BPA, epigenetic changes and heritable diabetes; soundness of US EPA’s evaluation of EDC dose-response curves; and more / June science digest #2 (lab and policy research)

June 10, 2014 at 10:53 am | Posted in News and Science Bulletins | Leave a comment
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June Science Digest #2 // Laboratory and policy research

Cancer, BPA | Dose-Dependent Incidence of Hepatic Tumors in Adult Mice following Perinatal Exposure to Bisphenol A. Apparently the first study reporting increased cancer incidence following BPA exposure. The researchers found hepatic tumors in 10-month-old mice which were exposed to 50mg/kg BPA in their diet. The researchers state that early disease onset, an absence of bacterial or viral infection and a lack of characteristic sexual dimorphism in tumor incidence “support a non-classical etiology”.

Science and Policy | Review of the US EPA’s Evaluation of Nonmonotonic Dose-Response Relationships as they Apply to Endocrine Disrupters. The US National Research Council’s appraisal of whether or not the EPA’s evaluation presents a scientifically sound and high-quality analysis of the literature on NMDRs. It recommends greater transparency and consistency to be achieved via systematic review methods, such as fuller documentation of search methods and use of risk of bias assessments. (See CEN coverage here. Also see the NRC’s review of EPA’s IRIS program.)

Semen Quality, EDCs | Direct action of endocrine disrupting chemicals on human sperm. A study of the action of 96 ubiquitous EDCs on human sperm, suggesting that many different EDCs can activate the same sperm-specific cation channel, inducing increase in motility response and other effects. The researchers conclude that EDCs interfere with various sperm functions and, thereby, might impair human fertilization. (See coverage in the UK Independent.)

Epigenetics, BPA, Diabetes | F0 maternal BPA exposure induced glucose intolerance of F2 generation through DNA methylation change in Gck. Study investigating whether or not BPA exposure can disrupt glucose homeostasis in second-generation offspring and any underlying epigenetic mechanism. The offspring were found to exhibit glucose intolerance and insulin resistance and down-regulation of the glucokinase (Gck) gene in liver. Methylation of the Gck promoter in offspring’s hepatic tissue was very different to controls.

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