Pregnant mice were given one of three treatment regimens during mid (11 to 13 d) or late (16 to 18 d) gestation: benzo[a]pyrene (BaP) (150 μg/g body weight), 150 R X‐irradiation, or X‐irradiation + BaP. A group of virgin mice were injected with BaP after birth (at 1 wk or 16 wk) with doses similar to or higher than those to which progeny of pregnant mice were exposed in utero. The offspring exposed during fetal life showed a marked suppression in anti‐SRBC plaque‐forming cells (PFC) 1 wk after birth (pups), followed by an apparent recovery at 4 wk. Return to the immuno‐suppressed state seen in pups was most noticeable in adults encountering BaP alone during gestation. In this group, increased tumor incidence was associated with a sustained reduction in PFC response. In contrast, after fetal exposure to X‐rays or injection with BaP postnatally, immune competence was not appreciably different from normal in late life and tumor incidence was only slightly higher than controls with X‐rays or a high dose (150 μg/g body weight) of BaP. When X‐rays were given in conjunction with BaP, it appeared that immune suppression was abated and tumor incidence reduced. The effect of BaP on PFC and tumor incidence varied according to the time in gestation when the carcinogen was given. After mid‐gestation insult, immune suppression was most pronounced in 19S PFC, while after late gestation, suppression was more severe in 7S antibody formation. The liver was the primary target for tumor growths in males. In females, a high incidence of ovarian tumors was seen, but only after mid‐gestation exposure. The frequency of lung tumors increased following late gestation insult in both sexes. These data show that (1) susceptibility to injury of different components of the developing humoral immune system and the disposition of the sexes for tumor induction are functions of the gestationai time of exposure to BaP, and (2) animals exposed prenatally to the carcinogen are more sensitive to immune suppression and increased tumor incidence than those exposed postnatally. The results support the contention that immune deficiency (suppression) influences the increase in neoplastic expression.