Recently, many researchers paid more attentions to the association between air pollution and chronic obstructive pulmonary disease (COPD). Haze, a severe form of outdoor air pollution, affected most parts of northern and eastern China in the past winter. In China, studies have been performed to evaluate the impact of outdoor air pollution and biomass smoke exposure on COPD; and most studies have focused on the role of air pollution in acutely triggering symptoms and exacerbations. Few studies have examined the role of air pollution in inducing pathophysiological changes that characterise COPD. Evidence showed that outdoor air pollution affects lung function in both children and adults and triggers exacerbations of COPD symptoms. Hence outdoor air pollution may be considered a risk factor for COPD mortality. However, evidence to date has been suggestive (not conclusive) that chronic exposure to outdoor air pollution increases the prevalence and incidence of COPD. Cross-sectional studies showed biomass smoke exposure is a risk factor for COPD. A long-term retrospective study and a long-term prospective cohort study showed that biomass smoke exposure reductions were associated with a reduced decline in forced expiratory volume in 1 second (FEV1) and with a decreased risk of COPD. To fully understand the effect of air pollution on COPD, we recommend future studies with longer follow-up periods, more standardized definitions of COPD and more refined and source-specific exposure assessments.
ObjectiveTo investigate the changes of lung function after exposure to fine particulate matter (PM2.5) for 60 days and the expression of miR-146 in mice.MethodsThirty SPF BALB/c mice were treated with noninvasive tracheal instillation of fine particulate matter suspension at different doses (2.5 mg/kg, 5.0 mg/kg, 10.0 mg/kg) for 2 months (two times one week), the blank group and normal saline group were set as control groups. The mice were examined and killed on the next day after the last instillation. Histopathological changes of the lungs, pro-infammatory factors levels in the lung tissues, pulmonary functions and the relative expression of miR-146a and miR-146b in the lung tissues were detected.ResultsPeak inspiratory flow (PIF) and peak expiratory flow (PEF) were decreased significantly after PM2.5 exposure, however, lung resistance increased and maximal voluntary ventilation reduced from the general tendency without significant difference. Hematoxylin-eosin stain showed lymphocyte infiltration and macrophage infiltration by phagocytic particles, alveolar spacer widening, inflammatory response increased with the increase of PM2.5 exposure dosage. Pro-infammatory factors as interleukin-6 in the bronchoalveolar lavage fluid, interferon-γ and tumor necrosis factor-α in the lung homogenate were increased significantly by enzyme linked immunosorbent assay. The relative expressions of miR-146a and miR-146b were up-regulated remarkablely in treatment groups compared to the control group by real-time fluorescence quantitative polymerase chain reaction, which had negative relationships with PIF and PEF.ConclusionsThe lung function of mice decreases significantly after exposure to fine particulate matter, and the expression of miR-146 is up-regulated.