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Oxychlordane reached lethal levels in birds given dietary dosages of HCS-3260 (70.75% cis-chlordane and 23.51% trans-chlordane) at 6 levels from 50 to 500 ppm. Oxychlordane ranged from 9.4 to 22.1 ppm in brains of cowbirds (Molothrus ater), grackles (Quiscalus quiscula), and red-winged blackbirds (Agelaius phoeniceus) that died on dosage and from 1.3 to 4.8 ppm in sacrificed birds, providing a clear diagnostic separation. Among starlings (Sturnus vulgaris), however, oxychlordane ranged from 5.0 to 19.1 ppm in brains of birds that died, significantly lower than in the other species, and from 1.4 to 10.5 ppm in sacrificed birds, overlapping the levels in those that died. Lethal levels, therefore, begin near 5.0 ppm, as in a previous study in which oxychlordane itself was fed, but the data from starlings emphasizes the need for confirmatory necropsy findings in diagnosis of poisoning. Nonachlor had a very low order of toxicity, killing only 1 of 12 birds dosed at 100 ppm for 35 d; 3 others died and 1 was incapacitated during a short period of food deprivation. Lethal levels of oxychlordane were present in the brains of birds that died. Oxychlordane accumulated in the bodies of birds on dietary dosage of HCS-3260 in proportion to dosage and time, but did not approach equilibrium at the levels (10, 50, and 100 ppm) that were fed. Loss rates of oxychlordane from HCS-3260, oxychlordane, or technical chlordane dosages (the last in a previous study) did not differ significantly from each other; respective half-lives were 57, 63, and 74 d. Residues of cis-chlordane in birds fed HCS-3260 were consistently lower than oxychlordane during the accumulation period and declined abruptly when dosage ceased; individual variation was high.

Formalin preservation, freezing, spoiling followed by freezing, and phenoxyethanol were compared in terms of concentrations of DDT, DDD, DDE, endrin, and heptachlor epoxide measured in brain, liver and carcass of birds fed dietary dosages of pesticides and in spiked egg homogenate. Phenoxyethanol proved to be an unsatisfactory preservative; the amount of 'extractable lipid' was excessive, and measurements of concentrations in replicates were erratic. Concentrations of residues in formalin-preserved and frozen samples did not differ significantly in any tissue. Percentage lipid in brains and eggs, however, were significantly lower in formalin-preserved samples. Samples of muscle and liver that had been spoiled before freezing yielded less DDD, and muscle samples yielded more DDT than formalin-preserved samples. We conclude that formalin preservation is a satisfactory method for preservation of field samples and that the warming and spoiling of samples that may occur unavoidably in the field will not result in misleading analytical results.