Abstract:BackgroundBisphenol A (BPA) and 4-tertiary-octylphenol (tOP) are industrial chemicals used in the manufacture of polycarbonate plastics and epoxy resins (BPA) and nonionic surfactants (tOP). These products are in widespread use in the United States.ObjectivesWe aimed to assess exposure to BPA and tOP in the U.S. general population.MethodsWe measured the total (free plus conjugated) urinary concentrations of BPA and tOP in 2,517 participants ≥ 6 years of age in the 2003–2004 National Health and Nutrition Examin… Show more
“…1. Before mating, female mice were assigned to each treatment group (2,20, and 200 μg/kg BPA or vehicle; n = 24 per treatment), and mice that became pregnant (∼70%) were exposed daily (oral administration) to the assigned treatment throughout gestation [gestational days (GD) 0-19]. Multiple BPA treatments permitted assessment of dose-dependent effects at doses above and below the current reference dose for humans (50 μg/kg/d).…”
Section: Resultsmentioning
confidence: 99%
“…We hypothesized that BPA may disrupt epigenetic programming of gene expression in the brain. Here, we provide evidence that maternal exposure during pregnancy to environmentally relevant doses of BPA (2,20, and 200 μg/kg/d) in mice induces sex-specific, dose-dependent (linear and curvilinear), and brain region-specific changes in expression of genes encoding estrogen receptors (ERs; ERα and ERβ) and estrogen-related receptor-γ in juvenile offspring. Concomitantly, BPA altered mRNA levels of epigenetic regulators DNA methyltransferase (DNMT) 1 and DNMT3A in the juvenile cortex and hypothalamus, paralleling changes in estrogen-related receptors.…”
mentioning
confidence: 95%
“…More than 90% of the examined US population has detectable levels of BPA in urine (2), with exposure occurring through diet, inhalation, and dermal absorption (1). Although potentially toxic throughout life, early-life exposure to BPA is of highest health concern (3,4) as this compound may accumulate in fetal and infant tissues, disrupting normal developmental processes (1).…”
Bisphenol A (BPA) is an estrogenic endocrine disruptor widely used in the production of plastics. Increasing evidence indicates that in utero BPA exposure affects sexual differentiation and behavior; however, the mechanisms underlying these effects are unknown. We hypothesized that BPA may disrupt epigenetic programming of gene expression in the brain. Here, we provide evidence that maternal exposure during pregnancy to environmentally relevant doses of BPA (2, 20, and 200 μg/kg/d) in mice induces sex-specific, dose-dependent (linear and curvilinear), and brain region-specific changes in expression of genes encoding estrogen receptors (ERs; ERα and ERβ) and estrogen-related receptor-γ in juvenile offspring. Concomitantly, BPA altered mRNA levels of epigenetic regulators DNA methyltransferase (DNMT) 1 and DNMT3A in the juvenile cortex and hypothalamus, paralleling changes in estrogen-related receptors. Importantly, changes in ERα and DNMT expression in the cortex (males) and hypothalamus (females) were associated with DNA methylation changes in the ERα gene. BPA exposure induced persistent, largely sex-specific effects on social and anxiety-like behavior, leading to disruption of sexually dimorphic behaviors. Although postnatal maternal care was altered in mothers treated with BPA during pregnancy, the effects of in utero BPA were not found to be mediated by maternal care. However, our data suggest that increased maternal care may partially attenuate the effects of in utero BPA on DNA methylation. Overall, we demonstrate that low-dose prenatal BPA exposure induces lasting epigenetic disruption in the brain that possibly underlie enduring effects of BPA on brain function and behavior, especially regarding sexually dimorphic phenotypes.environmental | fetal origin of adult disease
“…1. Before mating, female mice were assigned to each treatment group (2,20, and 200 μg/kg BPA or vehicle; n = 24 per treatment), and mice that became pregnant (∼70%) were exposed daily (oral administration) to the assigned treatment throughout gestation [gestational days (GD) 0-19]. Multiple BPA treatments permitted assessment of dose-dependent effects at doses above and below the current reference dose for humans (50 μg/kg/d).…”
Section: Resultsmentioning
confidence: 99%
“…We hypothesized that BPA may disrupt epigenetic programming of gene expression in the brain. Here, we provide evidence that maternal exposure during pregnancy to environmentally relevant doses of BPA (2,20, and 200 μg/kg/d) in mice induces sex-specific, dose-dependent (linear and curvilinear), and brain region-specific changes in expression of genes encoding estrogen receptors (ERs; ERα and ERβ) and estrogen-related receptor-γ in juvenile offspring. Concomitantly, BPA altered mRNA levels of epigenetic regulators DNA methyltransferase (DNMT) 1 and DNMT3A in the juvenile cortex and hypothalamus, paralleling changes in estrogen-related receptors.…”
mentioning
