During the 1992 breeding season, eggs of bald eagles (Haliaeetus leucocephalus) were collected within a gradient of exposure to chlorinated hydrocarbon pollutants, particularly from pulp mill point sources, on the southern coast of British Columbia, Canada. Twenty-five eggs were placed in a laboratory incubator, of which 18 hatched; chicks were sacrificed within 24 h. Hatching success was not significantly different between eggs taken from pulp mill sites and reference sites. A hepatic cytochrome P4501A (CYP1A) cross-reactive protein was induced nearly sixfold in chicks from near a pulp mill at Powell River compared to those from a reference site (p Ͻ 0.05). Hepatic ethoxyresorufin-O-deethylase (EROD) and benzyloxyresorufin O-dealkylase (BROD) activities were also significantly elevated in chicks from nests located near pulp mills compared to reference sites (p Ͻ 0.0005 and p Ͻ 0.02, respectively). A hepatic CYP2B cross-reactive protein was threefold higher in chicks from pulp mill versus reference sites, but the difference was not significant. Residual yolk sacs of eggs collected near pulp mill sites contained greater concentrations of 2,3,7,8substituted polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) compared to reference areas. No significant differences in concentrations of polychlorinated biphenyls (PCBs), non-ortho congeners, and organochlorine pesticides occurred among sites. Regressions showed that the hepatic CYP1A cross-reactive protein and EROD and BROD activities were positively correlated with 2,3,7,8-TCDD, 2,3,7,8-TCDF, and toxic equivalents (TEQs WHO -World Health Organization toxic equivalence factors) in yolk sacs. No significant concentration-related effects were found for morphological, physiological, or histological parameters, such as chick growth, edema, or density of thymic lymphocytes. Using hepatic CYP1A induction as a biomarker, a no-observedeffect-level (NOEL) of 100 ng/kg and a lowest-observed-effect-level (LOEL) of 210 ng/kg TEQs WHO on a whole egg (wet weight basis) are suggested for bald eagle chicks. Keywords-Bald eagleEmbryotoxicity TCDD Non-ortho PCBs P450Chlorinated hydrocarbon effects on bald eagles Environ. Toxicol. Chem. 15, 1996 783 Environ. Toxicol. Chem. 15, 1996 J.E. Elliott et al. Environ. Toxicol. Chem. 15, 1996 J.E. Elliott et al.Council of Canada. This project was part of a Ph.D. project on toxicology of chlorinated hydrocarbons in British Columbia bald eagles.

A great blue heron colony located near a pulp mill in British Columbia failed to fledge young in 1987, with a concurrent sharp increase in polychlorinated dibenzo-p-dioxin (PCDD) and polychlorinated dibenzofuran (PCDF) levels in their eggs. In 1988 we tested the hypothesis that the PCDD and PCDF contamination caused reproductive failure by increasing mortality of the heron embryos in ovo. Pairs of great blue heron eggs were collected from three British Columbia colonies with low, intermediate, and high levels of dioxin contamination: Nicomekl, Vancouver, and Crofton, respectively. One egg of each pair was incubated under laboratory conditions at the University of British Columbia (UBC) while the other egg was analyzed for PCDDs and PCDFs. All incubated eggs were fertile. All eggs from the Nicomekl colony hatched, while 13 of 14 eggs from Vancouver and 12 of 13 eggs from Crofton hatched. Subcutaneous edema was observed in 4 of 12 chicks from Crofton and 2 of 13 chicks from Vancouver. No edema was seen in the chicks from Nicomekl. There was a small, but significant, negative regression of plasma calcium concentration, yolk-free body weight, tibia length, wet, dry, and ash weight, beak length, and kidney and stomach weight of the hatched chicks on the tetrachlorodibenzo-p-dioxin (TCDD) level of the paired eggs. Fewer down follicles were present on the heads of TCDD-contaminated chicks. Hence while dioxins did not cause mortality of the heron embryos in ovo, the depression of growth and the presence of edema are suggestive that dioxins at the levels found in the environment have an adverse effect on the development of great blue heron embryos.

