The biologic interactions of potentially fibrogenic agents commonly occurring as environmental pollutants remain to be rigorously characterized. Two agents that produce pulmonary fibrosis were selected for this study. Separate groups of male Sprague‐Dawley rats were intratracheally instilled with 0, 2, 12, and 50 mg silica and then either sham‐exposed or exposed to 0.8 ppm ozone 6 h/d, 5 d/w, for 37 exposure days. Interaction was not detected between silica and ozone in the development of pulmonary fibrosis as determined by quantitative biochemical indices (hydroxypro‐line and lysyl oxidase) or by histopathologic examination of the lungs. Thus, environmentally relevant levels of ozone appear unlikely to affect the progression of a concurrent silicotic lesion.