Abstract
Pregnant mice were 1-3 treated mid (11-13 days) or late (16-18 days) gestation with benzo[a]pyrene (BaP) (150 .mu.g/g body weight), 150 R X-irradiation, or X-irradiation + BaP. 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. The offspring exposed during fetal life showed a marked suppression in anti-SRBC [sheep red blood cell] plaque-forming cells (PFC) 1 wk after birth (pups), followed by an apparent recovery at 4 wk. Return to the immunosuppressed 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. 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 slightly higher than controls with X-rays or 150 .mu.g/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. 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. 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 gestational time of exposure to BaP. Animals exposed prenatally to the carcinogen are more sensitive to immune suppression and increased tumor incidence than those exposed postnatally. Immune deficiency (suppression) influences the increase in neoplastic expression.