Interleukin (IL)-1, a pro-inflammatory cytokine, is expressed in the lung following ozone (O₃) exposure. IL-1 mediates its effects through the type I IL-1 receptor (IL-1RI), the only signaling receptor for both IL-1 and IL-1. The purpose of this study was to determine the role of IL-1RI in pulmonary responses to O₃. To that end, wildtype, C57BL/6 (IL-1RI^+/+) mice and IL-1RI-deficient (IL-1RI^-/-) mice were exposed to O₃ either subacutely (0.3 ppm for 72 h) or acutely (2 ppm for 3 h). Subacute O₃ exposure increased bronchoalveolar lavage fluid (BALF) protein, IP-10, sTNFR1, and neutrophils in IL-1RI^+/+ and IL-1RI^-/- mice. With the exception of IP-10, all outcome indicators were reduced in IL-1RI^-/- mice. Furthermore, subacute O₃ exposure increased IL-6 mRNA expression in IL-1RI^+/+, but not IL-1RI^-/- mice. Acute (2 ppm) O₃ exposure increased BALF protein, IL-6, eotaxin, KC, MIP-2, IP-10, MCP-1, sTNFR1, neutrophils, and epithelial cells in IL-1RI^+/+ and IL-1RI^-/- mice. For IL-6, eotaxin, MIP-2, and sTNFR1, there were small, but significant reductions of these outcome indicators in IL-1RI^-/- versus IL-1RI^+/+ mice at 6 h after exposure, but not at other time points, whereas other outcome indicators were unaffected by IL-1RI deficiency. These results suggest that IL-1RI is required for O₃-induced pulmonary inflammation during subacute O₃ exposure, but plays a more minor role during acute O₃ exposure. In addition, these results suggest that the induction of IL-6 via IL-1RI may be important in mediating the effects of O₃ during subacute exposure.