950s, recent research has focused on two broad sources of air pollution, namely, biomass fuel (BMF) and motor vehicle exhaust (MVE). Many studies have shown associations between air pollution PM and exacerbations of pre-existing COPD, but the role of air pollution PM in the development and progression of COPD is still uncertain. The current study indicates that rats can develop pronounced COPD following chronic exposure to air pollution PM (BMF and MVE), as characterized by lung function reduction, mucus metaplasia, lung and systemic inflammation, emphysema, and small airway remodeling. Comparative analyses demonstrate that both BMF and MVE activate similar pathogenesis that are linked to the development of COPD. These findings also show that some differences are found in the lungs of rats exposed to BMF or MVE, which might result in different phenotypes of COPD.
Highlights
Inhalable particulate matter (PM), a major component in air pollution, in the fine and ultrafine ranges has been implicated as having a detrimental role in the pathogenesis of COPD
PM mass concentrations and particle size distributions were measured during air pollution PM exposure
For the first time, that a rat model of air pollution PM-induced COPD, especially motor vehicle exhaust (MVE)-induced COPD, can be successfully established and that air pollution PM-exposed rats develop changes in their airways that are consistent with those occurring in human
Summary
Inhalable particulate matter (PM), a major component in air pollution, in the fine and ultrafine ranges (diameter
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