Effects of ambient PM2.5 on pathological injury, inflammation, oxidative stress, metabolic enzyme activity, and expression of c-fos and c-jun in lungs of rats.

Fine particulate matter (PM2.5) exposure is associated with morbidity and mortality induced by respiratory diseases and increases the lung cancer risk. However, the mechanisms therein involved are not yet fully clarified. In this study, the PM2.5 suspensions at different dosages (0.375, 1.5, 6.0, and 24.0 mg/kg body weight) were respectively given to rats by the intratracheal instillation. The results showed that PM2.5 exposure induced inflammatory cell infiltration and hyperemia in the lung tissues and increased the inflammatory cell numbers in bronchoalveolar lavage fluid. Furthermore, PM2.5 significantly elevated the levels of pro-inflammatory mediators including tumor necrosis factor-α (TNF-α), interleukin (IL)-6, IL-1β, and intercellular adhesion molecule 1 (ICAM-1) and the expression of c-fos and c-jun in rat lungs exposed to higher dose of PM2.5. These changes were accompanied by decreases of activities of superoxide dismutase and increases of levels of malondialdehyde, inducible nitric oxide synthase, nitric oxide, cytochrome P450s, and glutathione S-transferase. The results implicated that acute exposure to PM2.5 induced pathologically pulmonary changes, unchained inflammatory and oxidative stress processes, activated metabolic enzyme activity, and enhanced proto-oncogene expression, which might be one of the possible mechanisms by which PM2.5 pollution induces lung injury and may be the important determinants for the susceptibility to respiratory diseases.