Biological effects of polychlorinated dibenzo‐p‐dioxins, dibenzofurans, and biphenyls in double‐crested cormorant chicks (phalacrocorax auritus)

Abstract

The present project assessed the effect of environmental contamination with polychlorinated dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and biphenyls (PCBs) on hepatic microsomal ethoxyresorufin O-deethylase (EROD) activities and morphological parameters in matched double-crested cormorant (Phalacrocorax auritus) hatchlings from egg clutches chosen for chemical analysis. Double-crested cormorant eggs were collected from five colonies across Canada, with differing levels of contamination. Levels of contamination expressed in sum of 2,3,7,8-tetrachlorodibenzo-p-dioxin-toxic equivalents (TCDD-toxic equivalents or TEQ, ng/kg egg; mean +/- SEM) were: Saskatchewan, 250 +/- 50; Chain Islands, 672 +/- 73; Christy Islet, 276 +/- 14; Crofton, 131, n = 1; and Lake Ontario, 1606 +/- 118. In the hatchlings, hepatic EROD activities (pmol/min/mg protein; mean +/- SEM) were: Saskatchewan, 283 +/- 42; Chain Islands, 516 +/- 98; Christy Islet, 564 +/- 91; Crofton, 391 +/- 52; and Lake Ontario, 2250 +/- 156. Hepatic microsomal EROD activity (pmol/min/mg protein) regressed positively on TEQ (r2 = .69; p < .00005; n = 25). Yolk weight (g) regressed negatively on TEQ (r2 = .44; p = .00005). Wing length (mm) regressed negatively on PCB-169 (r2 = .28; p = .007). Monospecific antibodies raised against rat cytochrome P-450 1A1 recognized a protein in the hepatic microsomes of the double-crested cormorant, and also in those of the great blue heron (Ardea herodias), using immunoblotting. The intensity of the stained band increased with increased EROD activity, supporting the assumption that ethoxyresorufin is a suitable substrate for avian cytochrome P-450 1A1. These results validate the use of avian hepatic microsomal EROD activity as an index of cytochrome P-450 1A1 induction by environmental levels of polychlorinated aromatic hydrocarbons and as a useful screening tool to determine the extent of exposure to such chemicals. Furthermore, the induction of cytochrome P-450 1A1 observed in the cormorant indicates that the Ah receptor-mediated process, by which TCDD and related chemicals exert many of their toxicities, has been activated.

Toxic equivalency factors (TEFs) for PCBs, PCDDs, PCDFs for humans and wildlife.

“…The TEF and TEQ approaches were also succesfully applied in a biological monitoring study with great blue herons and double crested cormorants (224,225). Thus, as with fish, the additivity in the TEF concept is also supported by studies with (wild) birds.…”

Causes of Morbidity and Mortality and Their Effect on Reproductive Success in Double-Crested Cormorants From Saskatchewan

“…Ludwig et al (1996) ascribed similar lesions in cormorant embryos from the Great Lakes to exposure to planar halogenated compounds. However, Doré Lake is remote from direct industrial discharges, and the concentration of these compounds in cormorant eggs from another Saskatchewan colony, 400 km from Doré Lake, was onesixth of that in cormorant eggs from a Great Lakes colony (Sanderson et al, 1994).…”

Feminization in common terns (Sterna hirunda) : relationship to persistent organic contaminants

“…In addition, breeding birds may show abnormal parental behavior associated with prolonged incubation periods, egg loss, and nest inattentiveness. At the physiological level there are indications of altered thyroid function, increased aryl hydrocarbon hydroxylase activity, altered vitamin A homeostasis, and altered heme biosyntheses (porphyria), as well as hepatomegaly, necrosis, and fatty degeneration of the liver in embryos (Gilbertson 1983;Gilbertson, Kubiak et al 1991;Sanderson, Norstrom et al 1994). …”

“…As the embryo utilizes the yolk for nutrition, it is exposed to contaminants deposited in the yolk by the female. (Gilbertson, Kubiak et al 1991;Giesy, Ludwig et al 1994;Sanderson, Norstrom et al 1994;Murk, Boudewijn et al 1996). Cormorants, blackcrowned night-herons, gulls, great blue herons, and terns all have been affected.…”

“…In this study, AhR agonist activity of yolk sac contaminants was determined by measuring bioassay-derived dioxin-equivalents (TCDDEQs). Exposure to AhR agonists has been shown to cause increased embryo mortality and developmental abnormalities among colonial waterbirds including terns, gulls, and cormorants (Gilbertson 1983;Gilbertson, Kubiak et al 1991;Sanderson, Norstrom et al 1994). In addition, dioxin-like compounds have anti-estrogenic properties, alter testosterone levels, and may result in developmental and reproductive abnormalities (Gilbertson 1983;Gilbertson, Kubiak et al 1991;Sanderson, Norstrom et al 1994).…”