Background: Air pollution is a global issue not limited to areas with severe air pollution. PM (particulate matter) 2.5 lower than the current annual limit potentially remains harmful.

Objectives: To explore the effect of low-level PM2.5 exposure on the lungs, early pathological features, and potential novel therapeutic targets in progression.

Methods: Five-week-old male Balb/c mice (n=60) were exposed once daily to either low-level PM2.5 (10ug) or saline as the control for 4, 8 and 12 weeks (short, moderate and long term).

Results: Interestingly, low-dose PM2.5 exposure significantly induced airway hyperresponsiveness (AHR) regarding increased Rn (%) both in the short and long term (P<0.001 and P<0.05). As expected, short or moderate-term exposure to low-dose PM2.5 had no significant impact on ventilation function based on indexes (P>0.05). However, long-term exposure to low-dose PM2.5 increased Rn (P<0.05), indicating it induced airway resistance, mainly conducting airways. Differential cell counts from BALF showed low-dose PM2.5 significantly increased neutrophils in absolute and relative numbers after moderate and long-term exposure (P<0.001). Moreover, macrophages and eosinophils were only elevated by long-term PM2.5 exposure (P<0.05). Histological staining revealed inflammatory cell infiltration, increased collagen deposition around the large airway and thickness of smooth muscle layer rather than epithelium after long-term low PM2.5 exposure.

Conclusion: Low-dose PM2.5 exposure induced airway remodelling, impaired lung function and compliance in the long term. AHR and increased neutrophil-dominated inflammation occurred in the early stage of progression that could be therapeutically targeted.