Association of early life exposure to bisphenol A with obesity and cardiometabolic traits in childhood

Vafeiadi, Marina; Roumeliotaki, Theano; Myridakis, Antonis; Chalkiadaki, Georgia; Fthenou, Eleni; Dermitzaki, Eirini; Karachaliou, Marianna; Sarri, Katerina; Vassilaki, Maria; Stephanou, Euripides G.; Kogevinas, Manolis; Chatzi, Leda

doi:10.1016/j.envres.2016.01.017

Cited by 134 publications

(129 citation statements)

References 75 publications

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“…Prenatal exposure to BPA has been shown to be negatively associated with BMI, adiposity, and percent body fat in young girls (403) (143) as well as associated with decreased birth weight (269). On the other hand, early exposure to BPA in ages 4–15 has been associated with increased BMI, obesity, and waist circumference (403) (143) (405) (417) (394); however, one study did show a negative association between BPA levels and BMI in 6–9 year old girls (428). Therefore, prenatal exposure to BPA seems to decrease the risk of obesity later in life while postnatal early exposure in childhood seems to increase the risk of childhood obesity.…”

Section: Associations Between Pop Exposures and The Development Of Obmentioning

confidence: 99%

Adipose Tissue as a Site of Toxin Accumulation

Jackson

Shoemaker

Larian

et al. 2017

Comprehensive Physiology

136

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We examine the role of adipose tissue, typically considered an energy storage site, as a potential site of toxicant accumulation. Although the production of most persistent organic pollutants (POPs) was banned years ago, these toxicants persist in the environment due to their resistance to biodegradation and widespread distribution in various environmental forms (e.g., vapor, sediment, water). As a result, human exposure to these toxicants is inevitable. Largely due to their lipophilicity, POPs bioaccumulate in adipose tissue, resulting in greater body burdens of these environmental toxicants with obesity. POPs of major concern include polychlorinated biphenyls (PCBs), polychlorinated dibenzo-p-dioxins and furans (PCDDs/PCDFs), and polybrominated biphenyls and diphenyl ethers (PBBs/PBDEs), among other organic compounds. In this review, we 1) highlight the physical characteristics of toxicants that enable them to partition into and remain stored in adipose tissue, 2) discuss the specific mechanisms of action by which these toxicants act to influence adipocyte function, and 3) review associations between POP exposures and the development of obesity and diabetes. An area of controversy relates to the relative potential beneficial versus hazardous health effects of toxicant sequestration in adipose tissue.

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Section: Associations Between Pop Exposures and The Development Of Obmentioning

confidence: 99%

Adipose Tissue as a Site of Toxin Accumulation

Jackson

Shoemaker

Larian

et al. 2017

Comprehensive Physiology

136

View full text Add to dashboard Cite

show abstract

“…104–107,117,118,138 Three publications report that higher prenatal BPA exposure was associated with lower BMI and that these associations were stronger in girls. 104–106 Two other publications reported that prenatal BPA exposure was associated with increased waist circumference, BMI, and risk of being overweight or obese. 107,117 Two other publications reported no association between prenatal BPA exposure and child adiposity measures.…”

Section: Bpamentioning

confidence: 99%

Early-life exposure to EDCs: role in childhood obesity and neurodevelopment

2016

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Endocrine disrupting chemicals (EDCs) may increase the risk of childhood diseases by disrupting hormonally mediated processes critical for growth and development during gestation, infancy, or childhood. The fetus, infant, and child may have enhanced sensitivity to environmental stressors like EDCs due to rapid development and greater exposure to some EDCs that results from their developmentally appropriate behavior, anatomy, and physiology. This review summarizes epidemiological studies examining the relations of early-life exposure to bisphenol A (BPA), phthalates, triclosan, and perfluoroalkyl substance (PFAS) with childhood neurobehavioral disorders and obesity. The available epidemiological evidence suggests that prenatal exposure to several of these ubiquitous EDCs is associated with adverse neurobehavior (BPA and phthalates) and excess adiposity or increased risk of obesity/overweight (PFAS). Quantifying the effects of EDC mixtures, improving EDC exposure assessment, reducing bias from confounding, identifying periods of heightened vulnerability, and elucidating the presence and nature of sexually dimorphic EDC effects would result in stronger inferences from epidemiological studies. Ultimately, better estimates of the causal effects of EDC exposures on child health could help identify susceptible sub-populations and lead to public health interventions to reduce these exposures.

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“…Harley et al found that higher levels of urinary BPA in mothers during pregnancy were associated with lower BMI status in their 9-year old female offspring [56]. Another group found a similar inverse association between prenatal BPA exposure and BMI status in female children 1–4 years of age, but also found a positive association between prenatal BPA and BMI status in male offspring [57]. …”

Section: Prenatal Exposure To Pb and Bpa In Humansmentioning

confidence: 99%

Sexually Dimorphic Effects of Early-Life Exposures to Endocrine Disruptors: Sex-Specific Epigenetic Reprogramming as a Potential Mechanism

McCabe

Anderson

Montrose

et al. 2017

Curr Envir Health Rpt

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Purpose of review The genetic material of every organism exists within the context of regulatory networks that govern gene expression—collectively called the epigenome. Animal models and human birth cohort studies have revealed key developmental periods that are important for epigenetic programming and vulnerable to environmental insults. Thus, epigenetics represent a potential mechanism through which sexually dimorphic effects of early-life exposures such as endocrine disrupting chemicals (EDCs) manifest. Recent findings Several animal studies, and to a lesser extent human studies, have evaluated life-course sexually dimorphic health effects following developmental toxicant exposures; many fewer studies, however, have evaluated epigenetics as a mechanism mediating developmental exposures and later outcomes. Summary To evaluate epigenetic reprogramming as a mechanistic link of sexually dimorphic early-life EDCs exposures, the following criteria should be met: 1) well characterized exposure paradigm that includes relevant windows for developmental epigenetic reprogramming; 2) evaluation of sex-specific exposure-related epigenetic change; and 3) observation of a sexually dimorphic phenotype in either childhood, adolescence, or adulthood.

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Association of early life exposure to bisphenol A with obesity and cardiometabolic traits in childhood

Cited by 134 publications

References 75 publications

Adipose Tissue as a Site of Toxin Accumulation

Adipose Tissue as a Site of Toxin Accumulation

Early-life exposure to EDCs: role in childhood obesity and neurodevelopment

Sexually Dimorphic Effects of Early-Life Exposures to Endocrine Disruptors: Sex-Specific Epigenetic Reprogramming as a Potential Mechanism

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