Bisphenol A: An endocrine disruptor with widespread exposure and multiple effects

Rubin, Beverly S.

doi:10.1016/j.jsbmb.2011.05.002

Cited by 1,155 publications

(698 citation statements)

References 120 publications

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“…Genistein-induced epigenetic alterations seems to share important similarities with those found in intrauterine growth retardation neonates (Einstein et al, 2010), but the magnitude is markedly lower than the differences found between tissues or in cancer. As previously described, perinatal undernutrition (Jousse et al, 2011) or overnutrition (Plagemann et al, 2009), the intake of particular nutrients like methyl donors (Waterland et al, 2008) or PUFA (Kiec-Wilk et al, 2011), or the exposure to endocrine disruptors like bisphenol A (Rubin et al, 2011) are crucial in the in utero modulation of the epigenetic marks (DNA methylation or histone modifications), and more efforts must be made to unravel the epigenetic mechanisms involved in the pathogenesis of obesity and metabolic syndrome, including the doses of each compound, the interactions with the genotype and the period or length of the exposure. One interesting example of possible application of this research is the demonstration that leptin administration during the suckling period has protective effects against later obesity probably by inducing changes in promoter methylation of the hypothalamic POMC gene (Palou et al, 2011).…”

Section: Perinatal Events (Gestation and Lactation)mentioning

confidence: 98%

“…In this sense, endocrine disruptors act by inducing epigenetic alterations in estrogen responsive elements (ERE) sensitivity to estrogens (Bromer et al, 2010). As it is well established that early exposure to bisphenol A leads to adult obesity (Rubin, 2011), and that this compound induces profound alterations in DNA methylation and other epigenetic processes, it is necessary to design new perinatal and transgenerational experiments in rodents that could determine the targets and periods of life that are more sensitive to these endocrine disruptors, as well as the doses.…”

Section: Endocrine Disruptors and Toxicsmentioning

confidence: 99%

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Dietary factors, epigenetic modifications and obesity outcomes: Progresses and perspectives

Milagro

Mansego

Miguel

et al. 2013

Molecular Aspects of Medicine

252

161

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Nutritional factors play a life-long role in human health. Indeed, there is growing evidence that one of the mechanisms by which nutrients and bioactive compounds affect metabolic traits is epigenetics. Complex interactions among food components and histone modifications, DNA methylation, non-coding RNA expression and chromatin remodeling factors lead to a dynamic regulation of gene expression that controls the cellular phenotype. Although perinatal period is the time of highest phenotypic plasticity, contributing largely to developmental programming, also during adulthood there is evidence about a nutritional influence on epigenetic regulation. Similarly to type 2 diabetes, hypertension, atherosclerosis and other metabolic disorders, obesity predisposition and weight loss outcomes have been repeatedly associated to changes in epigenetic patterns. Different non-nutritional risk factors that usually accompany obesity seem also to be involved in these epigenetic modifications, especially hyperglycemia, inflammation, hypoxia and oxidative stress. There are currently three major objectives in epigenetic research in relation to obesity: to search for epigenetic biomarkers to predict future health problems or detect the individuals at most risk, to understand the obesity-related environmental factors that could modulate gene expression by affecting epigenetic mechanisms, and to study novel therapeutic strategies based on nutritional or pharmacological agents that can modify epigenetic marks. At this level, the major tasks are: development of robust epigenetic biomarkers of weight regulation, description of those epigenetic marks more susceptible to be modified by dietary exposures, identification of the active ingredients (and the doses) that alter the epigenome, assessment of the real importance of other obesity-related factors on epigenetic regulation, determination of the period of life in which best results are obtained, and understanding of the importance of the inheritance of these epigenetic marks.

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Section: Perinatal Events (Gestation and Lactation)mentioning

confidence: 98%

Section: Endocrine Disruptors and Toxicsmentioning

confidence: 99%

Dietary factors, epigenetic modifications and obesity outcomes: Progresses and perspectives

Milagro

Mansego

Miguel

et al. 2013

Molecular Aspects of Medicine

252

161

View full text Add to dashboard Cite

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“…BPA is used as a component of polycarbonate plastics and in epoxy resins (18) . The list of products currently made with polycarbonate plastics or lined with epoxy resins is extensive, and includes food and beverage storage containers and packaging (20) .…”

mentioning

confidence: 99%

Bisphenol A exposure and associations with obesity among adults: a critical review

Oppeneer

Robien

2014

Public Health Nutr.

