BIRDS 



LD-50 values computed 37 days after a single oral dose of 2,3,7,8-TCDD 

 varied from 15 ug/kg body weight in Northern bobwhite ( Colinus virginianus ), 

 with 95% confidence limits of 9.2 and 24.5 ug/kg, to more than 810 ug/kg Body 

 weight for the ringed turtle-dove ( Streptopelia risoria ). Mallards ( Anas 

 platyrhynchos ) were intermediate in sensitivity with an acute oral LD-50 value 

 of more than 108 ug/kg body weight (Hudson et al . 1984). For all 3 species, 

 death occurred 13 to 37 days after treatment; remission in survivors had 

 apparently occurred by day 30 posttreatment. Gross necropsy of ringed 

 turtle-doves that survived treatment showed enlarged livers, about twice 

 normal size. Bobwhites showed severe emaciation, high accumulations of uric 

 acid salts in connective tissues, and fluid accumulations in the pericardial 

 and abdominal cavities (Hudson et al . 1984). Some birds regurgitated within a 

 few minutes after treatment. Signs of intoxication that began 7 days after 

 treatment included excessive drinking, loss of appetite, hypoactivity, 

 emaciation, weakness, debility, muscular incoordination, increased reaction to 

 stimuli, fluffed feathers, huddled position, unkempt appearance, falling, 

 tremors, spasms, convulsions, and immobility (Hudson et al. 1984). 



Domestic chickens were relatively sensitive to PCDDs, especially 

 2,3,7,8-TCDD, with an estimated 2,3,7,8-TCDD oral LD-50 range of 25 to 50 

 ug/kg body weight (Kociba and Schwetz 1982a, b). Chickens fed 1 or 10 ug of 

 2,3,7,8-TCDD, 1 ,2,3,7,8,9-hexa CDD, or hepta-CODs per kg body weight daily for 

 21 days showed signs of chick edema disease, i.e., pericardial, subcutaneous, 

 and peritoneal edema; liver enlargement and necrosis with fatty degeneration; 

 and frequently resulted in death (NRCC 1981; Gilbertson 1983). Autopsies of 

 poultry killed by 2,3,7,8-TCDD in Seveso, Italy, in 1976 showed signs 

 characteristic of chick edema disease (Fanelli et al. 1980b). Pathological 

 signs of chick edema disease were also seen in herring gull chicks on the 

 lower Great Lakes in the early 1970's (Gilbertson 1983). Concentrations of 

 2,3,7,8-TCDD in eggs of the herring gull declined from about 1,000 ppt in 1971 

 to less than 80 ppt in 1981. This was accompanied by a decrease in the 

 frequency of chick edema disease (Gilbertson 1983). Decreases in levels of 

 other contaminants notably mirex were probably more important to the survival 

 of gulls in these colonies than 2,3,7,8-TCDD (Eisler 1985); however, little 

 data exist on the interaction of PCDDs, including 2,3,7,8-TCDD, with other 

 contaminants appearing concomitantly in bird tissues or their diets. 



Although there presently is no evidence of biomagnification of PCDDs in 

 birds (Gilbertson 1983), it is speculated that piscivorous birds have a 

 greater potential to accumulate PCDDs than the fish that they eat (NRCC 

 1981). 



MAMMALS 



The greater toxic potential of certain PCDD isomers involves two 

 properties: halogen atoms occupying at least 3 of the 4 lateral ring 



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