We hypothesized that indoor PM exposure from coal combustion exaggerates airway inflammation in the lung tissue of asthmatic mice induced with ovalbumin (OVA). Forty BALB/c mice, randomly divided into four groups ( = 10 per group), were intratracheally instilled with normal saline alone, PM (2.5 mg/ml PM alone), OVA (15 μg/ml OVA alone), and PM+OVA (2.5 mg/ml PM and 15 μg/ml OVA), respectively, four times at 2-wk intervals. Daily mean concentration of PM from indoor coal combustion was 156.95 μg/m. The highest metal composition in PM was Zn (34.81 ± 1.8 μg/m). Exposure to PM+OVA significantly elevated IL-4 and decreased IFN-γ production in mice compared with the control ( < 0.05). Exposure to PM+OVA showed a significant increase in the protein levels of granulocyte-macrophage colony-stimulating factor and IL-8 and a decrease in the protein level of transforming growth factor-β1 in bronchoalveolar lavage fluid of mice compared with the control ( < 0.05). The expression of IL-4 mRNA was significantly increased, whereas the expression of IFN-γ mRNA was decreased in lung tissue of the PM+OVA group ( < 0.05). The expression level of Foxp3 mRNA in the PM+OVA group was significantly lower than that in the control group in lung tissue ( < 0.05). Treatment with PM+OVA promoted a prominent neutrophil sequestration into the lung parenchyma, goblet cell proliferation, and severe inflammatory cell infiltration in the airways. Exposure to PM from indoor coal combustion might induce airway inflammatory immune responses and exacerbate peribronchiolar inflammation due to infiltration of inflammatory cells into the airway submucosa and airway structural pathological changes.