Study finds more reason to review the use of BPA

Deakin University scientists are part of the international research team
led by Professor Vincent Laudet at the Institute of Functional Genomics
of Lyon (ENS de Lyon, CNRS, France) that has discovered a new pathway
for bisphenol A (BPA) to spread through the body via a protein known as
ERRy (estrogen-related receptor gamma ESRRG ), which plays an important role in
metabolism. The involvement of ERRy adds weight to the possibility that
BPA could be a cause of obesity and diabetes.

BPA and related chemicals: Human safety thresholds for endocrine disrupting chemicals may be inaccurate -- ScienceDaily

Human and rat testes respond differently to endocrine disrupting
chemicals such as BPA in two thirds of all cases, according to a recent
review. As human safety levels are extrapolated from rodent data, the
study could lead to a re-evaluation of the acceptable daily intake for
many endocrine disruptors. Endocrine disruptors are compounds that
interfere with animal hormone (or endocrine) systems in various ways.

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Bisphenol A delays the perinatal chloride shift in cortical neurons by epigenetic effects on the Kcc2 promoter.

Bisphenol A (BPA) is a ubiquitous compound that is emerging as a possible toxicant during embryonic development. BPA has been shown to epigenetically affect the developing nervous system, but the molecular mechanisms are not clear. Here we demonstrate that BPA exposure in culture led to delay in the perinatal chloride shift caused by significant decrease in potassium chloride cotransporter 2 (Kcc2) mRNA expression in developing rat, mouse, and human cortical neurons. Neuronal chloride increased correspondingly. Treatment with epigenetic compounds decitabine and trichostatin A rescued the BPA effects as did knockdown of histone deacetylase 1 and combined knockdown histone deacetylase 1 and 2. Furthermore, BPA evoked increase in tangential interneuron migration and increased chloride in migrating neurons. Interestingly, BPA exerted its effect in a sexually dimorphic manner, with a more accentuated effect in females than males. By chromatin immunoprecipitation, we found a significant increase in binding of methyl-CpG binding protein 2 to the "cytosine-phosphate-guanine shores" of the Kcc2 promoter, and decrease in binding of acetylated histone H3K9 surrounding the transcriptional start site. Methyl-CpG binding protein 2-expressing neurons were more abundant resulting from BPA exposure. The sexually dimorphic effect of BPA on Kcc2 expression was also demonstrated in cortical neurons cultured from the offspring of BPA-fed mouse dams. In these neurons and in cortical slices, decitabine was found to rescue the effect of BPA on Kcc2 expression. Overall, our results indicate that BPA can disrupt Kcc2 gene expression through epigenetic mechanisms. Beyond increase in basic understanding, our findings have relevance for identifying unique neurodevelopmental toxicity mechanisms of BPA, which could possibly play a role in pathogenesis of human neurodevelopmental disorders.

Contaminated diet contributes to exposure to endocrine-disrupting chemicals: Phthalates and BPA

"According to a study published February 27 in the Nature Journal of Exposure Science and Environmental Epidemiology, we may be exposed to these chemicals in our diet, even if our diet is organic and we prepare, cook, and store foods in non-plastic containers. Children may be most vulnerable."

'via Blog this'

Plastic products and jet fuel exposures raising incidences of 'epigenetic transgenerational inheritance'

Writing in the online journal PLOS ONE, scientists led by molecular biologist Michael Skinner document reproductive disease and obesity in the descendants of rats exposed to the plasticizer bisephenol-A, or BPA, as well DEHP and DBP, plastic compounds known as phthalates. In a separate article in the journal Reproductive Toxicology, they report the first observation of cross-generation disease from a widely used hydrocarbon mixture the military refers to as JP8.

Read more at: http://medicalxpress.com/news/2013-01-plastic-products-jet-fuel-exposures.html#jCp

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Study shows BPA exposure in fetal livers

ScienceDaily (Dec. 3, 2012) — New research from the University of Michigan School of Public Health found BPA, or bisphenol A, in fetal liver tissue, demonstrating that there is considerable exposure to the chemical during pregnancy.

Toxicology: The learning curve : Nature News & Comment: Toxic effects of low doses

Endocrine disrupters include a large group of synthetic chemicals that interact with cellular hormone receptors. These compounds, which range from the common weed killer atrazine and the plasticizer bisphenol A (BPA) to the antibacterial agent triclosan (used in cleansers) and the vineyard fungicide vinclozolin, don't play by the usual rules of toxicology. On the basis of conventional high-dose testing, regulators have set maximum acceptable levels for each of them that assume all doses below that level are safe. But academic researchers who have studied a wider range of doses, including very low ones found in the everyday environment, say that their experiments usually do not generate the tidy, familiar 'ski-slope' dose-response graphs of classic toxicology. Instead, most endocrine disrupters have 'non-monotonic' dose-response curves, meaning that their slopes change at least once from negative to positive, or vice versa, forming 'U' shapes, inverted 'U's or even stranger shapes that resemble undulating Chinese dragons. 

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