Evaluation of the U.S. EPA/OSWER Preliminary Remediation Goal for Perchlorate in Groundwater: Focus on Exposure to Nursing Infants

Autor: Dale Hattis, Gary Ginsberg, Deborah C. Rice, R. Thomas Zoeller
Rok vydání: 2007
Předmět:
Zdroj: Environmental Health Perspectives
ISSN: 1552-9924
0091-6765
Popis: Perchlorate is a powerful oxidant that is used in rocket fuel, munitions, blasting operations, and fireworks [National Research Council (NRC) 2005]. Environmental contamination has occurred at military installations, at facilities that make perchlorate, and at various construction sites from the blasting of bedrock to build roads or homes. In addition, there are natural sources of perchlorate such as fertilizer produced in certain regions (e.g., Chilean nitrate), evaporite soils, and atmospheric sources (Dasgupta et al. 2005; Orris et al. 2003). Its high water solubility and environmental persistence have led to contamination of groundwater, with detection increasing in recent years as analytical methods have improved [Government Accountability Office (GAO) 2005]. There are no federal drinking water standards for perchlorate, although a number of states have recently developed or proposed values in the 2–6 μg/L range [Massachusetts Department of Environmental Protection (MADEP) 2006; New Jersey Drinking Water Quality Institute 2005; Ting et al. 2006]. These drinking-water targets are intended to prevent perchlorate’s neurodevelopmental effects resulting from its antithyroid action. Perchlorate can impair thyroid function by inhibiting the uptake of iodide, thereby reducing the amount of iodide stored in the thyroid and available for hormone production (NRC 2005; Ting et al. 2006). In those who have adequate iodide intake and stores of thyroid hormone, this impairment can be overcome with little to no consequence (Braverman et al. 2005). However, gestation can be a vulnerable period because the mother has increased nutritional demands for iodide and because thyroid hormone is critically important for fetal brain development (NRC 2005). The U.S. Environmental Protection Agency (EPA) reference dose (RfD) of 0.0007 mg/kg/day, as adopted from a report from the National Research Council (NRC 2005; U.S. EPA 2005), is intended to protect the general public, including vulnerable life stages such as in utero development, from perchlorate’s antithyroid effects. This RfD has been used in at least one case to derive a drinking-water limit for perchlorate (New Jersey Drinking Water Quality Institute 2005), whereas other states have used more stringent toxicity values to set a drinking-water limit (MADEP 2006; Ting et al. 2006). The case for a lower RfD has also been made by others (Ginsberg and Rice 2005). Recent data from the Centers for Disease Control and Prevention (CDC) indicate a low-dose effect of perchlorate, particularly on women with low iodine intake, and thus suggest a need to lower the RfD (Blount et al. 2006a). In the present article we do not focus on the issue of the appropriateness of the U.S. EPA RfD, but rather evaluate whether a groundwater cleanup guideline issued by U.S. EPA’s Office of Solid Waste and Emergency Response (OSWER) would keep exposure below the RfD for all vulnerable segments of the population. The OSWER guideline, released January 2006, sets a groundwater preliminary remediation goal (PRG) of 24.5 μg/L for Superfund sites containing perchlorate. Whereas this level corresponds to the amount that would deliver the RfD for a 70-kg adult ingesting 2 L/day, it is not necessarily protective of nursing and bottle-fed infants who consume more liquid per body weight than adults (U.S. EPA 2002). A recent analysis calculated perchlorate doses that were above the RfD for infants drinking reconstituted formula made with water containing perchlorate at 24 μg/L, the OSWER PRG (Baier-Anderson et al. 2006). Further, from a limited breast milk biomonitoring data set, Kirk et al. (2005) estimated that nursing infants could receive doses above the RfD even without considering the added exposure associated with the OSWER PRG. Our primary objective is to evaluate the perchlorate dose to nursing infants resulting from maternal ingestion of water contaminated by perchlorate at the OSWER PRG of 24.5 μg/L. As explained below and described elsewhere (Baier-Anderson et al. 2006), infants are likely also to be highly susceptible to perchlorate. The OSWER PRG did not explicitly consider exposure during this life stage. An additional objective is to evaluate whether the OSWER PRG protects the pregnant mother and her developing fetus. Exposure to the fetus depends on the mother’s intake of perchlorate from both diet and drinking water. In setting drinking-water maximum contaminant levels (MCLs), the U.S. EPA routinely applies a relative source contribution (RSC) to allow for the possibility that not all exposure will come from water, recognizing the importance of keeping the total exposure dose (e.g., water plus diet) below the RfD. The default RSC is 0.2, meaning that only 20% of the RfD would be allowed to come from drinking water. In the case of the OSWER PRG for perchlorate, the groundwater target is set at the water concentration that corresponds to the RfD—in effect, setting the RSC to unity. This appears to be contrary to the emerging database on perchlorate content of foods, which shows that perchlorate is common in the diet [El Aribi et al. 2006; U.S. Food and Drug Administration (FDA) 2004]. The limited human biomonitoring data suggest widespread exposure, with dietary perchlorate appearing to be a key source (Kirk et al. 2005; Valentin-Blasini et al. 2005). This indicates a need for careful consideration of the RSC. We provide a means to do this by analyzing the available human biomonitoring data. Some may be less concerned about exceedance of the RfD because it is based on a precursor effect, inhibition of iodide uptake by the thyroid. This implies that the RfD prevents a biochemical change that precedes a more serious toxic effect, and thus is not itself a critical health end point. This assumption lacks support; there are no data that show how much iodide uptake inhibition is needed to affect thyroid function. This relationship is likely to depend on a number of host-specific factors. For example, recent observations by Blount et al. (2006a) demonstrate that women in the lowest category of iodine intake were most sensitive to perchlorate’s effects on thyroid hormone production. Analogous to the low iodine women in the Blount et al. study (2006a), neonates are likely to be a sensitive life stage because of perchlorate’s direct effects on the thyroid and its ability to limit iodine transfer into breast milk, thereby reducing infant intake of this nutrient (Kirk et al. 2005; Tellez et al. 2005). Moreover, the simultaneous exposure to other breast milk contaminants (e.g., polychlorinated biphenyls, polybrominated diphenyl ethers, dioxins) that can disrupt thyroid function by other modes of action may interact with perchlorate in infants. Therefore, limiting perchlorate exposure should be a critical public health target not only during pregnancy but also in infants. This rationale is further described below.
Databáze: OpenAIRE
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