Bisphenol A (BPA), an endocrine disrupting compound, is of concern because of its wide presence throughout the environment and its harmful effects. The present study aimed to prepare an eco-friendly, low-cost, and efficient adsorbent for removal of BPA from wastewater. A natural Tunisian clay was used as a raw material. First, the clay was purified and then modified with hexadecyltrimethylammonium bromide (HDTMA) using microwave heating. The optimal conditions for clay modification were as follows: activation ratio = 0.3:(g/g), solid/liquid ratio = 5%, and microwave heating condition (2:min, 100:W). The purified and modified clays, abbreviated as HP and HMH, respectively, were characterized by scanning electron microscopy (SEM), Fourier-transform infrared spectroscopy (FTIR), X-ray diffraction (XRD), and nitrogen adsorption/desorption analysis (BET). Adsorption tests were conducted in a batch reactor process under various conditions. The tests showed that the BET specific surface area of HMH is considerably smaller than that of HP, whereas the basal spacing increased from 14.99 to 22.07 Å after modification, indicating the success of HP organophilization. The adsorption of BPA onto HMH was not affected by the pH of solution between 2 and 10 and only slightly by temperature variation from 23 to 50°C, but was affected significantly by the initial concentration of BPA, contact time, and organo-clay dose. At equilibrium, the data obtained were fitted to Langmuir and Freundlich models. The best fit was obtained by the Langmuir model with a maximum monolayer adsorption capacity of 217.39 mg/g at 23°C. The thermodynamic study suggested that the removal of BPA by HMH was spontaneous (ΔG < 0), exothermic (ΔH < 0), and favorable. The present study demonstrated that HMH synthesized from an abundant and cheap natural clay could be used successfully as a low-cost adsorbent for the removal of BPA from wastewater.

Plastic production has greatly increased in the past decades and has become central to modern human life. Realization is dawning that plastics break down into smaller pieces resulting in micro- or nanoplastics (MNP) that can enter humans directly via the environment. Indeed, MNP have been detected in every part of the human body, including the placenta, which is concerning for development. Early developmental stages are crucial for proper growth and genome programming. Environmental disruptors in MNP can have detrimental effects during this critical window as well and can increase the risk of developing disease and dysfunction. In addition, MNP may impact situations in which developmental pathways are reactivated after birth such as during organ repair. Currently, there is no overview of how MNP can impair (human) development and repair. Therefore, we provide an extensive overview of available evidence on MNP impacting developmental and regenerative processes in various organs in humans and rodent models. In addition, we have included the impact of some additives that can leach from these MNP. We conclude that MNP and their additives can have modulating effects on developing and regenerating organs.

Bisphenol-A (BPA) is associated with adverse health outcomes and is found in many canned foods. It is not understood if some BPA contamination can be washed away by rinsing. The objective of this single-blinded crossover experiment was to determine whether BPA exposure, as measured by urinary concentrations, could be decreased by rinsing canned beans prior to consumption. Three types of hummus were prepared from dried beans, rinsed, and unrinsed canned beans. Fourteen healthy participants ate two samples of each hummus over six experimental days and collected spot urine specimens for BPA measurement. The geometric mean BPA levels for dried beans BPA (GM = 0.97 ng/ml, 95%CI = 0.74,1.26) was significantly lower than rinsed (GM = 1.89 ng/ml, 1.37,2.59) and unrinsed (GM = 2.46 ng/ml, 1.44,4.19). Difference-in-difference estimates showed an increase in GM BPA from pre- to post-hummus between unrinsed and rinsed canned beans of 1.39 ng/ml, p-value = 0.0400. Rinsing canned beans was an effective method to reduce BPA exposure.

Low probability risks create challenges for individual decisions and potential pressures for government regulation. This article reports original survey evidence regarding the public’s perception and valuation of water-related risks from plastic bottles with bisphenol A, residues in drinking water of the herbicide atrazine, and trace amounts of prescription drugs in water. People who believe that they face high water-related risks generally believe that the risks apply and, given that belief, are willing to pay more to limit the risk. However, the expressed willingness to pay for risk reductions is inordinately high even among those who are unsure of whether they are even exposed to the risk, and therefore may not be reliable as values for the actual benefits.

