Abstract-Effects of PCBs were studied in common terns (Sterna hirundo).Hatchlings from eggs collected from Dutch breeding colonies and incubated artificially were raised to an age of 21 d. The birds were fed fish spiked with PCB 126 alone or in combination with PCB 153 (1:1,000), resulting in concentrations in the food ranging from 0.01 to 1.2 ng toxic equivalents (TEQs)/g wet weight.The most sensitive effect parameter was induction of hepatic CYP1A-associated ethoxyresorufin-O-deethylation (EROD) activity, and a nonlinear concentration-effect relationship could be determined with the TEQ concentration (r ϭ 0.967, p Ͻ 0.001). Induction of pentoxyresorufin-O-depenthylation and methoxyresorufin-O-demethylation activities was observed at dose levels similar to those that induced EROD activity. The estimated lowest-observed-effect level for induction of CYP1A in the common tern was approx. 25 ng TEQ/g liver lipid, which was caused by concentrations in the food of approx. 0.6 ng TEQ/g fish wet weight. At these concentrations, a 50% reduction in plasma total thyroxine compared with controls also was observed. Concentrations of plasma total thyroxine were negatively correlated with hepatic TEQ concentrations (r ϭ 0.523, p Ͻ 0.01), but the shape of the nonlinear concentration-effect relationship did not allow determination of a lowest-observed-effect level. No changes were found for hepatic hydroxylation of testosterone. Bursa weight decreased proportionally to hepatic concentrations of TEQs (r ϭ 0.433, p Ͻ 0.05) and showed a similar sensitivity as that observed for EROD activity. Concentrations of TEQs in The Netherlands are approx. 0.1 ng TEQ/g wet weight fish, which is approximately six times lower than the lowest-observed-effect level for CYP1A induction in terns as estimated in this study. It is concluded that no overt effects on growth and development in the common tern are expected with this background exposure during the posthatch period.

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Six groups of C57BL/6J mice received single oral doses of 1.5-10.6 nmol/kg 1,2,3,7,8-pentachlorodibenzo-p-dioxin (PnCDD), 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin (HxCDD) or 2,3,4,7,8-pentachlorodibenzofuran (PnCDF) as single compounds or in combination with 300 mumol/kg 2,2',4,4',5,5'-hexachlorobiphenyl (HxCB). Two other groups of mice received a mixture of the first three compounds, either with or without HxCB. The hepatic deposition and elimination of the compounds and their CYP1a dependent 7-ethoxyresorufin-O-deethylation (EROD) activity were studied until day 175. Interactive effects on the hepatic deposition of PnCDD were observed in most of the mixed dose groups. For HxCDD and PnCDF interactive effects were either very small or absent. No interactive effects were observed on hepatic elimination rates of PnCDD, HxCDD or PnCDF. No evidence was found for the influence of HxCB cotreatment on the hepatic concentration-response curves of the three compounds or their mixture. Based on the results from the present study it is concluded that PCDDs, PCDFs and PCBs may influence each other's, toxicokinetics when administered in mixtures.

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