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ABSTRACT
Assessment of long-term studies on the carcinogenic potential of certain environmental agents has indicated that all of the following appear to activate and/or promote the inherent tumors of the host strains of the animals used irrespective of the extent of additional immunological modulation accompanying the agents: tobacco smoke inhalation, the implantation and inhalation of the respirable fraction of iron ore mine dusts, acute neonatal reovirus 3 infection, urethane, and tobacco smoke inhalation following urethane treatment. It is proposed that these environmental agents function at the onc-gene level as promoters/activators rather than carcinogens, and that this now requires an understanding of the means by which certain environmental agents function at the onc-gene level.
