Il existe plusieurs études dans lesquelles l'utilisation de l'éthinylestradiol s'est révélée être bien plus effective que celle du bisphénol A. Ci-joint, un lien vers une étude menée sur des rats publiée en 2009 à ce sujet.
« EE2 (50 μg/kg/day) increased anogenital distance and reduced pup body weight at PND2, accelerated the age at vaginal opening, reduced F1 fertility and F2 litter sizes, and induced malformations of the external genitalia (5 μg/kg). F1 females exposed to EE2 also displayed a reduced (male-like) saccharin preference (5 μg/kg) and absence of lordosis behavior (15 μg/kg), indications of defeminization of the CNS. BPA had no effect on any of the aforementioned measures. These results demonstrate that developmental exposure to pharmacologically relevant dosage levels of EE2 can permanently disrupt the reproductive morphology and function of the female rat. »
« BPA is approximately a 10^5-fold less potent than estradiol and 10^6-fold less potent than EE2 in stimulating estrogen receptor (ER)–dependent gene expression. In vivo, sc administration of BPA or EE2 stimulates uterine weight (ED50 of 416 mg/kg/day for BPA versus 0.0008 mg/kg/day for EE2) and induces estrogen-dependent lordosis behavior in adult female rats. When given orally, EE2 stimulated uterine weight (ED50 of 2.5 μg/kg/day), whereas oral BPA at doses as high as 1 g/kg/day were insufficient to achieve an ED50 (doses of 20–375 mg/kg/day had no effect whereas 600 and 1000 mg/kg/day induced small but significant increases in weight). When administered to weanling female rat using the weanling female rat using the U.S. Environmental Protection Agency (USEPA), EE2 accelerated the onset of vaginal opening (VO) by 10 days after only 2–3 days of treatment and induced persistent vaginal estrus, whereas dosage levels of BPA up to 600 mg/kg/day were without effect on these estrogen-regulated end points. »
« In conclusion, the current study demonstrates that maternal exposure to 5–50 μg EE2/kg/day during gestation and lactation produces permanent adverse effects on the developing female rat reproductive system. EE2 affected several reproductive measures at doses ranging from 5 to 50 μg/day, dosage levels within the dose range used by girls and women for therapeutic purposes. In contrast, exposure to BPA at dosage levels 40-, 400-, and 4000-fold above the estimated median human exposure did not alter any end point included in our studies in F1 male or in female LE rats. [...] The lack of effect of BPA on female and male rat offspring after oral exposure to low doses in our studies is consistent with the lack of adverse effects on growth, VO, fertility, and fecundity of low doses of BPA in several other robust, well-designed, properly analyzed multigenerational studies. »