While in utero exposure to potent estrogenic drugs (personal communication) or steroids at high-dose levels does increase anogenital distance in female rats at birth, this effect is associated with malformations of the external genitalia (cleft phallus with hypospadias) in female offspring, an effect not observed in the PZ-exposed female offspring.
Prochloraz has been reported to activate the AHR (also known as the dioxin receptor) in vitro. However, in utero, AHR agonists produce a suite of reproductive tract effects that are distinct from those caused by in utero PZ treatment. Developmental effects of AHR agonists (i.e., 2, 3, 7, 8 tetrachlorodibenzo dioxin [TCDD]) in the male and female offspring differ markedly from the profile of effects seen in the current study. Effects of gestational TCDD exposure included female cleft phallus and persistent vaginal thread, delayed vaginal opening, and reduced ovarian weight in female rat offspring. In male rat offspring, TCDD causes epididymal agenesis and reduces sperm counts at low dosage levels, but unlike PZ, TCDD does not induce hypospadias or retained nipples in male offspring. Hence, the reproductive malformations induced by PZ in the current study are not a component of the dioxin profile of effects.