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EPA: Perchlorate in Drinking Water Can Harm Fetal Brain Development

Health + Wellness
EPA: Perchlorate in Drinking Water Can Harm Fetal Brain Development
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By Tom Neltner

Pursuant to a consent decree with the Natural Resources Defense Council (NRDC), the U.S. Environmental Protection Agency (EPA) is developing drinking water regulations to protect fetuses and young children from perchlorate, a toxic chemical that inhibits the thyroid's ability to make the hormone T4 essential to brain development. The rulemaking is part of a long process that began in 2011 when the agency made a formal determination that Safe Drinking Water Act standards for perchlorate were needed. Under the consent decree, EPA should propose a standard by October 2018.

In the latest step in that process, EPA's scientists released a draft report in September that, at long last, answers questions posed by its Science Advisory Board in 2013: does perchlorate exposure during the first trimester reduce production of T4 in pregnant women with low iodine consumption? Does reduction in maternal T4 levels in these women adversely affect fetal brain development? According to EPA's scientists, the answers are Yes and Yes.


For several years, EPA and the Food and Drug Administration (FDA) have developed and refined a model that would predict the effect of different doses of perchlorate on levels of T4 in pregnant women. The latest version of the model addresses women during the first trimester, especially those with low iodine intake. This is important because iodine is essential to make T4 (the number four indicates the number of iodine atoms present in the hormone); perchlorate inhibits its transport from the blood into the thyroid. The risk of perchlorate exposure to fetuses in the first trimester is greatest because brain development starts very early and is fully dependent on maternal T4. If the mother gets insufficient iodine to offset the perchlorate inhibition, she will not produce enough T4 for the fetal brain to develop properly. When free T4 (fT4) levels are low but without increase in thyroid stimulating hormone (TSH), the condition is known as hypothyroxinemia. When T4 production is lowered further, the pituitary gland releases TSH to increase T4 production by a feedback loop mechanism.

EPA's scientists reviewed 55 research studies and concluded, "Overall, the results of this literature review lend support to the concept that maternal fT4, especially in the hypothyroxinemic range, is critical to the offspring's proper neurodevelopment" and "the impact of altered fT4 is seen even with small incremental changes in fT4 (and in populations with fT4 across the "normal" range)."From the literature search, EPA identified IQ, motor skills, cognitive and language development and reaction time as measurements of neurodevelopment that enable them to quantify the effects of perchlorate exposure in the first trimester.

EPA also estimated the impact of perchlorate exposure in the population of pregnant women in the first trimester and with low iodine consumption; in other words, how many pregnant women will become hypothyroxinemic due to perchlorate exposure thus increasing the risk of adverse neurodevelopmental effects in their children. They predicted that a dose of:

  • 0.3-0.4 micrograms of perchlorate per kilogram of body weight/day (µg/kg bw/day) is associated with a one percent increase in pregnant women with hypothyroxinemia; and
  • 2.1-2.2 µg/kg bw/day is associated with a five percent increase in pregnant women with hypothyroxinemia.

While these percentages appear small, they represent a significant number of potentially affected children since neurodevelopmental harm is likely irreversible. EPA did not estimate the number of pregnant women or children potentially affected. We did. Based on four million children born in the U.S. each year, an estimated 400,000 were born to women with hypothyroxinemia. A one percent shift in the population of women with hypothyroxinemia associated with perchlorate exposure would correspond to an increase of 4,000 impacted children; if there is a five percent shift, the number of impacted children born to hypothyroxinemic mothers would increase to 20,000.

The agency is accepting public comments until Nov. 20, 2017 and will convene a peer review panel to review its findings in January 2018. After considering the panel's feedback, EPA will develop a Maximum Contaminant Level Goal (MCLG) and, eventually, a drinking water standard for perchlorate. The model's conclusions and identification of a new reference dose are also expected to inform EPA's standards for hypochlorite bleach to limit degradation to perchlorate and FDA's assessment of its decision to allow perchlorate to be added to plastic packaging and food handling equipment at concentrations as high as 1.2 percent.

EDF and NRDC submitted joint comments to EPA supporting the draft report and its analysis. We also made the following general observations:

  • Incremental changes in free T4 (fT4) are fundamental: Critical neurodevelopmental adverse effects could be missed by measuring full range maternal fT4. Windows of susceptibility are common in all organs during development. Hormonal control of brain development is no exception. Therefore, adverse neurodevelopmental outcomes will vary based on the time and duration of decreases in fT4 levels. We appreciate seeing the agency building a model based on this fundamental principle of developmental biology.
  • EPA's scientists provide an essential service: Academic researchers laid a solid foundation for the analysis. Without their work, typically funded by government grants, we would not have the evidence necessary to recognize the harm from perchlorate at the levels under consideration. But it took the independent scientists at EPA, building on a model developed by FDA, to provide the objective rigorous review of the evidence and adapt the model.

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