Engagement POST and Response post to peer TO DISCUSSION BOARD:
My Post-Factors that contribute to the efficacy at global level and sustainability of food interventions at the global level?
Xenophobic implications can vary depending on the xenobiotic itself, its mechanism of action, and its target, among other factors. In addition, xenobiotic exposures mainly occur through inhalation, ingestion, absorption, and injection, with drugs, pesticides, cosmetics, and industrial chemicals being some common examples. Specifically, BPA is primarily exposed through diet in food and beverages, yet air, dust, and water are other possible sources (National Institute of Environmental Health Sciences). BPA can leach into food from the protective internal epoxy resin coatings of canned foods and multiple consumer products such as polycarbonate tableware, storage containers, water bottles, etc. The degree to which BPA leaches from polycarbonate bottles depends on the temperature of the bottle and the age of the container (National Institute of Environmental Health Sciences).
One method for measuring BPA levels in urine is via enzymatic glucuronidation which involves the addition of 13C12-labeled BPA, enzymatic deconjugation, solid-phase extraction, and derivatization with pentafluorobenzyl bromide (Brock et al., 2001). The product of the derivatization is separated by gas chromatography followed by mass spectrometric detection using negative chemical ionization and selected ion monitoring (Brock et al., 2001).
The sex-specific classification in BPA urine concentrations is due to the difference in androgen-related enzyme activity levels in males and females (Caporossi & Papaleo, 2015). BPA could interact differently in males and females with estrogen receptors and steroidogenesis, (Caporossi & Papaleo, 2015). Ultimately, the adjustable gender difference plays a key role in understanding the toxic outcomes of BPA exposure.
The importance of socioeconomic information can give potential insight into lifestyle habits that can influence one’s exposure to BPA. There were no measurements up until 6 years, they were at 6 months, 14 months, and 4 years. This was relevant to gather the timeline of the potential effects of BPA. In doing so they found significance only at 4 years. As for the 2nd order Reed Model, the best fit was obtained via intensive statistical methods. Please see this link for more details! https://math.ucsd.edu/_files/undergraduate/honors-program/honors-program-presentations/2010-2011/Minji_Kim_Honors_Thesis.pdf
You guys had a great question about why exactly the exposure to BPA wasn’t strongly associated with increased BMI. In order to find the answer to this question, more research will have to be done in the field relating to prenatal BPA exposure and obesity, as mentioned in the future directions section. As mentioned in the results, prenatal exposure did present a weak association with BMI in children at 4 years, but not at 14 months. Perhaps this could be due to the obesogen exposure (BPA) acting more later in life, taking more time to show effects in its endocrine disruption. Still, the association isn’t strong, and more research should be performed to discover this severity and timing of the outcome.
Regarding public health, it is currently banned to manufacture or import any baby products or bottles which contain BPA. The Chemical Management Plan in Canada works to monitor the BPA exposure of Canadians, and information continues to be gathered regarding future directions on the phenol substance class (“Bisphenol A – Canada.ca,” n.d.). Future steps for the public could involve checking their own packaging for any BPA products, especially those imported from international countries, being sure to only store and microwave foods in BPA free containers – based on our study and its possible associations, this would be especially important for pregnant mothers to be aware of in order to decrease exposures to their fetus (“Bisphenol A – Canada.ca,” n.d.).
Your question mentions BPA being affected by mothers smoking; I believe you meant to mention smoking affecting BMI rather than BPA. In our presentation, smoking was mentioned as a possible confounder. The obesity in the child could potentially be linked to smoking rather than possible BPA exposures. Again, more research could be done in this regard, removing this confounder from studies. Looking at current research involving smoking during pregnancy and future obesity outcomes, there is a positive association seen between maternal smoking and childhood obesity (Ino, 2010). In this meta-analysis, children whose mothers had smoked during pregnancy experienced higher BMI measurements with an odds ratio of 1.52 (Ino, 2010). This yielded future obesity and potential metabolic syndromes (Ino, 2010). It is true that often smoking during pregnancy yields low birth weight, this is due to the effects of the nicotine vasoconstriction vessels supplying the fetus and carbon monoxide causing hypoxemia (Ino, 2010). As we have learned in the modules, often time children born with low birth weights can demonstrate rapid catch up during their childhood, demonstrating the thrifty phenotype hypothesis leading to future insulin metabolism and body fat distribution differences (Ino, 2010).