Objective To investigate whether airway inhalation of a PM2. 5 suspension at carious concentrations activates the NLRP3 inflammasome in rat myocardial tissue to induce cardiac damage and provide a reference to research drug treatments. Methods SD rats were randomly divided into a control group (Sham) and low (Low, 7. 5 mg/ kg), middle (Middle, 15 mg/ kg), and high (High, 30 mg/ kg) exposure groups with seven in each group. The exposure groups were instilled with the corresponding dose of suspension (1 mL/ kg) through a non-exposed trachea once every 6 days for 2 months, and rats in the Sham group were instilled with the same amount of normal saline. Physiological status was recorded daily. After the last infusion, the rats were fasted for 12 hours and then anesthetized with 1% sodium pentobarbital (50 mg/ kg). The cardiac function status was reflected by pathological sections of myocardial tissue, myocardial cell apoptosis, and changes in myocardial enzymes. Bcl-2 and Bax protein expression, and NLRP3, Caspase-1, and IL-1β protein and mRNA expression in myocardial tissue, and serum IL-1β, IL-6, TNF-α, and IL-18 levels reflected the NLRP3 inflammasome activation status in myocardial tissue. Results After instillation of various doses of PM2. 5 suspension, the rats in exposure groups became yellow, dull, and had decreased activity to varying degrees. There was no significant effect on diet or body weight. Decreased, irregular arrangement, nuclear pyknosis, edema. Compared with the Sham group, CK, LDH, and AST levels in myocardial tissue, Bcl-2 and IL-1β protein expression, NLRP3, IL-1β, and Caspase-1 mRNA expression, serum of IL-1β and IL-6. IL-18 and TNF-α levels were significantly increased, Bax protein expression, and the Bcl-2/ Bax ratio were decreased significantly. Cardiomyocyte apoptosis in Middle and High groups was significantly increased, and NLRP3 and Caspase-1 protein expression was significantly increased. Significantly increased; myocardial tissue apoptosis in the Low group and NLRP3 and Caspase-1 protein expression were not significantly different from those in the Sham group. Conclusions PM2. 5 exposure causes structural damage in myocardial cells, activates the NLRP3 inflammasome, promotes expression of proinflammatory factors and apoptotic proteins, and disrupts myocardial tissue functions.