Transfer of bisphenol A across the human placenta

Balakrishnan, Biju; Henare, Kimiora; Thorstensen, Eric B.; Ponnampalam, Anna P.; Mitchell, Murray D.

doi:10.1016/j.ajog.2010.01.025

Cited by 232 publications

(133 citation statements)

References 32 publications

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“…Differential tissue distribution of BPA in male and female offspring mice may play a critical role in gender dimorphic phenotypes (Doerge et al, 2011). These persistent disruptive effects by BPA may be associated with accumulation in the fetal and infant tissues through placenta and milk transfer (Balakrishnan et al, 2010). However, the molecular mechanisms underlying BPA-induced disruption of gender dimorphic and persistent phenotypes are not well understood.…”

Section: Discussionmentioning

confidence: 99%

Gestational and lactational exposure to low-dose bisphenol A increases Th17 cells in mice offspring

Luo

et al. 2016

Environmental Toxicology and Pharmacology

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Section: Discussionmentioning

confidence: 99%

Gestational and lactational exposure to low-dose bisphenol A increases Th17 cells in mice offspring

Luo

et al. 2016

Environmental Toxicology and Pharmacology

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“…Pregnant women are not directly at risk of adverse BPA activity, because their metabolic ability is not impaired [60]. Whereas, it is believed that the fetus is at a real risk of exposure [60,64]. Despite this, it is believed that exposure of the fetus depends on the concentration of BPA in the blood of the mother, because the human placenta does not metabolize BPA and consequently fetal should be protected from adverse effect of BPA by maternal metabolism [60].…”

Section: Papermentioning

confidence: 99%

Bisphenol A – Application, sources of exposure and potential risks in infants, children and pregnant women

Mikołajewska¹,

Stragierowicz²,

Gromadzińska³

2015

Int J Occup Med Environ Health

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Bisphenol A (BPA) is used in the chemical industry as a monomer in the production of plastics. It belongs to a group of compounds that disturb some of the functions of human body, the endocrine system in particular. Extensive use of BPA in manufacturing products that come in contact with food increases the risk of exposure to this compound, mainly through the digestive tract. Literature data indicate that exposure to bisphenol A even at low doses may result in adverse health effects. The greatest exposure to BPA is estimated among infants, children and pregnant women. The aim of this review is to show potential sources of exposure to bisphenol A and the adverse health effects caused by exposure to this compound in the group of particular risk.

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“…It has been shown that the placental barrier does not protect the unborn child in case of maternal exposure to acrylamide, dioxins, and estrogen-like compounds such as organochlorine pesticides and amphenones (10)(11)(12)(13).…”

Section: Introductionmentioning

confidence: 99%

Global Gene Expression Analysis in Cord Blood Reveals Gender-Specific Differences in Response to Carcinogenic Exposure In Utero

Hochstenbach

Leeuwen

Gmuender

et al. 2012

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Background: It has been suggested that fetal carcinogenic exposure might lead to predisposition to develop cancer during childhood or in later life possibly through modulation of the fetal transcriptome. Because gender effects in the incidence of childhood cancers have been described, we hypothesized differences at the transcriptomic level in cord blood between male and female newborns as a consequence of fetal carcinogenic exposure. The objective was to investigate whether transcriptomic responses to dietary genotoxic and nongenotoxic carcinogens show gender-specific mechanisms-of-action relevant for chemical carcinogenesis.Methods: Global gene expression was applied in umbilical cord blood samples, the CALUX-assay was used for measuring dioxin(-like), androgen(-like), and estrogen(-like) internal exposure, and acrylamide-hemoglobin adduct levels were determined by mass spectrometry adduct-FIRE-procedure TM . To link gene

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Transfer of bisphenol A across the human placenta

Cited by 232 publications

References 32 publications

Gestational and lactational exposure to low-dose bisphenol A increases Th17 cells in mice offspring

Gestational and lactational exposure to low-dose bisphenol A increases Th17 cells in mice offspring

Bisphenol A – Application, sources of exposure and potential risks in infants, children and pregnant women

Global Gene Expression Analysis in Cord Blood Reveals Gender-Specific Differences in Response to Carcinogenic Exposure In Utero

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