Tom Neltner, J.D., is Chemicals Policy Director and Maricel Maffini, Ph.D., Consultant
Pursuant to a consent decree with the Natural Resources Defense Council (NRDC), the 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.