A mechanism was proposed by which carcinogenesis can be explained as a byproduct of frustrated phagocytosis. The theory as advanced stated that enzymes involved in the processes of exocytosis and phagocytosis by neutrophils produce large amounts of the reactive superoxide radical which is very toxic. The dismutation products of this radical are hydrogen-peroxide and singlet oxygen which are also toxic. Ozone, a mutagen and considered radiomimetic is also associated with oxygen radicals. The author suggests that carcinogenesis by ionizing radiation, films, and fibers may be mediated by the same mechanism of oxygen radicals. When exocytosis occurs there is a danger that substantial amounts of oxygen radicals may emerge around the phagocyte edges. This danger is even greater when the foreign bodies being surrounded have smooth edges. Leaking oxygen radicals diffuse to nearby cells, injuring cell membranes to gain entry, and then reacting with DNA components before detoxification can occur. While some cells will be killed, others will have point mutations which can result in cancer. A modification of this process in application to fibers, but not to films, is that tissue motion may keep the free ends of fibers moving, allowing them to continue to puncture cell walls. During repeated attempts to phagocytize some types of foreign bodies, it is quite possible that sufficient reactive oxygen radicals would be liberated that fibrosis and tumor growth would occur. The common characteristics of such foreign bodies are their smoothness, flexibility, and a size too large for easy encompassing by phagocytes.