Abstract
Experiments in rodents indicate that during the post-embryonic period of prenatal development, the fetus is more sensitive than the adult to certain carcinogens, by several decimal orders of magnitude. Most such agents are direct-acting and independent of metabolism. To other substances, often those which require enzyme-mediated metabolic conversion to a chemically reactive derivative in order to effect carcinogenesis, the fetus may be less vulnerable than the adult. The neonate is also more susceptible than adults to some carcinogens, and may be more susceptible than the fetus to certain agents. Both rodent and primate studies indicate that gravid females are also at elevated risk for carcinogenesis, in part because of the presence in the placenta of trophoblastic tissue which may become malignant. The contributions of rapid growth rate, changing metabolic competence, and tissue differentiation to elevated perinatal susceptibility to carcinogens in rodents and primates are discussed, together with the implications of these findings for human beings subjected to industrial or environmental exposures to such chemicals.