Bisphenol A (BPA) is a chemical found in plastics that resembles oestrogen in organisms. Developmental exposure to endocrine-disrupting chemicals, such as BPA, increases the susceptibility to type 2 diabetes (T2DM) and cardiovascular diseases. Animal studies have reported a nephron deficit in offspring exposed to maternal diabetes. The aim of this study was to investigate the prenatal BPA exposure effects on nephrogenesis in a mouse model that was predisposed to T2DM. This study quantitatively evaluated the renal structural changes using stereology and histomorphometry methods. The OF1 pregnant mice were treated with a vehicle or BPA (10 or 100 μg/kg/day) during days 9–16 of gestation (early nephrogenesis). The 30-day-old offspring were sacrificed, and tissue samples were collected and prepared for histopathological and stereology studies. Glomerular abnormalities and reduced glomerular formation were observed in the BPA offspring. The kidneys of the BPA10 and BPA100 female offspring had a significantly lower glomerular number and density than those of the CONTROL female offspring. The glomerular histomorphometry revealed a significant difference between the female and male CONTROL offspring for the analysed glomerular parameters that disappeared in the BPA10 and BPA100 offspring. In addition, the kidney histopathological examination showed typical male cuboidal epithelial cells of the Bowman capsule in the female BPA offspring. Exposure to environmentally relevant doses of BPA during embryonic development altered nephrogenesis. These structural changes could be associated with an increased risk of developing cardiometabolic diseases later in life.

To explore the effects of maternal nutrition on offspring muscle characteristics, a total of 56 sows were assigned to one of the four dietary groups during gestation: control (CON), or control diets supplemented with methyl donor (MET), bisphenol A (BPA), and combined BPA and MET (BPA+MET). Compared with CON offspring, MET offspring showed a higher meat redness value, but lower glycogen content in the longissimus thoracis (LT). Moreover, compared with CON offspring, MET offspring showed lower LT glycogen synthase (GS) mRNA levels at birth and the finishing stage, and increased methylation at the GS promoter. Prenatal BPA exposure reduced the pH and redness value of meat, but increased the lightness value, lactate content, glycolytic potential and lactate dehydrogenase (LDH) enzyme activity in the LT muscle. Prenatal BPA exposure increased LDH mRNA levels in the LT muscle at birth and the finishing stage, and reduced methylation at the LDH promoter. Thus, maternal MET affects muscle GS and LDH expression via DNA methylation, thereby resulting in persistent effects on pork quality.

Bisphenol A (BPA), a monomer of polycarbonate plastics and epoxide resin, is a high-production-volume chemical implicated in asthma pathogenesis when exposure occurs to the developing fetus. However, few studies have directly examined the effect of in utero and early-life BPA exposure on the pathogenesis of asthma in adulthood. This study examines the influence of perinatal BPA exposure through maternal diet on allergen sensitization and pulmonary inflammation in adult offspring. Two weeks before mating, BALB/c dams were randomly assigned to a control diet or diets containing 50 ng, 50 μg or 50 mg BPA/kg of rodent chow. Dams remained on the assigned diet throughout gestation and lactation until postnatal day (PND) 21 when offspring were weaned onto the control diet. Twelve-week-old offspring were sensitized to ovalbumin (OVA) and subsequently challenged with aerosolized OVA. Sera, splenocytes, bronchoalveolar lavage fluid and whole lungs were harvested to assess allergen sensitization and pulmonary inflammation after OVA challenge. Serum anti-OVA IgE levels were increased two-fold in offspring exposed to 50 μg and 50 mg BPA/kg diet, compared with control animals. In addition, production of interleukin-13 and interferon-γ were increased in OVA-stimulated splenocytes recovered from BPA-exposed mice. Pulmonary inflammation, as indicated by total and differential leukocyte counts, cytokines, chemokines and pulmonary histopathology inflammatory scores, however, was either not different or was reduced in offspring exposed to BPA. Although these data suggest that perinatal BPA exposure beginning before gestation enhances allergen sensitization by increasing serum IgE and splenocyte cytokine production, a substantial impact of BPA on OVA-induced pulmonary inflammation in adulthood was not observed.

Bisphenol A (BPA) is a chemical compound that has adverse health outcomes in adults when exposed during the perinatal period. However, its effect on cardiovascular function remains to be elucidated. In this study, we examined the effects of daily administration of BPA to pregnant mice from gestational days 11 to 19 on cardiometabolic outcomes in the adult offspring. Prenatal BPA exposure resulted in altered growth trajectory and organ size, increase adiposity and impaired glucose homeostasis in male and female offspring. In addition, these BPA offspring exhibited raised systolic blood pressure, and in the males this was accompanied by impaired vascular tone. The aortas in females, but not in males, from the BPA group also showed reduced estrogen receptor gene expression. These results indicate that prenatal exposure to BPA increased susceptibility of the offspring to developing cardiovascular and metabolic dysfunction later in life.

While early-life estrogens are thought to play a physiologic role in prostate gland development, inappropriate estrogenic exposures either in dose, type or temporally can reprogram the prostate gland and increase susceptibility to abnormal prostate growth with aging including carcinogenesis. This review discusses the evidence for developmental estrogenic reprogramming that leads to adult prostate disease in a rat model. We propose that estrogen imprinting of the prostate is mediated through both structural reorganization of the gland early in life and epigenomic reprogramming that permits life-long memory of the inappropriate developmental exposures including heightened sensitivity to rising estradiol levels with aging. Complex interactions between early epigenetic programming and later-life experiences results in an emergence of multiple epigenomic outcomes, with some contributing to carcinogenesis with aging.