Abstract

The immunotoxic potential of a commercial polybrominated diphenyl ether (PBDE; Bromkal 70–5 DE) was compared with that of a commercial polychlorinated biphenyl (PCB; Aroclor 1254) in orally exposed rats and mice. In addition, mice were exposed to the PBDE congener 2,2’,4,4'‐tetrabromodiphenyl ether (TBDE), or to the PCB congener 2,3,3’,4,4'‐pentachloro‐biphenyl (CB‐105). The animals were given daily oral administrations of PCB (10 mg/kg body weight) or of PBDE (18 or 36 mg/kg body weight) for 14 days, which, in case of the lower PBDE dose, would result in approximately the same molar exposure for the two compounds. Liver weights were significantly higher in all of the exposed groups, except for rats exposed to the lower dose of PBDE, indicating induction of hepatic enzymes. In rats, exposure to Aroclor 1254 caused decreased thymus weights and cellularity, and flow cytometry studies showed an increased proportion of CD8+ and a decreased proportion of CD4‐CD8— (immature) cells in thymi. In mice, exposure to TBDE, as well as to Aroclor 1254 and the single PCB congener CB‐105, reduced the numbers of splenocytes. The reduced splenocyte numbers were reflected in decreased numbers of CD45R+, CD4+ and CD8+ cells in spleens from animals in these groups. Polyclonal IgG synthesis in vitro by pokeweed‐stimulated splenocytes from mice was significantly lower in cultures from animals exposed to the highest dose of Bromkal, as well as in animals exposed to Aroclor 1254. The present study shows that oral exposure of rats and mice to PCB induces certain immunological alterations in both species, while signs of immunotoxicity after PBDE exposure were only observed in mice. The results indicate that Bromkal may be less potent as an immunotoxin than Aroclor 1254.

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