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.