Subnormal expression of cell‐mediated and humoral immune responses in progeny disposed toward a high incidence of tumors afterin uteroexposure to benzo[a]pyrene

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Abstract
Pregnant mice were exposed to 150 .mu.g benzo[a]pyrene (BaP)/g body wt during fetogenesis (days 11-17 of gestation) and the progeny were assayed for humoral and cell mediated immune responses at different time intervals after birth. Immature offspring (1-4 wk) were severely suppressed in their ability to produce antibody-(plaque-) forming cells (PFC) against sheep red blood cells (SRBC) and in the ability of their lymphocytes to undergo a mixed lymphocyte response (MLR). Lymphocytes from these progeny showed a moderate to weak capacity to inhabit production of colony-forming units (CFU) in host spleens following transfer with semiallogeneic bone marrow (BM) cells into lethally X-irradiated recipients syngeneic to the BM (in vivo graft-vs-host response, GVHR). A severe and sustained suppression in the MLR and the PFC response occurred from the 5th-10 mo. The in vivo GVHR, also subnormal later in life, was not as severely suppressed as the other 2 parameters. Tumor incidence in the BP-exposed progeny was 8-10-fold higher than in those encountering corn oil alone from 18-24 mo. of age. In utero exposure to the chemical carcinogen BaP altered development of components needed for establishing competent humoral and cell-mediated functions of the immune apparatus and led to severe and sustained postnatal suppression of the defense mechanism. The immodeficiency exhibited, particularly in the T-cell compartment (MLR, GVHR), before and during the increase in tumor frequency, may have provided a favorable environment for the growth of nascent neoplasms inducecd by BaP.