Dioxin contamination and growth and development in great blue heron embryos

Abstract

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.

Biological effects of polychlorinated dibenzo‐p‐dioxins, dibenzofurans, and biphenyls in bald eagle (Haliaeetus leucocephalus) chicks

“…Previous studies in the British Columbia's Strait of Georgia used the great blue heron (Ardea herodias) as a sentinel species to assess wildlife exposure to PCDDs and PCDFs from bleached-kraft pulp mill and other forest industry sources that dominate industrial activity in that area [16]. Episodes of poor breeding success in the late 1980s were associated with sublethal effects on embryos, including edema, reduced body weight, and EROD (ethoxyresorufin O-deethylase) induction, which correlated well with TCDD levels [17][18][19]. Efforts by the pulp and paper industry to reduce PCDD and PCDF formation and release in effluents resulted by 1991 in significant decreases in contamination of heron eggs and improvements in the condition of embryos [19,20].…”

Importance of Proximity to Foraging Areas for the Pacific Great Blue Heron (Ardea herodias fannini) Nesting in a Developed Landscape

“…At one site near an industrial area at Crofton, biologists found extremely high levels of dioxins that may have caused eggshell thinning and reduced reproductive success (Elliott et al 1988 andWhitehead 1989;Sanderson et al 1994). Hart et al (1991) and Sanderson et al (1994) found that high levels of dioxins at the Crofton site, although not resulting in Great Blue Heron embryo mortality, may have had adverse effects on the development of the embryos. Dioxin levels have since declined significantly and are no longer a potential threat to herons (J.…”

Reproductive Effects in Birds Exposed to Pesticides and Industrial Chemicals

“…In addition to organochlorines as causative agents, heavy metals, petroleum hydrocarbons, and pesticides have been identified. Adverse effects on survival and hatchability of eggs are documented with bioaccumulation of dioxins (59,60) and selenium (61), both of which are pollutants more toxic to embryos than to adults and which bioaccumulate into yolk to concentrations that become toxic to embryos. Sublethal effects produced by these compounds include subcutaneous and cardiac edema and terata of the beak, axial skeleton, and heart.…”