Source: https://physiciansnews.com/2011/11/07/what-you-and-your-patients-need-to-know-about-bisphenol-a/
Timestamp: 2019-04-22 03:03:49+00:00

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Bisphenol A (BPA) is an environmental estrogen that can affect development and health by disrupting normal hormonal signaling. Estrogen, working at very low blood concentrations, triggers responses in cells and tissues and is critical during fetal development and in normal health and reproduction. BPA binds to the same cellular receptors as estrogen and may lead to detrimental health effects.
In June of this year, the American Medical Association formally recognized BPA as an endocrine-disrupting agent. Physicians can play an important role in educating their patients about this pervasive environmental contaminant. The first steps are to understand the potential health risks of BPA and how to limit those risks through simple lifestyle changes.
BPA is used in the production of polycarbonate plastics and epoxy resins. Many consumer products, such as some reusable water bottles, baby bottles, toys, cell phones, and DVDs, contain BPA. BPA is also found in the inner linings of metal food cans.1 The epoxy lining protects the metal can from rust and corrosion which may taint the food. It is present in various medical devices as well, including incubators, blood oxygenators, and dialysis machines. Given its wide uses, BPA ranks among the highest volume chemicals manufactured worldwide.
Although present in countless products, none of which is intended for consumption, the primary route of exposure is through ingestion. BPA has been shown to leach from products that contain it, such as food cans, into the foodstuffs stored in the container.1,2 When the food is then consumed, BPA enters the body through the digestive tract.
A 2007 survey by the Centers for Disease Control found that approximately 92% of Americans have detectable levels of BPA in their bodies.3 The survey is considered representative of the United States population even though it included only people older than six years old. It is notable, however, that the children (ages 6-11 years) in this study displayed the highest levels of BPA of all populations investigated. BPA has been found in placental tissue and fetal blood as well, indicating that fetuses are being exposed as a result of maternal exposure.4 An additional study looked at the levels of BPA in infants – specifically in premature infants housed in Neonatal Intensive Care Units.5 It was found that these infants displayed the highest level of BPA in their bodies of all populations.
While hundreds of studies, most focusing on animal models, point to the harmful health effects of BPA, there has been controversy over the past decade and a half regarding safety of the compound in humans. Nevertheless, scientific review panels have determined that some detrimental health effects may occur in humans.14-16 Likely human health effects that have been vetted through these review panels include advanced puberty in females14, 15 , effects on the brain and behavior15, 16, mammary gland and prostate abnormalities, and reproductive effects in males and females.
Humans are typically exposed to about 0.001 milligrams of BPA per kilogram of body weight per day. This is 50 times lower than the ‘safe’ limit set by the EPA and the Food and Drug Administration. Unfortunately, this level of exposure is still significantly higher than the low doses that have been shown to cause adverse health effects.
The concern of exposure is highest when fetuses, infants, and children are considered because of the adverse effects of BPA on normal developmental processes early in life.
It is clear that infants and children are burdened with the highest levels of BPA. This is likely due to several factors. First, the ability infants and children to metabolically detoxify contaminants such as BPA is not yet mature. While BPA will ultimately be removed from the blood through a liver-mediated process, BPA stays in the system of infants and children longer than in adults.16 Second, when compared to adults, infants and children consume proportionately more food when their overall body size is taken into account and therefore bodily concentrations are higher. The milk, formula, or food that is the main staple of an infant may be stored in containers (baby bottles, sippy cups) that are made with BPA.3, 22, 23 Infants and young children are also more likely to mouth plastic products, such as toys, that are not necessarily meant to be put in the mouth.
BPA can also pass from the mother to the fetus.5 In addition, breast milk can transmit BPA to an infant.24 Given this, it is not only the child, but the pregnant or nursing mother, that need to be protected from BPA exposure. Since the children cannot be responsible for making choices regarding BPA, clear information must be provided to parents (and potential parents) so that they can made the educated choices needed to protect themselves and their children.
