18 



birds that died from endrin plus chlordane 

 than in those dying from endrin alone. These 

 data indicate that closely related toxicants 

 may have an accumulative effect at the site of 

 action. 



Two of 14 male American kestrels (Falco 

 sparverius) died after 14 and 16 months on a 

 diet containing 2.8 ppm DDE (Porter and 

 Wiemeyer 1972). The brains of the two birds 

 contained DDE residues of 213 and 301 ppm 

 compared with an average of 14.9 ppm (range, 

 4.5-26.6 ppm) for 11 of the adult males that 

 were sacrificed after 12 to 16 months on 

 dosage. Each of the two birds that died had 

 lost about one-third of its weight since treat- 

 ment began and necropsy revealed typical 

 characteristics (reduced pectoral muscle and 

 badly depleted fat reserves) of organochlorine 

 poisoning. 



Endrin was consistently the most toxic of 

 89 pesticidal chemicals that were tested for 

 their lethal dietary toxicity to young bob- 

 whites, coturnix quail, ring-necked pheasants, 

 and mallards (Heath et al. 1972a). Aldrin and 

 dieldrin were among the six most toxic chemi- 

 cals of those tested on all species, and toxa- 

 phene was the only other organochlorine that 

 was particularly toxic to mallards. Major 

 species differences in vulnerability to various 

 chemicals such as were demonstrated in this 

 study must be considered whenever toxicity 

 of particular chemicals to avian species is un- 

 known. Further testing made this point in- 

 creasingly clear (Hill et al. 1975). Among the 

 more toxic organochlorine compounds, nearly 

 all are alicyclic hydrocarbons. Of these chemi- 

 cals tested, most of the aromatic chlorinated 

 hydrocarbons are among the less toxic. 



Toxicities of six PCB compounds (Aroclor 

 1232, 1242, 1248, 1254, 1260, and 1262) to 

 penned mallards, pheasants, bobwhite, and 

 coturnix quail were generally less than that of 

 DDT (Heath et al. 1972b). Aroclor toxicity 

 was positively correlated with chlorine per- 

 centage (last two digits of Aroclor number) for 

 the 2-week-old birds that were fed treated 

 diets for 5 days. The joint toxicity of Aroclor 

 1254 and DDE on coturnix was additive, not 

 synergistic. When 18 chemicals (including 8 

 organochlorines) were fed in 13 pairs to co- 

 turnix quail and ring-necked pheasant, the 

 effects of the organochlorines also were addi- 

 tive rather than synergistic (Kreitzer and 

 Spann 1973). 



To learn if the percentage of chlorine in a 



mixture of PCB's alone determines toxicity, 

 Hill et al. (1974) fed coturnix quail diets con- 

 taining Aroclor 1248, 1254, or 1260 at levels 

 that added equal amounts of chlorine to the 

 feed. Sublethal concentrations produced no 

 detectable effects. Lethal concentrations with 

 equal chlorine showed Aroclor 1248 to be the 

 least toxic of the three compounds at the 

 highest chlorine concentrations. At lower con- 

 centrations, Aroclor 1254 was the most toxic 

 Aroclor. Although chlorine percentage of a 

 PCB is positively correlated with its avian 

 toxicity, PCB toxicity is apparently not 

 simply a function of chlorination. Toxicity 

 also is related to the positions the chlorine 

 atoms occupy on the benzene rings. Toxicity 

 of hexachlorobiphenyl mixtures to bird em- 

 bryos has been shown to be correlated with 

 their dibenzofuran content (Vos and Koeman 

 1970; Vosetal. 1970). 



Experiments with coturnix quail were used 

 to simulate the stresses on wild birds of breed- 

 ing condition and of weight loss due to migra- 

 tion (Gish and Chura 1970). Light conditions 

 in the laboratory were manipulated to stimu- 

 late reproductive development in one group of 

 birds and suppress development in another 

 group. Within each of these groups, some 

 birds were partially starved before dosage 

 and some were fully fed. Birds were then fed 

 dietary levels of 0, 700, 922, 1,214, or 

 1,600 ppm (dry weight) of DDT for a period of 

 20 days or until death. Birds partially starved 

 before dosage were more susceptible to DDT 

 intoxication than nonstarved ones. Similarly, 

 males died earlier than females, and the 

 lighter birds died earlier than the heavier 

 ones. The heavier birds of each sex not only 

 survived longer than lighter individuals re- 

 ceiving the same treatments, but they also 

 lost a greater proportion of their weight 

 before death. During the early portion of the 

 dosage period, females in breeding condition 

 were less sensitive to DDT than were non- 

 breeding females and males. After 10 days on 

 dosage, however, the cumulative mortality of 

 females in breeding condition rapidly ap- 

 proached that of males and of females not in 

 breeding condition. 



Reproduction 



Field and experimental evidence indicates 

 that declines in eggshell thickness observed in 



