Free Perchlorate Exposure: An Advantageous Treatment Or A Harmful Disruptor? Critical Thinking Example
Perchlorate is a dissociated anion of inorganic perchlorate salts that are highly used in rocket fuel, defense industry, fireworks, paints and medicinal biology (Wu et al. 445). To understand the functioning of perchlorate inside human body it is necessary to know the biochemical as well as physiological base of its action as a competitor of iodine. Perchlorate intervenes with the accumulation of Iodine in the thyroid gland and hampers the hormone production. Adequate iodine is mandatory for the normal functioning of thyroid gland and Sodium Iodine Symporter (NIS) (Wu et al. 446). Due to a specific metabolic pathway it has been clinically useful for controlling excess iodine and hyperthyroidism. Wolff cited a proposed model pathway of Na+/K+ adenosine triphosphatase which involves the transportation of iodine and sodium ions. In NIS pathway perchlorate exhibits capabilities of inhibiting iodine intake (Wolff 90) because it has 30 times higher attraction towards perchlorate than iodide (Tran et al. 802). Several studies revealed that perchlorate also has a specific activity of reciprocal competitiveness with iodide and at higher extent iodide acts similarly on the perchlorate through inhibiting its accumulation (Wolff 91). Perchlorate has shown reversible impacts of obstructing thyroid hormone synthesis that results in iodine deficiency, reduction in thyroid hormones T3 and T4 and elevation in thyrotrophin (TSH) levels. This whole process affects the body growth and development (Wu et al. 446).
Now such evidences are sufficient to prove that perchlorate acts as a disrupter to the thyroid. The clinical usages of perchlorate in treating thyrotoxicity indicate that this disturbance is useful for human only under controlled quantity. The perchlorate interferes with thyroid in twofold way; first by reducing the excessive hormone synthesis and hyperthyroidism, secondly it lessens the thyroid inhibitor synthesis. It has been also valuable in tests for measuring the accumulated radio-iodide inside the thyroid due to other disruptions of iodide metabolism. The use of perchlorate as medication was considered safe since 1950’s. Firstly United States started treating thyrotoxicosis with perchlorates at higher doses (70,000–300,000 ppb). Even in some countries like Germany perchlorate was considered the best alternative against environmental radioiodine contamination. The first 6- 7 years has been very enthusiastic about the successful treatment of 1000 patients for thyroid via perchlorate, but in the period of 1961-66 the seven cases on aplastic anemia put a stop on it. Initially 400 mg dose was prescribed divided into 4-5 days because it was noticed that gradual administration of perchlorate was leading more satisfactory control of thyrotoxicity with minor effects. Afterwards the doses were increased for fast responses (Wolff 95).
Recently the drinking and ground water contamination has mounted due to perchlorate contaminant. Various agencies and authorities came forward to help controlling the possible adverse effects of perchlorate exposure on health. The United States Environmental Protection Agency (USEPA) is trying to evaluate the health hazard associated with environmental perchlorate exposure (Clewell et al. 17). Environmental Protection Agency (EPA) has decided a reference dose of perchlorate 0.7mg/kg/day (Gold et al. 6). A sample based study by Gold suggested that the perchlorate show no enduring and unfavorable thyroid effects. Though it is environmentally stable and prevalently increasing contaminant in drinking and irrigation water, it competitively hinders the iodide metabolism. Experiments illustrated that the half life of perchlorate in humans is approximately 7.5h, and an intake of 5.2mg/kg/day is sufficient to block the iodide uptake (Gold et al. 6). Several researches illustrate that perchlorate is not confined to the thyroid follicle, the anions of perchlorate reach to the follicular lumen (Clewell et al. 20). Further adding supportive lines Clewell cites that the organic binding in thyroid is highly impacted as a greater dose dependent fall was observed in organic iodides (Clewell et al. 21). The National Health and Nutrition Examination Survey (NHANES) reports in an epidemiological survey that exposure to perchlorate concentration is linked to altered TSH and thyroxine concentrations among iodine deficient women (Trans et al. 805).
Thus, under clinical supervision the controlled dose of perchlorate may be a precise treatment, but unnecessarily intake of perchlorate disturbs the iodine metabolism in humans resulting in thyroidal problems.
Clewell, Rebecca A., et al.. "Evidence for competitive inhibition of iodide uptake by perchlorate
and translocation of perchlorate into the thyroid." International journal of toxicology 23.1
Gold, Ellen B., et al.. "Thyroid hormones and thyroid disease in relation to perchlorate dose and
residence near a superfund site." Journal of Exposure Science and Environmental
Epidemiology 23.4 (2013): 399-408.
Tran, Neil, et al.. "Thyroid-stimulating hormone increases active transport of perchlorate into
thyroid cells." American Journal of Physiology-Endocrinology and Metabolism 294.4
Wolff, J. "Perchlorate and the thyroid gland." Pharmacological reviews 50.1 (1998): 89-106.
Wu, Fenghong, et al.. "The effects of ammonium perchlorate on thyroid homeostasis and
thyroid‐specific gene expression in rat." Environmental toxicology 27.8 (2012): 445-452.
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