Exposure to bisphenol A is associated with recurrent miscarriage

Department of Obstetrics and Gynecology, Nagoya City University Medical School, Nagoya, Japan.
Human Reproduction (Impact Factor: 4.59). 09/2005; 20(8):2325-9. DOI: 10.1093/humrep/deh888
Source: PubMed

ABSTRACT Little is known about the influence of high exposure to bisphenol A on recurrent miscarriage and immunoendocrine abnormalities.
Serum bisphenol A, antiphospholipid antibodies (aPLs), antinuclear antibodies (ANAs), natural killer cell (NK) activity, prolactin, progesterone, thyroid-stimulating hormone (TSH) and free T4 were examined in 45 patients with a history of three or more (3-11) consecutive first-trimester miscarriages and 32 healthy women with no history of live birth and infertility. Subsequent pregnancy outcome and embryonic karyotype of abortuses were examined prospectively.
The mean+/-SD values for bisphenol A in patients were 2.59+/-5.23 ng/ml, significantly higher than the 0.77+/-0.38 ng/ml found for control women (P=0.024). High exposure to bisphenol A was associated with the presence of ANAs but not hypothyroidism, hyperprolactinaemia, luteal phase defects, NK cell activity or aPLs. A high level of bisphenol A in itself did not predict subsequent miscarriage.
Exposure to bisphenol A is associated with recurrent miscarriage.

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Available from: Yasuhiko Ozaki, Jun 17, 2014
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    • "Indeed, elevated placental hCG levels have been linked to pregnancy complications, such as preterm birth [60], fetal growth restriction (FGR) [61], and preeclampsia [62]. Importantly , high placental concentrations of BPA are associated with preeclampsia [4], and elevated plasma levels of BPA in pregnant women are linked to recurrent miscarriages [5] as well as FGR [6]. Therefore, BPA-induced increases in placental hCG expression and secretion may contribute to the pathogenesis of these pregnancy complications. "
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    ABSTRACT: This study examined the effect of bisphenol A (BPA) on human placental gene expression using primary trophoblast cells as an in vitro model system. Trophoblast cells were isolated from human placentas at term, cultured and then exposed to environmentally relevant concentrations of BPA (0.1-2μg/ml) for up to 24h, after which levels of 11β-HSD2 mRNA, protein and activity were determined by standard radiometric conversion assay, western blotting, and qRT-PCR, respectively. The mRNA levels of several other prominent placental hormones/factors were also assessed by qRT-PCR. BPA dramatically increased levels of 11β-HSD2 activity, protein and mRNA in a time- and concentration-dependent manner (>4-fold). BPA also augmented aromatase, glucose transporter-1, CRH, and hCG mRNA levels while reducing the level of leptin mRNA. These findings demonstrate that BPA severely disrupts human placental gene expression in vitro, which suggests that exposure to BPA may contribute to altered placental function and consequent pregnancy complications. Copyright © 2015. Published by Elsevier Inc.
    Reproductive Toxicology 03/2015; 53. DOI:10.1016/j.reprotox.2015.03.001 · 2.77 Impact Factor
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    • "It is therefore possible that failure or deficiencies in trophoblast proliferation or differentiation may compromise placental development, since there have been studies showing elevated apoptosis in placenta from pregnancies complicated by IUGR [31] and preeclampsia [32]. Sugiura-Ogasawara et al. [33] reported an association between serum BPA levels and recurrent miscarriage. Blood BPA levels of patients with a history of three or more consecutive first-trimester miscarriages were approximately three times higher than those of controls. "
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    ABSTRACT: Introduction: Bisphenol A (BPA) is a weakly estrogenic compound that has been detected in a wide va-riety of food products and biological matrices (saliva, blood, urine, etc). Despite the potential risk of human exposure to BPA, little information exists concerning maternal and fetal exposure to BPA during pregnancy. The aim of this study is to evaluate the correlation between placental BPA concentration, infant birth weight and calculated birth weight centile, and several other maternal and infant parameters. Methods: Placental sample were collected from 200 subjects. BPA levels were measured by isotope dilution GCeMS. Additional maternal and infant data were gathered from medical charts and were potential correlates with placental BPA levels. Results: Placental BPA concentrations ranged from 4.4 ng/g to 273.9 ng/g in oven-dried tissue (average 103.4 ± 61.8 ng/g). There was a significant negative correlation between calculated birth weight centile and levels of placental BPA (p < 0.05). Low birth weight and small for gestational age infants also had significantly greater placental BPA concentrations as compared to normal weight infants and average/ large for gestational age infants. Infants born to African American mothers also had greater placental BPA concentrations as compared to infants born to Hispanic mothers. Discussion: Placental BPA concentrations are correlated with the growth potential of the fetus and may play a role in reduced fetal growth.
    Placenta 09/2014; DOI:10.1016/j.placenta.2014.08.091 · 3.29 Impact Factor
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    • "Thehypothesizedlinkbetweenendocrinedisruptorsand adiposityisbiologicallyplausibleandcoherentwiththe"environmentalobesogenhypothesis"andthe"developmentaloriginsof healthanddisease."Theenvironmentalobesogenhypothesispro- posesthatexposuretoatoxicchemicalburdenissuperimposedon energyimbalanceresultingfromdietandlifestyletoinitiateor exacerbatethedevelopmentofobesityanditsassociatedhealth consequences,includingtype2diabetes,cardiovasculardisease, hypertension,anddyslipidemias[2].Thedevelopmentaloriginsof healthanddiseaseparadigmproposesthatfetalandperinatal stagesofdevelopmentrepresentperiodsofheightenedsensitivity fortheestablishmentofpersistentchangestotheindividual's adaptivephysiology[2].BPAmaybeviewedasatoxicchemicalthat cantargetnuclearhormonereceptorsignalingpathways,resulting inperturbedadipocyteproliferation,differentiationormodulation ofsystemichomeostaticcontrols,withlong-termconsequences thatmaybemagnifiedifdisruptionoccursduringsensitivedevel- opmentalperiods[2].Ourstudyfindingsareconsistentwithpre- viousstudiesinvolvinganimalsandhumansubjectsthathave implicateddevelopmentalandpost-developmentalexposuresto endocrine-disruptingchemicalsinreproductiveanddevelopmental outcomes[58] [59],cancer[22] [32] [60],obesity[48] [53] [61] [62],insulin resistance[11] [56] [63],type2diabetes[2,11e14,48],hypertension [2] [51],dyslipidemia[2] [64] [65],metabolicsyndrome[66] [67],car- diovasculardisease[2] [11] [12] [68],anddepression[69]. "
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    Annals of epidemiology 08/2013; 24. DOI:10.1016/j.annepidem.2013.07.014 · 2.15 Impact Factor
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