Effects of 3,3′,4,4′,5‐pentachlorobiphenyl and 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin injected into the yolks of double‐crested cormorant (Phalacrocorax auritus) eggs prior to incubation

Abstract

Double-crested cormorant (Phalacrocorax auritus) eggs were injected with either 3,3Ј,4,4Ј,5-pentachlorobiphenyl (polychlorinated biphenyl [PCB] 126; 70-698 g/kg egg) or 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; 1.3-11.7 g/kg egg) prior to incubation. These compounds were injected into the yolks of cormorant eggs collected from incomplete clutches at isolated colonies on Lake Winnipegosis, Manitoba, Canada. Eggs were incubated for approximately 26 to 28 d. After hatching the brain, bursa, heart, liver, and spleen were dissected and weighed. Torsos were preserved in formalin for examination of the gonads. Median lethal doses (LD50s) calculated from mortality data at hatching were 177 and 4.0 g/kg egg for PCB 126 and TCDD, respectively. No significant differences were found in the incidence of developmental abnormalities in any of the treatment groups. Bursa weights were significantly less in the greatest (11.7 g/kg egg) TCDD group compared to the vehicle control group. Spleen weights were significantly less in the 349 g PCB 126/kg egg and the 5.4 and 11.7 g TCDD/kg egg groups when compared to the vehicle control group. No histological alterations of the gonads were found. Hepatic ethoxyresorufin-O-deethylase activity in all PCB 126 and TCDD dose groups was significantly greater compared to the control activity. The toxic equivalency factor for PCB 126 was 0.02.

Correlation between an in vitro and an in vivo measure of dioxin sensitivity in birds

“…Some of the LD50 values reported in Fig. 2 were affected by high mortality in the vehicle group or incomplete dose-response curves (Brunström 1989;Nosek et al 1993;Powell et al 1998). EROD data were not always reproducible as demonstrated by the almost 4-fold difference in EC50 values for PCB 126 in two common tern studies (Table 1).…”

“…This finding validates the EROD bioassay as a useful method for evaluating the relative sensitivity of dioxin-like compounds in avian species, reducing the need for extensive in vivo toxicity testing. Furthermore, by establishing a correlation between an AHR-mediated biochemical endpoint (EROD) and in vivo toxicity, our results add weight-of-evidence to an emerging EROD EC50 (nM) 10 -2 10 -1 10 0 10 1 LD50 (nmol/kg egg) Kennedy et al (1996a) b Sanderson et al (1998) c Bosveld (1995) d Lorenzen et al (1997) e Head et al (2008) f Nosek et al (1993) g Powell et al (1998) h Brunström (1989) i Hoffman et al (1998) j Normalized to account for different vehicle k Mean of two common tern values is presented in Fig. 2 l Turkey LD50 value was derived by linear interpolation between the LOAEL (20 lg/kg; 36% mortality), and the LD100 (60 lg/kg; 100% mortality) picture of the importance of AHR activation in differential biochemical responses to dioxin-like compounds in birds (Head et al 2008;Karchner et al 2006).…”

Multiple Lines of Evidence Risk Assessment of Terrestrial Passerines Exposed to PCDFs and PCDDs in the Tittabawassee River Floodplain, Midland, Michigan, USA

“…Additional egg-injection studies that were evaluated but not selected for deriving TRVs included studies of bobwhite quail ( Colinus virginianus ) (McMurry and Dickerson 2001) and double-crested cormorant ( Phalacrocorax auritus ) (Powell et al 1997b, 1998) studies. Reasons for not selecting them included limited sample size, failure to establish a dose–response relationship, and/or poor hatchability of non-or vehicle-injected controls.…”

Passerine Exposure to Primarily PCDFs and PCDDs in the River Floodplains Near Midland, Michigan, USA

“…These AhR-mediated responses include carcinogenicity, immunotoxicity, and adverse effects on reproduction, development, and endocrine functions (van den Berg et al 1998). In particular, AhR-mediated compounds have been shown to decrease hatching success, adult responsiveness, and immune function and to increase CYP1A enzyme induction of birds (Hoffman et al 1998; Nosek et al 1992a, 1993; Powell et al 1996, 1998; Thiel et al 1988). Recent findings provide evidence of the molecular basis for variation in avian species sensitivity to dioxinlike compounds (Head et al 2008; Karchner et al 2006).…”