confidence: 95%
“…More than 90% of the examined US population has detectable levels of BPA in urine (2), with exposure occurring through diet, inhalation, and dermal absorption (1). Although potentially toxic throughout life, early-life exposure to BPA is of highest health concern (3,4) as this compound may accumulate in fetal and infant tissues, disrupting normal developmental processes (1).…”
Bisphenol A (BPA) is an estrogenic endocrine disruptor widely used in the production of plastics. Increasing evidence indicates that in utero BPA exposure affects sexual differentiation and behavior; however, the mechanisms underlying these effects are unknown. We hypothesized that BPA may disrupt epigenetic programming of gene expression in the brain. Here, we provide evidence that maternal exposure during pregnancy to environmentally relevant doses of BPA (2, 20, and 200 μg/kg/d) in mice induces sex-specific, dose-dependent (linear and curvilinear), and brain region-specific changes in expression of genes encoding estrogen receptors (ERs; ERα and ERβ) and estrogen-related receptor-γ in juvenile offspring. Concomitantly, BPA altered mRNA levels of epigenetic regulators DNA methyltransferase (DNMT) 1 and DNMT3A in the juvenile cortex and hypothalamus, paralleling changes in estrogen-related receptors. Importantly, changes in ERα and DNMT expression in the cortex (males) and hypothalamus (females) were associated with DNA methylation changes in the ERα gene. BPA exposure induced persistent, largely sex-specific effects on social and anxiety-like behavior, leading to disruption of sexually dimorphic behaviors. Although postnatal maternal care was altered in mothers treated with BPA during pregnancy, the effects of in utero BPA were not found to be mediated by maternal care. However, our data suggest that increased maternal care may partially attenuate the effects of in utero BPA on DNA methylation. Overall, we demonstrate that low-dose prenatal BPA exposure induces lasting epigenetic disruption in the brain that possibly underlie enduring effects of BPA on brain function and behavior, especially regarding sexually dimorphic phenotypes.environmental | fetal origin of adult disease
“…The CDC detected this persistent, endocrine-disrupting chemical in 75 % of the US population (Calafat et al 2008). Despite one company's decision, triclosan remains unregulated and in widespread use.…”
Biomonitoring has chronicled hundreds of synthetic chemicals in human bodies. With the proliferation of biomonitoring studies from diverse stakeholders comes the need to better understand the public health consequences of synthetic chemical exposures. Fundamental disagreements among scientific experts as to the nature and purpose of biomonitoring data guide our investigation in this paper. We examine interpretations of biomonitoring evidence through interviews with 42 expert scientists from industry, environmental health and justice movement organizations (EHJM), academia, and regulatory agencies and through participant observation in scientific meetings where biomonitoring evidence is under debate. Both social movements and industry stakeholders frame the meaning of scientific data in ways that advance their own interests. EHJM scientists argue that biomonitoring data demonstrates involuntary Btoxic trespass^and underscores a policy failure that allows for the pervasive use of untested chemicals. Industry scientists seek to subsume biomonitoring data under existing regulatory risk assessment paradigms. Our analysis reveals one area of convergence (validity of Centers for Disease Control surveillance data) and seven areas of contestation regarding the scientific, public health, and policy implications of biomonitoring evidence, among regulatory, industry, and EHJM scientists including: chemical presence in bodies, biological mechanisms of health impact, use of biomonitoring equivalents, limits of targeted biomonitoring, limits of detection, policy influence of advocacy biomonitoring, and relevance of biomonitoring to motivate policy change. These areas of scientific contestation provide insight into the persistent challenges of regulating chemicals even in the midst of mounting evidence of widespread exposure to multiple compounds with implications for human health.
“…In such a case, gene and environment interaction is expected to be a possible explanation of the missing etiology that can not be explained by either established risk factors. BPA are environmental synthetic xenoestrogen involving in carcinogens can be widely detected in the urine samples of human population (Calafat et al, 2008). Although human population are widely exposure to environmental BPA and BPA exposure may plays an important role in osteosarcoma pathogenesis by disturbing estrogen metabolism pathways, few studies have focused on the potential effects of the genetic-BPA interactions following the initial findings of genetic polymorphism in osteosarcoma.…”
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