Hen pheasants (Phasianus colchicus) injected with graded single doses of TCDD (6.25, 25, or 100 micrograms/kg) exhibited delayed-onset body weight loss and mortality--classic signs of the wasting syndrome. The lowest single dose of TCDD to produce this effect was 25 micrograms/kg. When hen pheasants were treated weekly with far lower doses of TCDD (0.01-1.0 microgram/kg/wk) for 10 wk, signs of the wasting syndrome and mortality were also produced. The lowest cumulative TCDD dose required to produce the response, using a weekly dosing regimen, was 10 micrograms/kg. Furthermore, using this dosing regimen, egg production by hens treated with a cumulative TCDD dose of 10 micrograms/kg was reduced, as was hatchability of their eggs. We conclude that hen pheasants are responsive to the overt toxic effects of TCDD and that the lowest cumulative dose of TCDD that produces overt signs of toxicity, 10 micrograms/kg, also reduces egg production and egg hatchability.

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The T 1/2 for whole-body elimination of [3H]-2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) derived radioactivity in ring-necked pheasant hatchlings was 13 d, whereas in adult hen pheasants that were not producing eggs it was 378 d. All TCDD-derived radioactivity in hen tissues was from the parent compound. The oral bioavailability of TCDD in the adult hen pheasant varied with the environmental matrix, with 30% of the dose absorbed from a suspension of earthworms, 33% absorbed from a soil suspension, 41% absorbed from a suspension of paper mill sludge, and 58% absorbed from a suspension of crickets. A cumulative dose of 1.0 micrograms TCDD/kg body weight, administered as weekly doses of 0.1 micrograms/kg for 10 wk, did not adversely affect hen condition or egg production. Under these exposure conditions, hens translocated about 1% of their cumulative TCDD dose to each of the first 15 eggs laid. All of the TCDD-derived radioactivity in the eggs was the parent compound and was confined entirely to the yolk; no TCDD was detected in egg albumin. We conclude that TCDD was more persistent in pheasant hens than in chicks and that egg laying was an important route of elimination in the hen.

Fertilized eggs of ring‐necked pheasants (Phasianus colchicus) were injected into the albumin or yolk with vehicle or graded doses of 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin (TCDD) (0.01, 0.1, 1, 10, 100, 1,000, 10,000, or 100,000 pg TCDD/g egg) on day 0 of embryonic development and toxicity was assessed in 1‐d‐old hatchlings and 28‐d‐old chicks. The most sensitive effect of in ovo TCDD exposure was induction of hepatic ethoxyresorufin‐O‐deethylase (EROD) activity in 1‐d‐old hatchlings. The ED50 for this response was 312 pg TCDD/g egg. Embryo mortality was the most sensitive sign of toxicity. The TCDD dose that caused 50% mortality above control (LD50) when injected into the egg albumin or yolk was 1,354 and 2,182 pg TCDD/g egg, respectively. At egg TCDD doses up to and including 1,000 pg TCDD/g egg, no effect was detected in 1‐d‐old hatchlings and 28‐d‐old chicks in body growth, organ weights, carcass morphometrics, incidence of edema, or incidence of histological alterations in the liver, spleen, heart, Bursa of Fabricius, or thymus. Egg TCDD doses as high as 1,000 pg TCDD/g egg also had no effect on cardiac morphometrics or incidence of cardiac malformations in 1‐d‐old hatchlings, or on antibody‐mediated immunity in 28‐d‐old chicks. We conclude that embryo mortality is the most sensitive sign of TCDD toxicity in the ring‐necked pheasant following in ovo exposure. The ring‐necked pheasant embryo is less sensitive than the chicken (Gallus domesticus) embryo and more sensitive than the eastern bluebird (Sialia sialis) embryo to TCDD toxicity.

Fertilized eggs of ring-necked pheasants (Phusiunus colchicus) were injected into the albumin or yolk with vehicle or graded doses of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (0.01, 0.1, 1, 10, 100, 1,000, 10,000, or 100,000 pg TCDD/g egg) on day 0 of embryonic development and toxicity was assessed in 1-d-old hatchlings and 28-d-old chicks. The most sensitive effect of in ovo TCDD exposure was induction of hepatic ethoxyresorufin-0-deethylase (EROD) activity in 1-d-old hatchlings. The ED50 for this response was 312 pg TCDD/g egg. Embryo mortality was the most sensitive sign of toxicity. The TCDD dose that caused 50% mortality above control (LD50) when injected into the egg albumin or yolk was 1,354 and 2,182 pg TCDD/g egg, respectively. At egg TCDD doses up to and including 1,000 pg TCDD/g egg, no effect was detected in 1-d-old hatchlings and 28-d-old chicks in body growth, organ weights, carcass morphometrics, incidence of edema, or incidence of histological alterations in the liver, spleen, heart, Bursa of Fabricius, or thymus. Egg TCDD doses as high as 1,000 pg TCDD/g egg also had no effect on cardiac morphometrics or incidence of cardiac malformations in 1-d-old hatchlings, or on antibody-mediated immunity in 28-d-old chicks. We conclude that embryo mortality is the most sensitive sign of TCDD toxicity in the ring-necked pheasant following in ovo exposure. The ring-necked pheasant embryo is less sensitive than the chicken (Gullus domesticus) embryo and more sensitive than the eastern bluebird (Siuliu siulis) embryo to TCDD toxicity.