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Particulate matter 2.5 (PM 2.5) exposure can increase the prevalence of allergic rhinitis (AR), the mechanism underlying which may include oxidative stress and inflammatory response. As a ROS quenching agent, N -acetylcysteine (NAC) can attenuate the accumulation of inflammatory cells and hyper-responsiveness in animal asthma models. To explore the effect of NAC on the oxidative stress and inflammatory reactions in AR rats exposed to PM 2.5 , we analyzed the components of PM 2.5 and examined the nasal symptoms, redox level in nasal mucosa, Th1/Th2-related serum cytokines, nasal mucosal histopathology and ultrastructure in AR rat models with NAC intervention after PM 2.5 exposure. The results showed that the high concentrations of metal cations and PAHs in PM 2.5 could aggravate Th2-dominant allergic inflammation in AR model and cause redox imbalance, accompanied by nasal epithelial cell stripping and eosinophil infiltration, while NAC intervention could alleviate the clinical symptoms of AR model after PM 2.5 exposure, correct the redox imbalance, reduce the Th2 cytokines, reduce eosinophil infiltration, and promote the moderate regeneration of epithelial cells. The mechanism of NAC reversing PM 2.5 -mediated action may be related to its anti-oxidant and anti-inflammatory effects, which may provide some new insights for the prevention of AR exacerbated by exposure to PM 2.5. • PM 2.5 can aggravate allergic rhinitis. • The chemical composition of PM 2.5 can affect Th2 allergic inflammation. • NAC can relieve the symptoms of allergic rhinitis in rats after PM 2.5 exposure. • NAC can reverse the structural changes of epithelial cells after PM 2.5 exposure. [ABSTRACT FROM AUTHOR]