Endocrine disrupting chemicals (EDCs) are chemicals that mimic, block, or interfere with hormones in the body. Increasing use of EDCs over the past 20 years may contribute to the growing number of people with infertility, diabetes, early onset of puberty in girls and early menopause in women, cancer, birth defects, and neurobehavioral disorders, as described in a guide to EDCs developed by The Endocrine Society and IPEN.
While it is not clear exactly how many EDCs exist, common EDCs include:
Known EDCs such as PCBs, BPA, and phthalates are found in blood, fat, and umbilical cord blood samples taken from people around the world. While some EDCs (eg, DDT and PCBs) have been banned, these chemicals may remain in the environment and food supply for decades. Some EDCs may be stored in fat cells for years after exposure, and may be passed on to children during pregnancy or when breastfeeding.
In contrast, BPA does not accumulate in the body, and studies have shown that minimizing the use of canned foods and plastic containers can reduce BPA levels found in the body. However, BPA is still used in so many products that the U.S. Centers for Disease Control and Prevention has estimated that more than 96% of Americans have BPA in their bodies.
How EDCs Affect Hormones
Endocrine disrupting chemicals may bind to an endocrine hormone’s receptor, activating the hormone’s receptor and triggering physiological processes. Alternately, some EDCs block endocrine hormones by binding their receptors and not allowing the receptors to be activated even in the presence of the natural hormones.
Like natural hormones, even small levels of EDCs can affect body functions.
Specifically, recent studies have shown the following:
Tips for Avoiding EDCs
Companies that make BPA-free canned foods include Amy’s, Eden Foods, Bionaturae canned tomatoes, Bumble Bee tuna, Earth’s Best, Farmer’s Market, Health Valley, Hain Pure Foods, Westbrae Natural, and many others. Some companies like Trader Joe’s list what foods are in BPA-free packages.
Commentary by Steven G. Hentges, PhD
Polycarbonate/BPA Global Group
American Chemistry Council
Bisphenol A (BPA) is a chemical that is primarily used to make polycarbonate plastic and epoxy resins, both of which are commonly used in consumer products. Polycarbonate is a hard clear plastic that is used in electronic products, automotive products, and many household products, including food storage containers. It also is commonly used in a range of medical devices, including syringe barrels, components of dialysis equipment, and blood oxygenation equipment.
Epoxy resins are commonly used in coating applications. For example, epoxy resins are the most common type of protective coating used in food and beverage cans. The coating is applied to prevent erosion of the can and possible contamination of food and drink from metal or bacteria.
These materials—BPA, polycarbonate, and epoxy resins—have been used safely for decades. Epoxy resins have been used in food cans for 30 to 40 years, and polycarbonate and epoxy resins have been used in numerous applications for approximately 50 years.
During that time, BPA has become one of the best-tested substances in commerce, perhaps even the most tested. In general, government agencies, including the U.S. Food and Drug Administration (FDA) and European Food Safety Authority (EFSA) have concluded that BPA is safe when used in the form of polycarbonate or epoxy resins for food contact applications.1 Based on the FDA’s ongoing safety review of scientific evidence, “the available information continues to support the safety of BPA for the currently approved uses in food containers and packaging.”2 The FDA offers extensive documentation that supports this conclusion.
Pharmacokinetics and Metabolism of BPA
Pharmacokinetic and metabolism data from the National Toxicology Program (NTP), FDA, and other researchers show that when BPA enters the body through food exposure, it is metabolized almost completely into a biologically inactive metabolite at the point of absorption in the intestinal wall and the liver.3,4 It is primarily the inactive metabolite that enters the bloodstream, with only trace levels of BPA found in blood. The metabolite is then quickly eliminated from the body through urine, with a half-life of few hours.
Extensive data from the Centers for Disease Control and Prevention and the National Health and Nutrition Examination Survey (NHANES) indicate that human exposure to BPA is extremely low.5 Typical human exposure is in the range of approximately 25 nanograms of BPA per kilogram of body weight per day.6 Together, this data shows that, on average, we are exposed to low levels of BPA, and what does enter the body is metabolized and quickly eliminated from the body typically on the same day as exposure.
Even under extreme conditions, including high temperatures, the amount of BPA that could be released from polycarbonate plastic and epoxy resins is still well below any level that could conceivably cause harm.
Data on the toxicity of BPA is more controversial, because there are a wide range of studies on BPA, and all studies are not the same in terms of design. Many smaller studies conducted on BPA were really intended to develop hypotheses about BPA, including possible types of toxicity related to BPA. A smaller number of large-scale studies have been conducted specifically to test hypotheses, evaluate toxicity and resolve uncertainties.
