Fifty white leghorn chicken (Gallus domesticus) eggs per group were injected with 0.1, 1.0, 10.0, or 20.0 microg perfluorooctane sulfonate (PFOS)/g egg before incubation to investigate the effects of PFOS on the developing embryo. Hatchlings were weighed, examined for gross developmental abnormalities, and transferred to a battery brooder, where they were raised for 7 d. Chicks were then weighed, and 20 birds per treatment were randomly chosen for necropsy. The brain, heart, kidneys, and liver were removed and weighed. Livers were processed further for determination of PFOS concentrations and histological assessment. Hatchability was reduced significantly in all treatment groups in a dose-dependent manner. The calculated median lethal dose was 4.9 microg PFOS/g egg. Perfluorooctane sulfonate did not affect posthatch body or organ weights. Exposure to PFOS caused pathological changes in the liver characterized by bile duct hyperplasia, periportal inflammation, and hepatic cell necrosis at doses as low as 1.0 microg PFOS/g egg. Perfluorooctane sulfonate concentrations in the liver increased in a dose-dependent manner. Based on reduced hatchability, the lowest-observed-adverse-effect level was 0.1 microg PFOS/g egg.

Autoradiography with 3H-labeled spermatozoa was utilized to study spermatozoal oviductal interrelationships. Results demonstrated that sperm displacement from the uterovaginal sperm-host glands did not occur in domestic fowl. Furthermore, there was no indication that phagocytosis of labeled spermatozoa by sperm gland epithelium occurred. Associated studies demonstrated that extensive head-to-head agglutination occurred between freshly ejaculated spermatozoa, but the ability to agglutinate was lost as the sperm cells aged. On the basis of these observations, it was proposed that agglutination may be the basic mechanism controlling sperm storage and release from the uterovaginal sperm-host glands. A working model to this effect was presented.

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