Distribution of bisphenol-A, triclosan and n-nonylphenol in human adipose tissue, liver and brain

Geens, Tinne; Neels, Hugo; Covaci, Adrian

doi:10.1016/j.chemosphere.2012.01.002

Cited by 273 publications

(157 citation statements)

References 46 publications

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“…Studies have demonstrated higher levels of BPA in adipose tissue versus liver and brain tissues in human samples. 52 It is possible obese individuals store BPA differently than nonobese individuals, thus leading to higher concentrations of BPA in the urine. It is unclear if a single measure of BPA would be indicative of long-term exposure to BPA, as humans metabolize and excrete BPA relatively rapidly (half-life of 6 hours with nearly complete urinary excretion by 24 hours).…”

Section: Discussionmentioning

confidence: 99%

Bisphenol A and Chronic Disease Risk Factors in US Children

Eng¹,

Lee²,

Gebremariam³

et al. 2013

Pediatrics

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WHAT'S KNOWN ON THIS SUBJECT: Bisphenol A (BPA) is a known endocrine disruptor found in many products with which children come into contact. Although BPA in adults is associated with obesity, diabetes, and cardiovascular disease, little is known about its effects in children. WHAT THIS STUDY ADDS:This study found that higher BPA levels are associated with obesity and abnormal waist circumferenceto-height ratio in children. abstract OBJECTIVE: To evaluate the relationship between urinary bisphenol A (BPA) levels and measures of adiposity and chronic disease risk factors for a nationally representative US pediatric sample. METHODS:We used the NHANES 2003-2010 to evaluate cross-sectional associations between urinary BPA and multiple measures of adiposity, cholesterol, insulin, and glucose for children aged 6 to 18 years, adjusting for relevant covariates (eg, demographics, urine creatinine, tobacco exposure, and soda consumption). RESULTS:We found a higher odds of obesity (BMI $95th percentile) with increasing quartiles of BPA for quartiles 2 vs 1 (odds ratio [OR] 1.74, 95% confidence interval [CI] 1.17-2.60, P = .008), 3 vs 1 (OR 1.64, 95% CI 1.09-2.47, P = .02), and 4 vs 1 (OR 2.01, 95% CI 1.36-2.98, P = .001). We also found a higher odds of having an abnormal waist circumference-to-height ratio (quartiles 2 vs 1 [OR 1.37, 95% CI 0.98-1.93, P = .07], 3 vs 1 [OR 1.41, 95% CI 1.07-1.87, P = .02], and 4 vs 1 [OR 1.55, 95% CI 1.12-2.15, P = .01]). We did not find significant associations of BPA with any other chronic disease risk factors.CONCLUSIONS: Higher levels of urinary BPA were associated with a higher odds of obesity (BMI .95%) and abnormal waist circumference-to-height ratio. Longitudinal analyses are needed to elucidate temporal relationships between BPA exposure and the development of obesity and chronic disease risk factors in children. Pediatrics 2013;132:e637-e645 AUTHORS:

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Section: Discussionmentioning

confidence: 99%

Bisphenol A and Chronic Disease Risk Factors in US Children

Eng¹,

Lee²,

Gebremariam³

et al. 2013

Pediatrics

View full text Add to dashboard Cite

show abstract

“…It is possible that obese individuals store, metabolize, and/or excrete BPA differently from non-obese individuals, leading to higher BPA levels in their urine. 44,45 Nonetheless, a recent prospective cohort study of women showed that higher urinary BPA concentration at baseline was associated with greater weight gain during a 10-year follow-up, 46 although additional longitudinal studies in both sexes are warranted. Second, single spot urine measures may not be representative of long-term exposure to BPA.…”

Section: Strengths and Limitationsmentioning

confidence: 99%

Urinary bisphenol A and obesity in adults: results from the Canadian Health Measures Survey

