Abstract: Background　Allergic rhinoconjunctivitis is a common IgE-mediated disorder, and environmental pollution plays a significant role in its pathogenesis. PM2.5, characterized by its small particle size and strong adsorptive capacity, may exacerbate immune dysregulation by directly irritating mucous membranes or carrying allergens. However, the mechanisms underlying its impact on nasal-ocular co-allergy remain unclear. Objective　To establish a murine model of allergic rhinoconjunctivitis and investigate the effects of PM2.5 on the disease.Methods　Thirty-six female C57 mice (SPF grade) were randomly divided into control group, model group, and PM2.5 exposure group. On day 0, 4, 7, 14 and 21, the model group and the PM2.5 exposure group received 0.2 mL/piece intraperitoneal injection medicine containing OVA 100ug and adjuvant Al(OH)3 4 mg respectively. After an interval of 3 days, each eye and nose was dosed withb10 μL of 5% OVA for 5 consecutive days a week to induce allergic symptoms. The PM2.5 intervention group was performed with 10 μL of 0.05% PM2.5 for each eye and nose, 10-20 minutes later, 10 μL of 5% OVA was used for each eye and nose. In the sensitization and stimulation stage, the control group was replaced with equal amount of PBS. Ocular and nasal symptoms were observed and scored. The contents of OVA specific IgE(OVA-sIgE), IL-4, IL-17 and IL-18 in serum were detected by ELISA. The expressions of NLRP3 and TNF-α in eyelid conjunctiva and nasal mucosa were detected by Western blot. The expression of NLRP3 in eyelid conjunctiva and nasal mucosa of mice was detected by immunohistochemistry. Results　The nasal and ocular allergic symptoms were induced in both the model group and the PM2.5 exposure group, and the onset time of nasal and eye allergy in the PM2.5 exposure group was significantly earlier than that in the model group (P<0.05). The expression levels of OVA-sIgE, IL-4, IL-17 and IL-18 in the model group and the PM2.5 exposure group were significantly higher than those in the control group (P<0.05), and the expression of OVA-sIgE in the PM2.5 exposure group was significantly higher than that in the model group (P<0.05). Compared with the control group, the expression levels of NLRP3 and TNFa in the eyelid conjunctiva and nasal mucosa of the model group and the PM2.5 exposure group were significantly increased (P<0.05). The expression levels of NLRP3 and TNFa in eyelid conjunctiva and nasal mucosa of the PM2.5 exposure group were significantly increased compared with the model group (P<0.05). The expression of NLRP3 in the eyelid conjunctiva and nasal mucosa of the model group and the PM2.5 exposure group were significantly increased by immunohistochemistry.Conclusion　PM2.5 obviously accelerates the occurrence and aggravation of allergic rhinoconjunctivitis, and it may play a certain role in promoting the onset of allergic rhinoconjunctivitis through the NLRP3 signaling pathway.