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Teratogenic effects of the organophosphate insecticide dicrotophos (Bidrin): Histological characterization of defects

White Leghorn chicken eggs, specific pathogen free, were treated with the organophosphate insecticide dicrotophos and the early defects thus induced were characterized histologically. Eggs were incubated for 24, 48, 72, or 96 hr, injected with doses of dicrotophos ranging from 250 μg to 2.0 mg per egg, and observed after an additional 48 hr of incubation. Treated embryos displayed general developmental retardation as well as unilateral retardation of the cranial sense organs, the youngest embryos being most severely affected. Many embryos injected with insecticide at 24 hr, and all but one injected at 48 or 72 hr, displayed notochordal folding, usually restricted to the cervical region; most of these also showed deformities of the adjacent spinal cord. Other defects, seen on a less consistent basis, included branching of the neural canal in the lumbar region, bifurcation of the neural epiphysis, deformation of the lens vesicle, and distention of the major blood vessels. The incidence and severity of epiphyseal, lens, and vascular defects were greatest among embryos treated at 24 hr, whereas notochordal and both types of neural defects were greatest among those treated at 48 hr. The incidence and severity of the abnormalities diminished with increasing age such that by 96 hr the only defect noted was a weak notochordal folding in one embryo. To a lesser extent, incidence and severity were dose‐related also. Histological similarities between embryos displaying vascular distention and recently dead treated embryos suggested that this abnormality is a precursor to death. All defects were associated with the presence of the insecticide at the time the affected structures were undergoing initial or early morphogenesis or else the deposition of a supportive sheath, suggesting these activities as targets of the teratogen.