Minh

Chang

Mendez

et al. 2017

Health Promot Chronic Dis Prev Can

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Introduction Exposure to bisphenol A (BPA) has been shown to affect lipid metabolism and promote weight gain in animal studies. Recent epidemiological studies also support a link between BPA and obesity in human populations, although many were limited to a single adiposity measure or have not considered potential confounding by dietary factors. The purpose of this study is to examine associations between urinary BPA and adiposity measures in a nationally representative sample of Canadian adults. Methods We performed analyses using biomonitoring and directly measured anthropometric data from 4733 adults aged 18 to 79 years in the Canadian Health Measures Survey (2007–2011). We used multinomial and binary logistic regression models to estimate associations of urinary BPA with body mass index (BMI) categories (overweight vs. under/normal weight; obesity vs. under/normal weight) and elevated waist circumference (males: ≥ 102 cm; females: ≥ 88 cm), respectively, while controlling for potential confounders. Linear regression analyses were also performed to assess associations between urinary BPA and continuous BMI and waist circumference measures. Results Urinary BPA was positively associated with BMI-defined obesity, with an odds ratio of 1.54 (95% confidence interval [CI]: 1.002–2.37) in the highest (vs. lowest) BPA quartile (test for trend, p = .041). Urinary BPA was not associated with elevated waist circumference defined using standard cut-offs. Additionally, each natural-log unit increase in urinary BPA concentration was associated with a 0.33 kg/m2 (95% CI: 0.10– 0.57) increase in BMI and a 1.00 cm (95% CI: 0.34–1.65) increase in waist circumference. Conclusion Our study contributes to the growing body of evidence that BPA is positively associated with obesity. Prospective studies with repeated measures are needed to address temporality and improve exposure classification.

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“…Due to its lipophilicity, TCS can easily pass through biological barriers and can be accumulated in living organisms [6,8]. A number of studies have revealed the presence of TCS in human tissues, such as in fat, the liver, brain and also in blood or breast milk [9][10][11][12]. Alarming concentrations of TCS have been detected in fish (13-88 ng/g) and human (0.23 ng/g) brains [10,13].…”

Section: Introductionmentioning

confidence: 99%

Triclosan-Evoked Neurotoxicity Involves NMDAR Subunits with the Specific Role of GluN2A in Caspase-3-Dependent Apoptosis

et al. 2018

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Triclosan (TCS) is an antimicrobial agent that is used extensively in personal care and in sanitising products. A number of studies have shown the presence of TCS in different human tissues such as blood, adipose tissue, the liver, brain as well as in breast milk and urine. N-Methyl-D-aspartate receptors (NMDARs) are glutamate-gated ion channels that are widely expressed in the central nervous system and which play key roles in excitatory synaptic transmission. There is, however, no data on the involvement of NMDAR subunits in the apoptotic and neurotoxic effects of TCS. Our experiments are the first to show that TCS used at environmentally relevant concentrations evoked NMDA-dependent effects in neocortical neurons in primary cultures, as MK-801, an uncompetitive NMDA receptor antagonist, reduced the levels of TCS-induced ROS production as well as caspase-3 activity and LDH release. TCS caused a decrease in protein expression of all the studied NMDA receptor subunits (GluN1, GluN2A, GluN2B) that were measured at 3, 6 and 24 h post-treatment. However, at 48 h of the experiment, the level of the GluN1 subunit returned to the control level, and the levels of the other subunits showed a tendency to increase. In TCS-treated neocortical cells, protein profiles of NMDAR subunits measured up to 24 h were similar to mRNA expression of GluN1 and GluN2A, but not to GluN2B mRNA. In this study, cells transiently transfected with GluN1, GluN2A or GluN2B siRNA exhibited reduced levels of LDH release, which suggests the involvement of all of the studied NMDAR subunits in the neurotoxic action of TCS. According to our data, GluN1 and GluN2A were mainly responsible for neuronal cell death as evidenced by neutral red uptake, whereas GluN2A was involved in TCS-induced caspase-3-dependent apoptosis. We suggest that TCS-evoked apoptosis and neurotoxicity could be related to transient degradation of NMDAR subunits in mouse neurons. Furthermore, recycling of NMDAR subunits in response to TCS is possible. Because transfections with specific siRNA did not completely abolish the effects of TCS as compared to cells transfected with negative siRNA in this study, other NMDAR-independent mechanisms of TCS action are also possible.

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Distribution of bisphenol-A, triclosan and n-nonylphenol in human adipose tissue, liver and brain

Cited by 273 publications

References 46 publications

Bisphenol A and Chronic Disease Risk Factors in US Children

Bisphenol A and Chronic Disease Risk Factors in US Children

Urinary bisphenol A and obesity in adults: results from the Canadian Health Measures Survey

Triclosan-Evoked Neurotoxicity Involves NMDAR Subunits with the Specific Role of GluN2A in Caspase-3-Dependent Apoptosis

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