Distribution and Estrogenic Risk of Alkylphenolic Compounds, Hormones and Drugs Contained in Water and Natural Surface Sediments, Morelos, Mexico

This study evaluated the distribution and potential estrogenic risk of the presence of bisphenol A (BPA), 4-nonylphenol (4NP), naproxen (NPX), ibuprofen (IBU), 17-β-estradiol (E2) and 17-α-ethinylestradiol (EE2) in water and sediments of the Apatlaco river micro-basin (Morelos, Mexico). The concentration of the determined compounds ranged between <LOD to 86.40 ng·L−1 and <LOD to 3.97 ng g−1 in water and sediments, respectively. The Log Kd distribution obtained (from 1.05 to 1.91 L Kg−1) indicates that the compounds tend to be adsorbed in sediments, which is probably due to the hydrophobic interactions confirmed by the significant correlations determined mainly between the concentrations and parameters of total organic carbon (TOC), total suspended solids (TSS), biological oxygen demand (BOD5) and chemical oxygen demand (COD). Of five sites analyzed, four presented estrogenic risk due to the analyzed endocrine-disrupting compounds (EEQE2 > 1 ng·L−1).

The impact of bisphenol a (BPA) on the placenta

Bisphenol A (BPA) is an endocrine-disrupting chemical (EDC) that is used in a wide-variety of plastic and common house-hold items. Therefore, there is potential continual exposure to this compound. BPA exposure has been linked to certain placenta-associated obstetric complications such as preeclampsia, fetal growth restriction, miscarriage, and preterm birth. However, how BPA exposure results in these disorders remains uncertain. Hence, we have herein summarized the reported impact of BPA on the morphology and metabolic state of the placenta and have proposed mechanisms by which BPA affects placentation, potentially leading to obstetric complications. Current findings suggest that BPA induces pathological changes in the placenta and disrupts its metabolic activities. Based on exposure concentrations, BPA can elicit apoptotic or anti-apoptotic signals in the trophoblasts; and can exaggerate trophoblast fusion while inhibiting trophoblast migration and invasion to affect pregnancy. Accordingly, the usage of BPA products by pregnant women should be minimized and less harmful alternative chemicals should be explored and employed where possible.

Developmental exposure to the DE-71 mixture of polybrominated diphenyl ether (PBDE) flame retardants induce a complex pattern of endocrine disrupting effects in rats

Polybrominated diphenyl ethers (PBDEs) are legacy compounds with continued widespread human exposure. Despite this, developmental toxicity studies of DE-71, a mixture of PBDEs, are scarce and its potential for endocrine disrupting effects in vivo is not well covered. To address this knowledge gap, we carried out a developmental exposure study with DE-71. Pregnant Wistar rat dams were exposed to 0, 40 or 60 mg/kg bodyweight/day from gestation day 7 to postnatal day 16, and both sexes were examined. Developmental exposure affected a range of reproductive toxicity endpoints. Effects were seen for both male and female anogenital distances (AGD), with exposed offspring of either sex displaying around 10% shorter AGD compared to controls. Both absolute and relative prostate weights were markedly reduced in exposed male offspring, with about 40% relative to controls. DE-71 reduced mammary gland outgrowth, especially in male offspring. These developmental in vivo effects suggest a complex effect pattern involving anti-androgenic, anti-estrogenic and maybe estrogenic mechanisms depending on tissues and developmental stages. Irrespective of the specific underlying mechanisms, these in vivo results corroborate that DE-71 causes endocrine disrupting effects and raises concern for the effects of PBDE-exposure on human reproductive health, including any potential long-term consequences of disrupted mammary gland development.