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Objective: To review the literature on bisphenol A (BPA) exposure and obesity in human populations. Design: Systematic review of the literature via searches of PubMed, EMBASE, Web of Science and reference lists for articles published to 1 August 2014. Setting: China, Italy, Japan, Republic of Korea, Sweden, UK, USA. Subjects: Adults (≥18 years). Results: Eighteen articles were identified and included in the review. Twelve studies included secondary evaluations of BPA exposure and BMI, and six studies evaluated body composition as the primary outcome. All analyses were crosssectional and no study included in the review received a positive quality rating (twelve negative, six neutral). Eight studies observed a statistically significant positive association between urinary or serum BPA levels and BMI, and ten studies observed no association. Studies where BMI was a primary outcome and studies of neutral quality were more likely to observe an association. Conclusions: Study results are conflicting and significant methodological issues limit the ability to draw conclusions from these studies. Prospective studies that measure BPA exposure and changes in body weight and composition are needed to establish temporality, causality and the direction of any observed associations.

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“…Conclusions: Known dietary sources of BPA exposure explained less than half the variability in uBPA levels, regardless of diet assessment method. Findings suggest that a questionnaire approach may be insufficient for ranking BPA exposure level and additional important sources of BPA exposure likely exist.Bisphenol A (BPA), used in the manufacture of polycarbonate plastics and epoxy resins, is one of the highest-volume chemicals produced worldwide (1,2) and production is predicted to reach more than 4·09 Mt (9 billion lb) by 2020 (3) . Biomonitoring data indicate widespread, chronic low-level exposure to BPA (2,(4)(5)(6) .…”

mentioning

confidence: 99%

“…Biomonitoring data indicate widespread, chronic low-level exposure to BPA (2,(4)(5)(6) . Animal and in vitro data indicate exposure adversely affects health, but limited and conflicting human epidemiological data is often cited as a barrier for risk assessment by regulatory agencies (7)(8)(9) .…”

mentioning

confidence: 99%

Estimating bisphenol A exposure levels using a questionnaire targeting known sources of exposure

Nomura

Harnack

Robien

2015

Public Health Nutr.

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Objective: To develop a BPA Exposure Assessment Module (BEAM) for use in large observational studies and to evaluate the ability of the BEAM to estimate bisphenol A (BPA) exposure levels. Design: The BEAM was designed by modifying an FFQ with questions targeting known sources of BPA exposure. Frequency of intake of known dietary sources of BPA was assessed using the BEAM and three 24 h food records as a reference diet measurement tool. Urinary BPA (uBPA) levels were measured as the criterion tool in a pooled urine sample (nine spot samples per participant). Spearman correlations, linear regression and weighted kappa analysis were used to evaluate the ability of the BEAM and food records to estimate BPA exposure levels. Setting: Minneapolis/Saint Paul, MN, USA. Subjects: Sixty-eight healthy adult (20-59 years) volunteers. Results: Dietary BPA intake assessed by the BEAM was not associated with uBPA levels and was unable to predict participants' rank by uBPA levels. BEAM models with all a priori predictors explained 25 % of the variability in uBPA levels. Canned food intake assessed by food records was associated with uBPA levels, but was unable to rank participants by uBPA levels. Multivariable-adjusted food record models with a priori predictors explained 41 % of the variability in uBPA levels. Conclusions: Known dietary sources of BPA exposure explained less than half the variability in uBPA levels, regardless of diet assessment method. Findings suggest that a questionnaire approach may be insufficient for ranking BPA exposure level and additional important sources of BPA exposure likely exist.Bisphenol A (BPA), used in the manufacture of polycarbonate plastics and epoxy resins, is one of the highest-volume chemicals produced worldwide (1,2) and production is predicted to reach more than 4·09 Mt (9 billion lb) by 2020 (3) . Biomonitoring data indicate widespread, chronic low-level exposure to BPA (2,(4)(5)(6) . Animal and in vitro data indicate exposure adversely affects health, but limited and conflicting human epidemiological data is often cited as a barrier for risk assessment by regulatory agencies (7)(8)(9) . While recent epidemiological data suggest that BPA may be associated with alterations in sex and thyroid hormone levels (10)(11)(12)(13)(14)(15)(16)(17)(18) , infertility and polycystic ovary syndrome (19)(20)(21) , obesity (18,(22)(23)(24)(25)(26)(27)(28)(29) , pre-diabetes/type 2 diabetes (23,(30)(31)(32) and CVD (23,31,(33)(34)(35) , most are crosssectional analyses with important limitations, such as lack of long-term exposure data which are more relevant for chronic disease risk (36) . Diet has been considered the primary source of BPA exposure (37)(38)(39)(40)(41)(42)(43) and previous studies support diet as the major route of human BPA exposure (44)(45)(46)(47)(48)(49)(50) . The use of polycarbonate plastics in the production of food and beverage storage containers has been largely phased out in the USA. However, BPA is still used in epoxy resin linings of metal cans and lids (1,2,6,51...

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Bisphenol A: An endocrine disruptor with widespread exposure and multiple effects

Cited by 1,155 publications

References 120 publications

Dietary factors, epigenetic modifications and obesity outcomes: Progresses and perspectives

Dietary factors, epigenetic modifications and obesity outcomes: Progresses and perspectives

Bisphenol A exposure and associations with obesity among adults: a critical review

Estimating bisphenol A exposure levels using a questionnaire targeting known sources of exposure

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