Abstract-During the 1992 breeding season, eggs of bald eagles (Haliaeetus leucocephalus) were collected within a gradient of exposure to chlorinated hydrocarbon pollutants, particularly from pulp mill point sources, on the southern coast of British Columbia, Canada. Twenty-five eggs were placed in a laboratory incubator, of which 18 hatched; chicks were sacrificed within 24 h. Hatching success was not significantly different between eggs taken from pulp mill sites and reference sites. A hepatic cytochrome P4501A (CYP1A) cross-reactive protein was induced nearly sixfold in chicks from near a pulp mill at Powell River compared to those from a reference site (p Ͻ 0.05). Hepatic ethoxyresorufin-O-deethylase (EROD) and benzyloxyresorufin O-dealkylase (BROD) activities were also significantly elevated in chicks from nests located near pulp mills compared to reference sites (p Ͻ 0.0005 and p Ͻ 0.02, respectively). A hepatic CYP2B cross-reactive protein was threefold higher in chicks from pulp mill versus reference sites, but the difference was not significant. Residual yolk sacs of eggs collected near pulp mill sites contained greater concentrations of 2,3,7,8-substituted polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) compared to reference areas. No significant differences in concentrations of polychlorinated biphenyls (PCBs), non-ortho congeners, and organochlorine pesticides occurred among sites. Regressions showed that the hepatic CYP1A cross-reactive protein and EROD and BROD activities were positively correlated with 2,3,7,8-TCDD, 2,3,7,8-TCDF, and toxic equivalents (TEQs WHO -World Health Organization toxic equivalence factors) in yolk sacs. No significant concentration-related effects were found for morphological, physiological, or histological parameters, such as chick growth, edema, or density of thymic lymphocytes. Using hepatic CYP1A induction as a biomarker, a no-observedeffect-level (NOEL) of 100 ng/kg and a lowest-observed-effect-level (LOEL) of 210 ng/kg TEQs WHO on a whole egg (wet weight basis) are suggested for bald eagle chicks.

1993. Metabolizable energy of fish when fed to captive Great Blue Herons (Ardea herodias). Can. J. Zool. 71: 1767-1771. The efficiency with which the gross energy content of herring (Clupea harengus), mackerel (Scomber scombrus), and trout (Oncorhynchus mykiss) is metabolized was determined for 11 captive Great Blue Herons (Ardea herodias). There was a linear relationship between apparent metabolized energy and gross energy intake for the mackerel and trout. This relationship was lower and more variable for herring. Estimates of the apparent metabolizable energy coefficient for mackerel and trout were affected by the level of energy intake. Correcting for endogenous energy losses in the excreta yielded estimates of true metabolizable energy coefficients that were independent of gross energy intake. The true metabolizable energy coefficient of mackerel and trout did not differ and averaged 0.866 (SD = 0.014, n = 3 diets). Correcting for nitrogen retention did not improve the estimate of the metabolizable energy coefficient. The metabolizable energy coefficient of herring was highly variable and showed no consistent pattern in relation to energy intake.

The proliferation of peripheral blood lymphocytes, cultured with Con A, can be inhibited by ionizing radiation. Lymphocytes from patients with conditions associated with autoimmunity, such as rheumatoid arthritis, systemic lupus erythematosus and polymyositis, are more radiosensitive than those from healthy volunteers or patients with conditions not associated with autoimmunity. The nuclear material isolated from the lymphocytes of patients with autoimmune diseases is, on average, lighter in density than the nuclear material from most healthy controls. This difference in density is not related to increased sensitivity to ionizing radiation but the degree of post-irradiation change in density (lightening) is proportional to the initial density, i.e. more dense nuclear material always shows a greater upward shift after radiation. The recovery of preirradiation density of nuclear material, 1 h after radiation exposure, taken as an indication of DNA repair, correlates with the radiosensitivity of lymphocyte proliferation (Con A response); failure to return to pre-irradiation density being associated with increased sensitivity of proliferative response. These results require extension but, taken with previously reported studies of the effects of DNA methylating agents, support the idea that DNA damage and its defective repair could be important in the aetio-pathogenesis of autoimmune disease.