Data from the larger studies that were specifically designed to evaluate toxicity show a consistent picture, and it is exactly what would be expected from the pharmacokinetic data: BPA does not have high toxicity. For example, carcinogenicity studies by the National Toxicology Program show that BPA does not appear to be carcinogenic.7 In addition, at least 5 large-scale multi-generation studies on BPA are available, and all of these studies consistently showed that BPA does not cause reproductive or developmental effects, in particular, at low doses.8-12 Like any chemical, it will cause systemic toxicity at very high doses; however, at doses that are anywhere close to human exposure levels, no toxic effects are found.
In January 2014, FDA published what is probably the largest scale toxicity study ever conducted on BPA. The study was primarily designed to evaluate the potential for BPA to cause developmental effects as had been suggested by small-scale studies. The FDA study found no evidence for developmental health effects at low doses of BPA that are in the range of human exposure.13
In conclusion, although we have many studies that are controversial and suggest that BPA might be harmful, those studies are mainly hypothesis generating studies that required further investigation. When those hypotheses were tested in larger-scale studies, health effects of BPA exposure were not found. The American Chemical Council’s view, which is consistent with the views of government agencies such as the FDA and EFSA, is that BPA is not a risk to human health in the way that it is used today at these very low exposure levels. This conclusion is built on the 3 scientific pillars of 1) pharmacokinetic/metabolism data, 2) low levels of human exposure, and 3) the low toxicity demonstrated in large-scale studies that were designed to evaluate toxicity.
1. U.S. Food and Drug Administration. Questions & Answers on Bisphenol A (BPA) Use in Food Contact Applications. Available at: http://www.fda.gov/Food/IngredientsPackagingLabeling/FoodAdditivesIngredients/ucm355155.htm. Accessed June 29, 2015.
2. U.S. Food and Drug Administration. Bisphenol A (BPA): Use in Food Contact Application. Available at: http://www.fda.gov/NewsEvents/PublicHealthFocus/ucm064437.htm. Accessed June 29, 2015.
3. Teeguarden JG, Calafat AM, Ye X, et al. Twenty-four hour human urine and serum profiles of bisphenol a during high-dietary exposure. Toxicol Sci. 2011;123(1):48-57.
4. Thayer KA, Doerge DR, Hunt D, et al. Pharmacokinetics of bisphenol A in humans following a single oral administration. Environ Int. 2015;83:107-115.
5. Centers for Disease Control and Prevention. National Center for Environmental Health. Fourth National Report on Human Exposure to Environmental Chemicals. 2009. Available at: http://www.cdc.gov/exposurereport/pdf/fourthreport.pdf. Accessed July 15, 2015.
6. LaKind JS, Naiman DQ. Temporal trends in bisphenol A exposure in the United States from 2003-2012 and factors associated with BPA exposure: Spot samples and urine dilution complicate data interpretation. Environ Res. 2015;142:84-95.
7. 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. September 2008. NIH Publication No. 08-5994. Available at: http://cerhr. niehs.nih.gov/chemicals/bisphenol/bisphenol.pdf
8. Tyl RW, Myers CB, Marr MC, et al. Two-generation reproductive toxicity study of dietary bisphenol A in CD-1 (Swiss) mice. Toxicol Sci. 2008;104(2):362-384.
9. Tyl RW, Myers CB, Marr MC, et al. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats. Toxicol Sci. 2002;68(1):121-146.
10. Kobayashi K, Ohtani K, Kubota H, Miyagawa M. Dietary exposure to low doses of bisphenol A: effects on reproduction and development in two generations of C57BL/6J mice. Congenit Anom (Kyoto). 2010;50(3):159-170.
11. Kobayashi K, Kubota H, Ohtani K, Hojo R, Miyagawa M. Lack of effects for dietary exposure of bisphenol A during in utero and lactational periods on reproductive development in rat offspring. J Toxicol Sci. 2012;37(3):565-573.
12. Ema M, Fujii S, Furukawa M, Kiguchi M, Ikka T, Harazono A. Rat two-generation reproductive toxicity study of bisphenol A. Reprod Toxicol. 2001;15(5):505-523.
13. Delclos KB, Camacho L, Lewis SM, et al. Toxicity evaluation of bisphenol A administered by gavage to Sprague Dawley rats from gestation day 6 through postnatal day 90. Toxicol Sci. 2014;139(1):174-197.
Updated July 15, 2015
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