COMPARATIVE TOXICITY OF POLYCHLORINATED-BIPHENYLS TO JAPANESE-QUAIL (COTURNIX CAMELLIA-JAPONICA) AND AMERICAN KESTRELS (FALCO-SPARVERIUS)

Polychlorinated biphenyls (PCBs) and related halogenated hydrocarbons bioaccumulate to high concentrations in top predators, such as raptori al birds, yet little is known of PCB toxicity to such species. This st udy explored several aspects of both the acute and chronic response of American kestrels (Falco sparverius) to three purified PCB congeners and a commercial mixture, Aroclor 1254, and compared the response to t hat of the Japanese quail(Coturnix c. japonica), a more studied specie s known Co be PCB sensitive. In one experiment, adult female birds wer e given single oral doses of either Aroclor 1254, 3,3',4,4'-TCB (PCB 7 7, IUPAC nomenclature), 3,3',4,4',5-PCB (PCB 126) or 2,2',4,4',5,5'-HC B (PCB 153) and sacrificed after 5 d. In kestrels, neither the pure co mpounds nor the mixture affected hepatic or renal porphyrin levels. Th ere was slight but significant hepatic and renal ethoxyresorufin O-dee thylase (EROD) induction in birds dosed with PCBs 77 and 126. A cytoch rome P-4501A (CYP1A) cross-reactive protein was detected in liver and kidney of kestrels given PCBs 77 and 126, but not in Aroclor 1254-dose d birds. In quail, an acute dose of Aroclor 1254 caused significant li ver weight increases, hepatic and renal EROD and aminopyrine n-demethy lase (APND) induction, and dose-related hepatic and renal porphyria. Q uail treated with PCB 126 developed hepatic and renal porphyria; EROD and APND were also induced. Administration of PCB 77 caused only sligh t induction of hepatic EROD activity. PCB 153 caused some hepatic and renal porphyria and induced EROD to the same degree as PCB 126. A hepa tic CYP1A cross-reactive protein was induced about ZOO-fold in all ind ividual quail that exhibited significant EROD induction and was also i nduced in kidney of I quail given Aroclor 1254. A second experiment ex amined chronic exposure to Aroclor 1254 by feeding adult females of bo th species a daily dose of 7 mg/kg/d for 4-, 8-, and 12-wk periods. Th ere were no effects on hepatic porphyrins in kestrels. APND and aldrin epoxidase (AE) were induced; EROD was not induced, although a hepatic CYP1A-like protein was detected in 1 kestrel dosed for 12 wk. Chronic exposure of quail to Aroclor 1254 caused highly significant increases in mean hepatic porphyrin levels and in activity of EROD, APND, and 4 -chlorobiphenyl hydroxylase; a CYP1A-like protein was also induced abo ut 200-fold. In both studies, Aroclor 1254 residues accumulated in tis sues of both species, but there was no significant relationship betwee n residue levels and effects. In conclusion, adult American kestrels w ere relatively insensitive to the effects of PCBs, from both acute and chronic exposure, on hepatic and renal porphyrin levels. Although con centrations of a CYP1A-like protein were increased in some kestrels gi ven PCBs, EROD activity was only marginally increased, suggesting chat catalytic activity of this protein differed among the two species.