Polychlorinated biphenyls (PCB), which are
tumor promoters, have been found in human tissues for decades. Their contribution to
cancer risk may only now start to appear, due to long human
cancer latency and the nature of
tumor promotion. Epidemiological associations have been seen between PCB exposure or tissue content and
cancer at several sites. In rodents,
tumor promotion by
PCBs has been little studied in tissues other than liver. Previously, in an experiment modeling infant
carcinogen exposure following
PCBs received in milk, lung and liver
tumors, initiated neonatally in mice by the environmental
nitrosamine N-nitrosodimethylamine (NDMA), were promoted by later treatment with
Aroclor 1254. The present study was undertaken to confirm and characterize the effects of
Aroclor 1254 on
tumor number, latency, size and
malignancy. Male Swiss mice were given NDMA on postnatal day 4 and
Aroclor 1254 (250 mg/kg) on day 8, and killed at intervals. Eight PCB congeners were quantified in the carcasses. Incidences of mice with NDMA-initiated lung
tumors at 28 weeks of age were increased 2.5-fold by
PCBs. Multiplicities of lung
tumors were enhanced four-fold by
PCBs at 28 and 52 weeks. By 72 weeks
tumor numbers were similar in the NDMA-only and NDMA-PCB groups. Liver
tumors first occurred in significant numbers at 52 weeks and only in mice receiving both NDMA and
PCBs. As for the lung, at 72 weeks the incidence was high in both the NDMA-only and NDMA-PCB groups. Sizes of
tumors and liver
carcinoma incidence were not altered by PCB treatment. Carcass analysis revealed a significant positive association between lung
tumor numbers at 28 weeks and relative percentage of
2,2',4,4',5-pentachlorobiphenyl, with no other correlations. The results confirm that
PCBs promote lung as well as liver
tumors, by triggering the early appearance of latent initiated
tumors otherwise presenting in old age.