Breast Milk Iodine and Perchlorate Concentrations in Lactating Boston-Area Women

Pearce, Elizabeth N.; Leung, Angela M.; Blount, Benjamin C.; Bazrafshan, Hamidreza; He, Xuemei; Pino, Sam; Valentín-Blasini, Liza; Braverman, Lewis E.

doi:10.1210/jc.2006-2738

Cited by 158 publications

(136 citation statements)

References 22 publications

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“…Further research is needed to assess the toxicological implications of NIS expression in both placental and mammary tissue (11a) and the modulation of perchlorate transport by iodide. Active transport of perchlorate across membranes is also consistent with the active secretion of perchlorate in human and bovine milk (7,15,19,24).…”

Section: Discussionsupporting

confidence: 59%

Thyroid-stimulating hormone increases active transport of perchlorate into thyroid cells

Tran

Valentín-Blasini²,

Blount³

et al. 2008

American Journal of Physiology-Endocrinology and Metabolism

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Section: Discussionsupporting

confidence: 59%

Thyroid-stimulating hormone increases active transport of perchlorate into thyroid cells

Tran

Valentín-Blasini²,

Blount³

et al. 2008

American Journal of Physiology-Endocrinology and Metabolism

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“…It is perhaps not surprising that this association was greater in women with urinary iodine below 100 µg/L, and stronger still among these women who smoke, 90 since cigarettes contain thiocyanates that also inhibit iodine uptake. Because infants are particularly vulnerable to thyroid hormone insufficiency 29 and because perchlorate levels are particularly high in breast milk, 91 it is of concern that perchlorate may be affecting TH signaling in early infant development in some proportion of the US population. 92 Predicting the consequences of environmental perchlorate exposure on thyroid function and thyroid hormone action reveals several serious weaknesses in our understanding of the thyroid system as we employ this information for risk assessment.…”

Section: Perchloratementioning

confidence: 99%

Environmental chemicals targeting thyroid

Zoeller¹

2010

132

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Thyroid hormones (THs) are required for normal brain and somatic development and for the proper regulation of physiology in both children and adults. Thyroid function is controlled by the dynamic interrelationships between the hypothalamus, the pituitary and the thyroid. These dynamic relationships maintain circulating levels of THs within a narrow range under normal conditions. Normally, there is likely to be a tight relationship between changes in circulating levels of THs and changes in TH action in various target tissues. This relationship is maintained by tissue-level mechanisms that include TH metabolism and transport. Environmental chemicals that interfere with TH signaling mechanisms (Endocrine Disrupting chemicals, EDcs) may produce adverse effects both in the individual and in a population. Because of the complex nature of the regulation of thyroid function and TH action, the consequences of EDc exposure is also likely to be complex and our ability to understand these effects as well as to screen for potential EDcs must consider this complexity. Specifically, if there are chemicals in the environment that directly interfere with TH action through their receptors but do not affect circulating TH levels, they would not be identified as thyroid toxicants by currently applied screening methods or by epidemiological studies. The goal of this review is therefore to identify the issues that must be clearly resolved before effective risk assessment can be performed. HORMONES 2010, 9(1) the hypothalamic pituitaRy thyRoid axis (hpt) axis To develop efficient risk assessment strategies for thyroid toxicants, it is important to understand both the normal functioning of the hypothalamic-pituitary-thyroid axis (HPT) and what we know about individual thyroid toxicants. To this end, background information about the HPT axis and its relevance to thyroid toxicology is reviewed here. Key words: Thyroid hormones, Endocrine disruptors, Environmental chemicals, Thyroid toxicants ReviewCirculating levels of Thyroid Hormones (THs) are maintained within a relatively narrow range 1 in large part by a negative feedback relationship between circulating levels of THs and those of Thyroid Stimulating Hormone (TSH). THs appear to exert this effect by acting on one subtype of the TH receptor (TR). TRs are encoded by two separate genes,  and , the primary transcripts of which are alternatively spliced

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“…Perchlorate is typically detected in breast milk (Kirk et al, 2005) and thus the data presented here underestimate perchlorate exposure for breast fed infants. Specifically, using the range of mean perchlorate levels in breastmilk extracted from Kirk et al, 2005;Pearce et al, 2007;Kirk et al, 2007, and breastmilk intake estimates compiled by the US EPA (USEPA, 2002. Child-specific Exposure Factors Handbook [interim final].…”

Section: Consumption Datamentioning

confidence: 99%

Perchlorate exposure from food crops produced in the lower Colorado River region

Sanchez

Barraj

Blount

et al. 2008

J Expo Sci Environ Epidemiol

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The Colorado River shows low levels of perchlorate derived from aerospace-and defense-related fuel industries once located near the Las Vegas Wash. At sufficiently high dosages perchlorate can disrupt thyroid function by inhibiting uptake of iodide. The Colorado River is the primary source of irrigation water for most food crops grown in Southern California and Southwestern Arizona. The objective of this study was to evaluate potential perchlorate exposure from food crops produced in the lower Colorado River region (LCRR). The major food commodities produced in the region were sampled and perchlorate levels were determined by ion chromatography followed by detection using either conductivity or tandem mass spectrometry, depending on analyte levels. The Monte Carlo module of the Dietary Exposure Evaluation Model (DEEMt) was used to derive an estimate of the 2-day average perchlorate intakes. Data were derived assuming that individuals residing in the LCRR get their fruits and vegetables from within the LCRR as well as from other areas in the United States, or assuming individuals living in the LCRR get their fruits and vegetables from the LCRR only. Perchlorate exposure estimates derived in this study are comparable to exploratory estimates by the US Food and Drug Administration. For infants and children, over 50% of the estimated perchlorate exposure was from milk. The relative impact of vegetables and fruit toward perchlorate exposure increased by age through adulthood. Cumulative perchlorate exposure estimates based on this hypothetical analysis could approach or exceed the NAS reference dose (RfD) for some population groups as drinking water levels exceeded 6 mg/l. However, few individuals are exposed to perchlorate in drinking water at levels above 4 mg/l in the United States and very few would be exposed to perchlorate levels exceeding the RfD, whether consuming food crops from within or outside the LCRR.

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Breast Milk Iodine and Perchlorate Concentrations in Lactating Boston-Area Women

Cited by 158 publications

References 22 publications

Thyroid-stimulating hormone increases active transport of perchlorate into thyroid cells

Thyroid-stimulating hormone increases active transport of perchlorate into thyroid cells

Environmental chemicals targeting thyroid

Perchlorate exposure from food crops produced in the lower Colorado River region

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