PubMed · 9845068
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C J Tabin. 1998-11-26. A developmental model for thalidomide defects.. https://doi.org/10.1038/24516
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Gestational and lactational exposure to di(n-butyl) phthalate (DBP) at >/=250 mg/kg/day disrupts male rat reproductive development and function. Although this indicates an antiandrogenic mechanism, DBP and its biologically active metabolite do not interact with the androgen receptor (AR) in vitro. In the present study, we compared the effects of DBP and the antiandrogen flutamide using a shorter exposure during the prenatal period of male sexual differentiation in rats. Pregnant CD rats received DBP at 0, 100, 250, or 500 mg/kg/day po (n = 10) or flutamide at 100 mg/kg/day po (n = 5) from Gestation Days 12 to 21. In F1 males, DBP (500 mg/kg/day) and flutamide caused hypospadias; cryptorchidism; agenesis of the prostate, epididymis, and vas deferens; degeneration of the seminiferous epithelium; and interstitial cell hyperplasia of the testis. Flutamide and DBP (250 and 500 mg/kg/day) also produced retained thoracic nipples and decreased anogenital distance. Interstitial cell adenoma occurred at 500 mg DBP/kg/day in two males. The only effect seen at 100 mg DBP/kg/day was delayed preputial separation. In contrast to flutamide, DBP caused a low incidence of prostate agenesis and hypospadias with no vaginal pouch. The low incidence of DBP-induced intraabdominal testes contrasted with the high incidence of inguinal testes seen with flutamide. Thus prenatal male sexual differentiation is a sensitive period for the reproductive toxicity of DBP. A no observed adverse effect level was not established and the lowest observed (adverse) effect level was 100 mg/kg/day. Flutamide and DBP disrupted the androgen signaling necessary for male sexual differentiation but with a different pattern of antiandrogenic effects. DBP is an example of an environmental antiandrogen that disrupts androgen-regulated male sexual differentiation without interacting directly with the AR, as does flutamide.
Several studies suggest that toxic chemicals in hair products may be absorbed through the scalp in sufficient amounts to increase the risks of adverse health effects in women or their infants. This case-control study of 525 Black women from three counties in North Carolina who had delivered a singleton, liveborn infant examined whether exposure to chemicals used in hair straightening and curling increased the odds that the infant was preterm or low birth weight. Cases consisted of 188 preterm and 156 low birth weight births (for 123 women, their infant was both low birth weight and preterm). Controls were 304 women who delivered term and normal birth weight infants. Women who used a chemical hair straightener at any time during pregnancy or within 3 months prior to conception had an adjusted odds ratios (OR) of 0.7 (95% confidence interval (CI) 0.4-1.1) for preterm birth and 0.6 (95% CI 0.4-1.1) for low birth weight. Exposure to chemical curl products was also not associated with preterm delivery (adjusted OR = 0.9, 95% CI 0.5-1.8) or low birth weight (adjusted OR = 1.0, 95% CI 0.5-1.9). Despite this failure to find an association, continued search for risk factors to which Black women are uniquely exposed is warranted.
BACKGROUND: In areas endemic for hookworm, routine antenatal mebendazole therapy could greatly reduce the prevalence of anaemia in pregnancy. At present, however, this is not a widely accepted control strategy because of a lack of data on the safety of the drug. We assessed the effect of mebendazole therapy during pregnancy on birth outcome. METHODS: A cross-sectional study was done in Sri Lanka, where prescription of mebendazole to women in the second trimester of pregnancy is recommended. Two hospitals were chosen for the study, and women who gave birth there between May, 1996, and March, 1997, were recruited. We compared the rates of major congenital defects, stillbirth, perinatal death, and low birthweight (< or = 1500 g) among babies of mothers who had taken mebendazole during pregnancy with those whose mothers had not taken an anthelmintic (controls). FINDINGS: The rate of major congenital defects was not significantly higher in the mebendazole group than in the control group (97 [1.8%] of 5275 vs 26 [1.5%] of 1737; odds ratio 1.24 [95% CI 0.8-1.91], p=0.39). Among 407 women who had taken mebendazole in the first trimester (contrary to medical advice), 10 (2.5%) had major congenital defects (odds ratio vs controls 1.66 [0.81-3.56], p=0.23). The proportions of stillbirths and perinatal deaths were significantly lower in the mebendazole group (1.9 vs 3.3%, 0.55 [95% CI 0.4-0.77]), as was the proportion of low-birthweight babies (1.1 vs 2.3%, 0.47 [95% CI 0.32-0.71]). INTERPRETATION: Mebendazole therapy during pregnancy is not associated with a significant increase in major congenital defects, but our results indicate that it should be avoided during the first trimester. This therapy could offer beneficial effects to pregnant women in developing countries, where intestinal helminthiases are endemic.