Rapid report

Association between bisphenol A and waist-to-height ratio among children: National Health and Nutrition Examination Survey, 2003–2010

Bisphenol A (BPA) is a typical endocrine disrupting chemical with extensive applications, and has been correlated with various hazardous health effects, including obesity and other metabolic-related diseases. Human mesenchymal stem cells (hMSCs), due to their abilities to differentiate into adipocytes and osteoblasts, can be a good in vitro model to assess chemical-dependent toxicity on adipogenesis or osteogenesis. Here, we employed hMSCs as an evaluation system to assess BPA-related effects on cell viability, oxidative stress induction, self-renewal, and differentiation. Our results revealed that low concentrations (1 and 10 nM) of BPA did not impair cell proliferation nor self-renewal capacity, but stimulated adipogenesis and osteogenesis. Our findings support the concern of BPA contributing to the epidemic of obesity, and also reveal its underlying toxicity on osteogenesis.

To assess the relationship between in utero and concurrent child urinary exposures to bisphenol A (BPA) and phthalates with BMI z-score, waist circumference, and sum of triceps and subscapular skinfold thickness in Mexican children.

Among participants (N=249) from the Early Life Exposure in Mexico to ENvironmental Toxicants study, we evaluated associations between maternal third trimester and concurrent urinary BPA and individual and summed phthalates metabolites (∑Di(2-ethylhexyl phthalate), ∑high molecular weight, ∑low molecular weight) with measures of weight status and adiposity in children aged 8–14 years. Linear regressions with specific-gravity corrected and natural log-transformed urinary concentrations were estimated, adjusting for covariates. Effect modification by sex was explored.

Prenatal urinary exposure to monobenzyl phthalate (MBzP) was inversely associated with child's BMI z-score (β=−0.21, 95%CI: −0.41, −0.02) and child urinary exposure to mono(2-ethylhexyl)phthalate (MEHP) was inversely associated with waist circumference (β=−1.85, 95%CI: −3.36, −0.35) and sum of skinfold thicknesses (β=−2.08, 95%CI: −3.80, −0.37) after adjusting for confounders. In the childhood exposure period, sex modified the relationships with BPA, MEHP, MBzP, monoethyl phthalate (MEP), mono(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP), mono(2-ethyl-5-oxohexyl) phthalate (MEOHP), and mono(2-ethyl-5-carboxypentyl) phthalate (MECPP). In girls, increased BPA exposure was positively associated with sum of skinfold thickness (β=3.47, 95%CI: 0.05, 6.40) while increased MEHP was inversely associated with sum of skinfold thicknesses in boys (β=−2.95, 95%CI: −5.08, −0.82); these results remained in sensitivity analyses after excluding children who had initiated pubertal development (Tanner stage >1 for pubic hair). We did not observe relationships between summed phthalates metabolites at any exposure period with outcome measures.

Our results identified associations between urinary BPA and phthalates metabolites with measures of weight status and adiposity that differed by timing of exposure, sex, and pubertal status. Additional studies are needed to explore how associations may differ between those who are pre- and post-pubertal.

The incidence of childhood obesity, type 2 diabetes, and other forms of metabolic disease have been rising over the past several decades. Although diet and physical activity play important roles in these trends, other environmental factors also may contribute to this significant public health issue. In this article, we discuss the possibility that widespread exposure to endocrine-disrupting chemicals (EDCs) may contribute to the development of metabolic diseases in children. We summarize the epidemiological evidence on exposure to environmental chemicals during early development and metabolic outcomes in infants and children. Prenatal exposure to EDCs, particularly the persistent organic pollutant DDT and its metabolite DDE, may influence growth patterns during infancy and childhood. The altered growth patterns associated with EDCs vary according to exposure level, sex, exposure timing, pubertal status, and age at which growth is measured. Early exposure to air pollutants also is linked to impaired metabolism in infants and children. As a result of these and other studies, professional health provider societies have called for a reduction in environmental chemical exposures. We summarize the resources available to health care providers to counsel patients on how to reduce chemical exposures. We conclude with a discussion of environmental policies that address chemical exposures and ultimately aim to improve public health.

Bisphenol A (BPA) and triclosan (TCS) were determined in urine of Belgian overweight and obese (n = 151) and lean (n = 43) individuals. After the first urine collection (0 M), obese patients started a diet program or have undergone bariatric surgery. Hereafter, three additional urine samples from obese patients were collected after 3 (3 M), 6 (6 M) and 12 (12 M) months. Both compounds were detected in > 99% of the samples. BPA had median concentrations of 1.7 and 1.2 ng/mL in obese and lean groups, respectively, while TCS had median concentrations of 1.5 and 0.9 ng/mL in the obese and lean groups, respectively. The obese group had higher urinary concentrations (ng/mL) of BPA (p < 0.5), while no significant differences were found for TCS between the obese and lean groups. No time trends between the different collection moments were observed. The BPA concentrations in the obese group were negatively associated with age, while no gender difference or relationship with body mass index was observed. For TCS, no relationships with gender, BMI, or age were found. The temporal variability of BPA and TCS was assessed with calculation of the intraclass correlation coefficient, Spearman rank correlation coefficients, and surrogate category analysis. We observed evidence that single spot urine samples might be predictive of exposure over a longer period of time. Dietary intakes of BPA and TCS did not differ significantly among the time points considered after obese individuals started losing weight (6 and 12 months). Multiple linear regression analyses after adjusting for age and weight loss revealed negative associations between urinary TCS and serum FT4 in the 0 M and 3 M female obese individuals and positive associations between urinary BPA and serum TSH in the lean group.