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They Are What You Eat - Endocrine-Disrupting Chemicals and the Failure to Protect

EDCs can affect fetuses and babies at very low exposure levels and current regulatory programs can't quite figure out how to protect you. You need to do it.

An important article was recently published but will likely go unnoticed in most circles. Its unarresting title is “Hormones and Endocrine-Disrupting Chemicals: Low Dose Effects and Non-Monotonic Dose Responses.”[i] Don’t turn away, I will interpret as best I can and put it into some context for you. You need to know this.

The study deals with a group of chemicals called endocrine-disrupting chemicals, or EDCs. As the name indicates, these are chemicals that disrupt chemicals in the body’s endocrine system. The endocrine system comprises various glands in the body that secrete hormones. These include not only the first-thought-of ovaries and testes, but also the pituitary, thyroid, and adrenal glands, the pancreas, the hypothalamus, and other organs.

Collectively, endocrine glands, through the secretion of hormones, are involved in most workings of the human body, including growth, development, reproduction, metabolism, response to stress, and just about anything else you can think of.  The unique, and important, fact is that hormones are active at very low concentrations in the body, in the parts-per-billion to parts-per-trillion range (one part per trillion is roughly equivalent to 50 drops (a half teaspoon) of water in a filled Olympic-sized swimming pool).

EDCs are pervasive in our environment, and include some recognizable names: PCBs (formerly used as a coolant and now often found in inland and farm-raised fish), BPA (in plastics and on thermal receipts), triclosan (the antibacterial in many hand soaps), vinclozolin (a fungicide registered for use on raspberries, lettuce, snap beans, turf grass, and other crops), and DDT, a banned pesticide that is still present in our environmental from past uses for mosquito control).

Because of EDC’s effects on hormonal systems, fetal and neonatal periods are especially sensitive to EDCs. For example, in animal studies, low level (part-per-billion) exposure to BPA during late fetal development or soon after birth has been shown to change the response of the mammary gland to estrogen, to produce alterations in breast tissue during puberty and adulthood, and make breast tissue more sensitive to mammary carcinogens and produce pre-cancerous lesions later in life. Higher dose studies did not show these effects.

The Vanderberg article discusses the dose/response relationship for EDCs. A dose/response relationship, as it suggests, describes what kind and magnitude of a response (effect) a chemical elicits in the body over a range of doses or exposures. “The dose makes the poison” adage, ascribed to Paracelsus in the 1500s, has been the assumed rule of toxicology for centuries, wherein the higher the dose, the greater or more frequent the response; the lower the dose, the smaller or less frequent the same response.

Consequently, because most environmental exposures occur at low concentrations, toxicological studies on chemicals have typically been performed on high exposure levels and extrapolated ownward to predict effects at low exposure levels. It is a common assumption in EPA, FDA, and USDA regulatory programs that most chemicals follow this pattern.

The problem is, EDC chemicals don’t respond like this. The “non-monotonic” in the paper’s title refers to a situation where the dose/response relationship is not linear, where the slope of the curve changes over different exposure levels. Often these curves are “U” shaped or inverted “U” shaped rather than linear, where the maximum effect or even a different effect occurs at low or moderate exposure levels, rather than at or in contrast to higher exposure levels. There are complexities in the endocrine system that can account for these non-linear relationships, and the paper provides numerous examples of this.

So what? The paper identifies several implications and recommendations for the way in which toxicological studies are performed for EDCs, but for us it means is that the current regulation of EDCs is based on a flawed assumption of how, and at what concentration, EDCs produce adverse effects. The regulatory agencies assume that high dose studies can adequately identify the types and incidence of effects at low, environmental, doses, and use this assumption as the basis for setting air, water, soil, and food standards. It means that, for this class of chemicals, we may not be protected even when the regulations are enforced.

A local example of this low dose effect through possible hormonal pathways was recently reported in Environmental Health Perspectives, a peer-reviewed scientific journal.[ii] This article discussed an on-going epidemiological study of a group of children born to mothers residing near PCB-contaminated sites in New Bedford between 1993 and 1998. These children were exposed to low levels of PCBs while their mothers were pregnant, as determined by chemical analysis of umbilical cord blood. The researchers have followed these children and tested them periodically for a variety of endpoints.

Of the nearly 600 children tested eight years after birth, the researchers found that boys exposed to PCBs in the womb had lower test scores for attention and impulse control, using standardized tests used to screen for ADHD. Joe Braun, an epidemiologist at the Harvard School of Public Health, commented that “[i]t’s possible that these compounds can impact brain development by altering the hormonal balance of a developing fetus…boys and girls have different hormonal patterns.” 

Here is real life proof (or as close to proof one can get for an environmental contaminant) that low dose exposure can affect children years after the exposure at levels not previously thought to be of concern. While this is tragic for the individual child, it is downright scary when you think about potential population or cultural effects. And the current regulation of PCBs does not protective against this effect.

In a move on another EDC, the FDA recently (March 30, 2012), denied a petition from the Natural Resources Defense Council to ban BPA from all food and drink containers. The FDA’s response in the denial was that the petition “did not provide the scientific evidence to change current regulations”, but that it would continue to examine studies on the effects of BPA, which it claims are conflicting.

This position, even though in 2008, the National Toxicology Program expressed “some concern for effects on the brain, behavior, and prostate gland in fetuses, infants, and children at current human exposures to bisphenol A”[iii] and eleven states have already banned BPA from infant feeding containers. In addition, the 2003-2004 National Health and Nutrition Examination Survey by the CDC found BPA in the urine of nearly 93 percent of the 2,517 U.S. participants of the study,[iv] so we are being exposed.

So what does this mean?  The government is slow to accept the non-linear does/response relationship of EDCs and is having trouble reconciling these newer studies with conventionally performed studies. Therefore, the current regulation of these chemicals does not consider these low dose effects and does not protect against them.  The Republican Party and similar conservative (read: industry-aligned) groups want to reduce the government’s already weak ability to regulate chemicals. This leaves, us, the consumers, as the only ones who are going to protect our children. 

You, particularly you moms and women of child-bearing age, need to be vigilant in what you expose yourself and your children to. Don’t assume that the government is protecting you and don’t assume that, because something is on the market, it is safe. Do your homework, examine what you eat and eat with, what you wash your hands with, and what you put on your grass. Look beyond the partisan hype, question authority, make your own decisions, and pressure your government representatives to protect you and yours. 

[i] Vanderberg et al (2012). Hormones and Endocrine-Disrupting Chemicals: Low Dose Effects and Non-Monotonic Dose Responses” (Endocrine Reviews, published ahead of print March 14, 2012, as doi:10.1210/er.2011-1050).
[ii] Sagiv SK, Thurston SW, Bellinger DC, Altshul LM, Korrick SA (2012).  Neuropsychological Measures of Attention and Impulse Control among 8-Year-Old Children Exposed Prenatally to Organochlorines. (Environ Health Perspect :-http://dx.doi.org/10.1289/ehp.1104372).  

[iii] NTP-CERHE Monograph on the Potential Human Reproductive and Development Effects of Bisphenol A;  NIH Publication No., 08-5994, September 2008

[iv] Calafat AM, Ye X, Wong LY, Reidy JA, Needham LL. Exposure of the U.S. Population to Bisphenol A and 4-tertiary-Octylphenol: 2003–2004. Environ Health Perspect 2008 Jan;116(1):39-44.



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