The concurrent administration of a cocarcinogenic carrier particle such as ferric oxide (Fe2O3)and the polycyclic aromatic hydrocarbon lung carcinogen benzo[a]pyrene (BaP) results in a decreased latency and an increased incidence in the production of lung tumors in hamsters compared to the administration of BaP alone. The pulmonary alveolar macrophage (AM), the primary lung defense cell, has been shown to endocytize BaP, metabolize BaP to a more biologically active form, and then release the metabolites. Therefore, a study was undertaken to determine in a dose‐response manner the effect of AM phagocytosis of a carrier particle (Fe2O3)on the metabolism of a carcinogen (BaP) and on the production of reactive oxygen. The AM were lavaged from hamsters and cultured in suspension (2.5 x 106cells/vial) with BaP (62.5 nmol,14C labeled) alone or adsorbed onto 0.5, 1.0, or 2.0 mg Fe2O3in the presence of cytochromec. Following separate ethyl acetate extractions of the AM and medium, the metabolites were isolated by high‐performance liquid chromatography (HPLC) and quantified by liquid scintillation spectrometry. The production of superoxide anions was monitored by the reduction of cytochromec.