Comparative toxicity of polychlorinated biphenyls to Japanese quail (Coturnix c. japonica) and American kestrels (Falco sparverius).

Abstract

Polychlorinated biphenyls (PCBs) and related halogenated hydrocarbons bioaccumulate to high concentrations in top predators, such as raptorial birds, yet little is known of PCB toxicity to such species. This study 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 that of the Japanese quail (Coturnix c. japonica), a more studied species known to be PCB sensitive. In one experiment, adult female birds were given single oral doses of either Aroclor 1254, 3,3',4,4'-TCB (PCB 77, IUPAC nomenclature), 3,3',4,4',5-PCB (PCB 126) or 2,2',4,4',5,5'-HCB (PCB 153) and sacrificed after 5 d. In kestrels, neither the pure compounds nor the mixture affected hepatic or renal porphyrin levels. There was slight but significant hepatic and renal ethoxyresorufin O-deethylase (EROD) induction in birds dosed with PCBs 77 and 126. A cytochrome P-4501A (CYP1A) cross-reactive protein was detected in liver and kidney of kestrels given PCBs 77 and 126, but not in Aroclor 1254-dosed birds. In quail, an acute dose of Aroclor 1254 caused significant liver weight increases, hepatic and renal EROD and aminopyrine n-demethylase (APND) induction, and dose-related hepatic and renal porphyria. Quail treated with PCB 126 developed hepatic and renal porphyria; EROD and APND were also induced. Administration of PCB 77 caused only slight induction of hepatic EROD activity. PCB 153 caused some hepatic and renal porphyria and induced EROD to the same degree as PCB 126. A hepatic CYP1A cross-reactive protein was induced about 200-fold in all individual quail that exhibited significant EROD induction and was also induced in kidney of 1 quail given Aroclor 1254. A second experiment examined chronic exposure to Aroclor 1254 by feeding adult females of both species a daily dose of 7 mg/kg/d for 4-, 8-, and 12-wk periods. There 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 about 200-fold. In both studies, Aroclor 1254 residues accumulated in tissues of both species, but there was no significant relationship between residue levels and effects. In conclusion, adult American kestrels were relatively insensitive to the effects of PCBs, from both acute and chronic exposure, on hepatic and renal porphyrin levels. Although concentrations of a CYP1A-like protein were increased in some kestrels given PCBs, EROD activity was only marginally increased, suggesting that catalytic activity of this protein differed among the two species.