Developmental effects associated with exposure of humans to endrin have not been reported. Prenatal exposure of animals to concentrations of endrin sufficient to cause maternal toxicity has resulted in a statistically significant increase in the incidence of fused ribs, cleft palate, exencephaly, microencephaloceles, and open eyes in hamsters and mice. Adverse developmental effects generally have not been observed in rats except for temporary increase in locomotor activity of pups and delayed ossification at doses which resulted in maternal toxicity.
No in vivo studies of genotoxic effects in humans were located.
Endrin was not mutagenic in vitro in microbial assays with or without metabolic activation or in the mouse lymphoma cell assay. Exposure of primary rat, mouse, or hamster hepatocytes to endrin did not cause unscheduled DNA synthesis or repair. Sister chromatid exchange frequencies were not significantly elevated in activated and nonactivated human lymphoid cells. Chromosomal aberrations observed in testicular cells of rats following injection of endrin are of questionable relevance to human risk assessment due to the route of exposure, which was direct, intratesticular injection. The ability of endrin to cause an increase in hepatic DNA damage (single strand breaks) is attributed to endrininduced oxidative damage, and is not suggestive of a direct, genotoxic effect of endrin. Data suggest that genotoxicity is not an area of concern in humans.
No reports of reproductive effects in endrinexposed humans have been located. Early single and 3generation reproductive studies in dogs and rats, respectively, were inadequate for assessing potential reproductive effects.