Integrative characterization of fine particulate matter-induced chronic obstructive pulmonary disease in mice.

The impacts of ambient fine particulate matter (PM) on public health are a worldwide concern. Epidemiological evidence has shown that PM-triggered inflammatory cascades and lung tissue damage are important causes of chronic obstructive pulmonary disease (COPD). However, most laboratory studies of COPD have focused on animal models of cigarette smoke exposure or combined exposure to cigarette smoke and PM. Furthermore, a single method is used to evaluate the development of COPD without integrality. In this study, we investigated pulmonary pathophysiological alterations using integrated functional, morphological, and biochemical techniques and a mouse model exposed to PM alone for 3 months. Emphysema in this model was confirmed by reconstructed three-dimensional micro-CT images. Typical histopathological signs were neutrophil/macrophage infiltration and accumulation at 2 months after exposure and emphysema/atelectasis at 3 months. Respiratory mechanical parameters confirmed that PM caused a decline in respiratory function. PM also triggered complex cytokine profile changes in the lungs with characteristic inflammation-related tissue destruction. This study showed that chronic PM exposure impaired lung function, triggered emphysematous lesions, and induced pulmonary inflammation and airway wall remodeling. Most importantly, prolonged exposure to PM alone caused COPD in mice. These results improve the understanding of the mechanisms and mediators underlying PM-induced COPD.