10 Tips to Lessen Exposure to Endocrine Disrupting Chemicals

Avoidance of Endocrine Disrupting Chemicals (EDCs) requires greater due diligence and wiser choices especially with regard to children and pregnant women.

Written by Amy Hess-Fischl MS, RD, LDN, BC-ADM, CDE

Endocrine disrupting chemicals (EDCs) are environmental chemicals that mimic, block, or interfere with hormones in the body. Increasing exposure to  EDCs over the past 20 years appear responsible for 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, according to a statement issued by The Endocrine Society and IPEN, a global network of more than 500 public interest NGOs in more than 100 countries around the world.

These environmental toxins have been found in our air, water, and soil as well as in a range of household products, including children’s toys, furniture, and beauty products.

While it is not clear exactly how many EDCs exist, the most 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.

The Impact of EDCs on Hormones, and Health

Endocrine disrupting chemicals may bind to an endocrine hormone’s receptor, activating the hormone’s production and triggering physiological processes. Conversely, some EDCs block endocrine hormones by binding to their receptors and blocking normal activation even in the presence of the natural hormones.

The concern has grown since even a low level of exposure to EDCs can affect body functions, particularly in the most vulnerable populations including infants and children, pregnant women, and those who are immune compromised or frail.

Of particular note, recent studies have shown the following:

Tips for Reduce Your Family's Exposure to EDCs

First and foremost, consult the Environmental Working Group’s guides to beauty products, cleaning products, and foods so you have a better sense of the ways to make avoiding EDCs part of your life. 

There are 10 key suggestions to get you started, and that will go a long way to help keep you and your family safer:

Compelling Reasons Behind the Need to Rid Your Life of EDCs

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. 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, explains Steven G. Hentges, PhD, is Executive Director of the Polycarbonate/BPA Global Group of the American Chemistry Council.

In general, government agencies, including the US Food and Drug Administration (FDA) maintains 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.”

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

Extensive data from the Centers for Disease Control and Prevention and the National Health and Nutrition Examination Survey 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 high temperatures, the amount of BPA that could be released from polycarbonate plastic and epoxy resins is still well below governmental limits for alarm despite public concern.

Data on the toxicity of BPA is more controversial, but the intensty of public pressure has generated a willingness by manufacturers to remove this chemical from many products including those of plastic bottles.

Even so, carcinogenicity studies by the National Toxicology Program show that BPA does not appear to be carcinogenic.7 However, like any chemical, it will cause systemic toxicity at high doses, and is likely to have the greatest negative effect in babies, children and pregnant women where lower levels of exposure may be sufficient to cause harm.



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.

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