Fortunately, BPA is metabolized and cleared from the body so decreasing daily exposure to BPA can make a difference in overall body levels.25, 26 In Japan, industries voluntarily reduced BPA use in their products between 1998 and 2003 and studies showed a dramatic decline in body levels of BPA in the population.27, 28 Educating your patients about a few simple lifestyle changes can make a difference in their overall BPA exposure and potentially reduce their risk for adverse health effects.
Second, minimizing the use of polycarbonate plastics food and beverage containers will also help. Polycarbonate plastics are usually hard, clear, and shatter-resistant. They may be labeled with recycle number 7, although not all number 7 products contain BPA.
Children are also more likely to mouth plastic products, such as toys or the hard plastic portion of a pacifier. Caregivers should be mindful of products aimed at children that may contain BPA, such as sippy cups, tableware, and toys.3, 22, 26 Thankfully, manufacturers are increasingly labeling products as “BPA-free”. The American Medical Association adopted a new policy in 2011 supporting continued industry efforts to produce BPA-free baby products as well as a total ban on the sale of such products.
As of 2011, ten states have passed legislation limiting the use of BPA in products aimed at children. Pennsylvania has similar legislation, spearheaded by Representative Lawrence Curry, that is currently in the House Health Committee. In New Jersey, Senator Linda Greenstein introduced a related bill in 2010 that has been referred to the Senate Commerce Committee.
While the current BPA legislation is an important step, the direct education of patients about BPA and the simple steps that can be taken to minimize their BPA exposure may lead to health improvements within the community.
Rebecca Roberts, Ph. D., is an Associate Professor in the Department of Biology and Coordinator of the Biochemistry and Molecular Biology Program at Ursinus College in Collegeville, PA, where she studies the effect of hormonal regulation of the immune system, with a focus on the roles of estrogen and bisphenol A in Systemic Lupus Erythematosus. She has been active in educating the public about bisphenol A and recently presented expert testimony to the Pennsylvania House of Representatives Democratic Policy Committee regarding toxin-free toddler and baby products.
1. Goodson, A., H. Robin, W. Summerfield, and I. Cooper, 2004. Migration of bisphenol A from can coatings – effects of damage, storage conditions and heating. Food Addit Contam, v. 21(10), pp. 1015-26.
2. Brede, C., P. Fjeldal, I. Skjevrak, and H. Herikstad. 2003 Increased migration levels of bisphenol A from polycarbonate baby bottles after dishwashing, boiling and brushing. Food Addit Contam, v. 20(7), pp. 684-9.
4. Calafat A.M., J. Weuve, X. Ye, L.T. Jia, H. Hu, S. Ringer, K. Huttner, and R. Hauser, 2009. Exposure to bisphenol A and other phenols in neonatal intensive care unit premature infants. Environ Health Perspect, v. 117, pp. 639-644.
5. Schonfelder, G., W. Wittfoht, H. Hopp, C.E. Talsness, M. Paul, and I. Chahoud, 2002. Parent bisphenol A accumulation in the human maternal-fetal-placental unit. Environ Health Perspect, v. 110(11), pp. A703-7.
6. Takeuchi, T., O. Tsutsumi, Y. Ikezuki, Y. Takai, and Y. Taketani, 2004. Positive relationship between androgen and the endocrine disruptor, bisphenol A, in normal women and women with ovarian dysfunction. Endocr J., v. 51, pp. 165-169.
7. Sugiura-Ogasawara, M., Y. Ozaki, S. Sonta, T. Makino, and K. Suzumori, 2005. Exposure to bisphenol A is associated with recurrent miscarriage. Hum Reprod, v. 20, pp.2325-2329.
8. Melzer, D., Rice, N.E., Lewis, C., Henley, W.E., Galloway, T.S. (2010). Association of urinary bisphenol a concentration with heart disease: evidence from NHANES 1003/06. PLoS One, v. 5(1), pp8673.
9. Singleton, D.W., Y. Feng, Y. Chen, S.J. Busch, A.V. Lee, A. Puga, and S.A. Khan, 2004.Bisphenol-A and estradiol exert novel gene regulation in human MCF-7 derived breast cancer cells. Mol Cell Endocrinol, v. 221(1-2), pp. 47-55.
10. Lee, C.K., S.H. Kim, D.H. Moon, J.H. Kim, B.C. Son, D.H. Kim, C.H. Lee, H.D. Kim, J.W. Kim, J.E. Kim, and C.U. Lee, 2005. Effects of bisphenol A on the placental function and reproduction in rats. J Prev Med Pub Health. v. 38(3), pp. 330-336.
11. Markey, C.M., P.R. Wadia, B.S. Rubin, C. Sonnenscheine, and A.M. Soto, 2005. Long Term Effects of Fetal Exposure to Low Doses of the Xenoestrogen Bisphenol-A in the Female Mouse Genital Tract. Biol Reprod, v. 72(6), pp. 1344-51.
12. Nikaido, Y., K. Yoshizawa, N. Danbara, M. Tsujita-Kyutoku, T. uri, N. Uehara, and A.Tsubura, 2004. Effects of maternal xenoestrogen exposure on development of the reproductive tract and mammary gland in female CD-1 mouse offspring. Reprod Toxicol, v. 18(6), pp. 803-811.
13. Rubin, B.S., J.R. Lenkowski, C.M. Schaeberle, L.N. Vandenberg, P.M. Ronsheim, and A.M. Soto, 2006. Evidence of altered brain sexual differentiation in mice exposed perinatally to low, environmentally relevant levels of bisphenol A. Endocrinology, v.147(8), pp. 3681-3691.
14. National Toxicology Program’s Report of the Endocrine Disruptors Low Dose Peer Review (2001).
15. U.S. Department of Health and Human Services, National Institutes of Health, National Toxicology Program, Center for the Evaluation of Risks to Human Reproduction. NTP-CERHR monograph on the potential human reproductive and developmental effects of bisphenol A (NIH Publication No. 08-5994).
16. Vom Saal, F.S. et al., 2007. Chapel Hill bisphenol A expert panel consensus statement: Integration of mechanisms, effects in animals and potential to impact human health at current levels of exposure. Reproductive Toxicology, v. 24, pp. 131-138.
17. Kudakovic, M. and F.A. Champagne, 2011. Epigenetic perspective on the developmental effects of bisphenol A. Brain, Behavior, and Immunity. V. 25(6), pp. 1084-93.
18. Dolinoy, D.C., D. Huang, and R.L. Jirtle, 2007. Maternal nutrient supplementation counteracts bisphenol A-induced DNA hypomethylation in early development. PNAS, v. 104(32), pp. 13056-13061.
19. Walker, D.M. and A.C. Gore, 2011. Transgenerational neuroendocrine disruption of reproduction. Nat Rev Endocrinol. v. 7(4), pp197-207.
20. U.S. Environmental Protection Agency, 2010. Bisphenol A (BPA) action plan summary.
21. U.S. Department of Health and Human Services, 2010. Bisphenol A (BPA) information for parents.
22. Vandenberg, L.N., R. Hauser, M. Marcus, N. Olea, and W.V. Welshons, 2007. Human exposure to bisphenol A (BPA). Reproductive Toxicology, v. 24, pp. 139-177.
23. Kuo, H.W. and W.H. Ding, 2004. Trace determination of bisphenol A and phytoestrogens in infant formula powders by gas chromatography-mass spectrometery. J. Chromatogr A, v. 1027, pp. 67-74.
24. Houlihan, J., 2007. Toxic plastics chemical in infant formula. Environmental Working Group.
25. Carwile JL, Luu HT, Bassett LS, Driscoll DA, Yuan C, Chang JY, Ye X, Calafat AM, Michels KB, 2009. Polycarbonate bottle use and urinary bisphenol A concentrations. Environ Health Perspect, v. 117(9), pp. 1368-1372.
26. Vökel, Wl, Kiraoglu, M., Fromme, H., 2011. Determination of free and total bisphenol A in urine of infants. Environ Res, v. 111(1), pp.143-148.
27. Matsumoto A KN, Kitagawa K, Isse T, Oyama T, Foureman GL, Morita M, Kawamoto T. 2003. Bisphenol A levels in human urine. Environ Health Perspect 111(1): 101-4.
28. Research Center for Chemical Risk Management (2005). Bisphenol A Risk Assessment Document. AIST Risk Assessment Document Comprehensive Chemical Substance Assessment and Management Program. Japan.
30. Breast Cancer Fund (2011). BPA in Kids’ Canned Food.
Well, I can not compete with the highly scientific studies quoted above. But what I can offer is this: meet my 13 year old daughter, who has markedly low estradiol, elevated (although blessedly not *too* elevated) androgens, and body hair in keeping with those androgens – possibly PCOS, although she does not have most of the other symptoms outside the Labwork.
What she *did* have was a definitive reaction when we abruptly eliminated BPA from our diet. After over two years of stable periods (beyond the erratic first six months) she skipped a cycle, then began bleeding every 16-18 days for the next four months. Our very limited, gluten/corn/casein free diet did not alter, either before, during or after this event, nor were there any other changes that could be considered remotely likely to affect the menses. Our only change was to rid the house and diet of all plastics, cans, non stick coatings and even TP made from recycled paper.
She has apparently stabilized, however, labs indicate that her last two cycles may have been anovulatory.
I hope the relevance of this real-world example is obvious, and thank those who research and publish what history will write: filling our bodies with endocrine disruptors will not be seen as a Very Bright Idea in the future.
You wrote: “Likely human health effects that have been vetted through these review panels include advanced puberty in females14, 15 , effects on the brain and behavior15, 16, mammary gland and prostate abnormalities, and reproductive effects in males and females.
Regarding Rebecca Roberts’s recent article, BPA has an active and an inactive form in the human body. It is well known that when ingested, almost all BPA is converted into the inactive form and excreted. In fact, the amount of BPA that CDC measured in urine is encouraging, as it is evidence that the amount of BPA to which people, including children, are exposed is extremely small. Also, FDA studies have shown that ingested BPA does not reach the fetus, even at levels well above typical human exposures.
Drs. Ronald Lorentzen and David Hattan, FDA toxicologists, recently discussed how some scientists opining on the human health risks of BPA do not have the appropriate experience in applying results of laboratory studies to assess these risks. They suggested that these scientists have not considered that not all laboratory studies are equally informative regarding human health risks. For example, rats metabolize BPA much less efficiently than humans, and many studies in animals use exposure routes that are not informative for human risk assessment (e.g., injection).
With respect to the human studies, Dr. Mary Wolff, a prominent epidemiologist, noted that certain epidemiology methods are not appropriate for assessing BPA health effects, and that few (if any) took precautions to prevent sample contamination or deal with statistical noise, complicating the interpretation of results.
The only appropriate scientific way to assess BPA toxicity and epidemiology studies is to consider each one in the context of all other relevant studies that have been conducted. Those who claim that BPA could cause harm do not conduct such analyses. When one analyzes these studies in the appropriate manner, the weight of evidence does not indicate harm from human exposures to BPA among fetuses, newborns, infants, children, or adults. Doctors and other health professionals should take this information into account as they consider how to counsel their patients.
Excellent! A Beautiful article! I have been waiting for this for years! BPA in coated, thermally activated papers should have been mentioned though, do not underestimate that route of exposure. Also the mechanism of anovulatory cycles raising testosterone producing ovarian cysts which deprive females of much needed progesterone because of the absence of a corpus luteum, and instead drench her body with excess androgens. A woman with obvious belly fat, facial and torso hair, and shoulders that are much wider than the hips is a sure tip off that she has pcos caused by bpa exposure.
Also manufacturers did not willingly remove bpa from their products, consumers removed it from the list of products they are willing to buy. Government and industry have played catch up to public opinion and have banned bpa products only after no one would buy them anymore. Also there has been excellent progress by corporations who DON’T manufacture bpa like BASF who recently discovered phenol free coatings for receipt paper, and a recent advance in developing a bpa free epoxy coating for use in rail cars that carry food products.
The massive disinformation war that occurs around the world in every regulatory jurisdiction is outside the scope of this article but I’m not complaining. The human race has a wonderful ally in the form of Dr. Rebecca Roberts, bravo again on your excellent work!

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