Toxicity of Selenium and Its Mechanisms on Children Health - Coursework Example

Toxi of selenium and its mechanisms on children health Introduction Selenium is an essential naturally occurring trace element (micronutrient) within human and animal nutrition. Selenium contributes to the defence against the toxicity of reactive oxygen species. It does this by performing the role of oversight on thyroid hormone metabolism, as well as overseeing the redox state of cells (Watts 1994, p.111). The imperative significance of selenium within both human and animal diet was hampered by its exceedingly toxic potential, and by fears that selenium might be carcinogenic. Most of these fears have been dislodged by evidence, which outlines that selenium may avail protection against certain cancers. Exposure to high levels of selenium is injurious to health, which forms the basis for setting of the minimum dietary levels of selenium that may be needed for good health. Conversely, not eating enough selenium may result to health effects because selenium may be utilized by the body in antioxidant enzymes that shield against damage to tissues inflicted by oxygen, and in an enzyme that influences growth and metabolism. Failure to consume adequate selenium can lead to heart problems and muscle pain (Barceloux 1999, p.146). The quantity of selenium in foodstuff is a function of the selenium content of the soil released through the weathering of rocks or volcanic emissions. Anthropogenic sources of selenium include activities such as mining, milling, refining, and oil and gas emissions. Elemental selenium remains commercially produced, principally as a by-product of copper refining. Selenium enters the food chain through incorporation into plant proteins. Like any other trace elements, selenium may be unevenly distributed in the world’s soil (Levander 1986, p.209). Fatigue, irritation of mucous membranes, and dizziness may be reported in individuals exposed to selenium at concentrations higher than the legal levels. In rare cases, collection of fluid within the lungs (pulmonary edema) and acute bronchitis have been reported. The precise levels at which the outlined effects might occur are unknown; however, they may become apparent with increasing amounts and frequency of exposure to selenium (Barceloux 1999, p.147). The severity of the effects of excess selenium hinges on the amount of selenium consumed and the frequency of intake. Deliberate or accidental swallowing of significant amounts of sodium selenate or sodium selenite could be fatal if immediate medical treatment is availed. Even mildly disproportionate amounts of selenium consumed for extensive periods may yield deformed nails and brittle hair (Levander 1986, p.210). In extreme cases, individuals may lose feeling and control of their arms and legs. History and Epidemiology Selenium is a critical component of the human diet and equally a deadly poison. Much of what is known about selenium revolves around its function as a critical trace element required in the diet of majority of living things, rather than its toxic properties. In the 1970s, selenium was cited as a critical cofactor of the enzyme glutathione peroxidase. Keshan disease, which represents an endemic cardiomyopathy linked to multifocal myonecrosis, mitochondrial disruption, and pancreatic fibrosis, was illustrated in 1979 among Chinese women and children who constantly consumed a selenium-poor diet (Lombeck et al. 1984, p.91). Kashin-Beck disease can be associated with shortened stature from chondrocyte necrosis as described in young children in Korea, China, and Russia. Nevertheless, additional factors may lead to the condition. Selenium supplementation renders partial improvement in the children (Yang et. al. 1983, p.972). The daily allowance that averages around 55µg/d is guided by the level of supplementation critical to attainment of optimal glutathione peroxidase activity in the selenium-deficient study populations, and the amounts likely to cause toxicity (Mairrino, Thomas, Girotti and Ursini 1991, p.131). Chronic selenium toxicity (selenosis) has transpired throughout history. The condition was first described in animals whereby acute syndrome of “blind stagers” and the highly chronic “alkali disease” influenced livestock eating highly seleniferous plants. Recently, there have been reported cases of chronic selenium toxicity due to improperly packaged dietary supplements (Ge and Yang 1993, p. 259). People in seleniferous areas of China and Venezuela also developed analogous integumentary symptoms such as hair loss, nail changes, and dermatitis after an intake of close to 600µg/d, which represents more than 100 times the RDA (Bratter et al. 1991, p.269). Dietary selenium remains readily acquired via grains, meats, and cereals. Chemical Properties Selenium exists in organic, inorganic, and elemental forms, with four critical oxidation states; these states include selenide (Se2-), selenite (Se+4), elemental (Se0), and selenate (Se+6). The element’s solubility in water mainly increases with oxidation state. Hydrogen selenide (H2Se) results from the reaction of water with metal selenides or the reaction of hydrogen with soluble selenium compounds. The organic alkyl selenides are the least toxic while inorganic salts and acids are responsible for all instances of acute toxicity (Mairrino, Thomas, Girotti and Ursini 1991, p.132). Selenious acid (H2SeO3), which results from the reaction of selenium dioxide with water, can be regarded as the most toxic form of selenium because its ingestion is frequently lethal. Pharmacology and Pathophysiology Selenium exists in one of three states, in the body. First, it exists as selenoproteins, comprising of selenocysteine residues that play certain selenium-dependent functions in oxidation-reduction reactions. Secondly, it may exist as non-specific plasma proteins bind and may help in transport of selenium and directly binding of albumin and globulins. Thirdly, there are a number of inorganic forms of selenium in transit, in the body; these include elemental selenium (Se0) (Arthur and Beckett 1994, p.615). Pharmacokinetics and Toxicokinetics Elemental selenium can be regarded as the least bioavailable (50%), followed by inorganic selenite and selenate salts (75%), then followed by selenious acid that is well absorbed into the lungs and GI tract (85% based on animal studies). Organic selenium compounds are the best absorbed at close to 90% as dictated by isotope tracers as demonstrated in human studies. The effects of a toxic dose of selenium differ broadly between selenium compounds with elemental selenium reporting no undesirable effects in acute overdose. The selenium salts, especially selenite, are acutely toxic, in the same way as selenium oxide (SeO2) via its conversion to selenious acid through reaction with water. Selenious acid may be fatal with as little as a tablespoonful of 4% solution in children. Selenium Toxicity Individuals are mainly exposed to low levels of selenium daily through food, air, and water. Individuals receive the bulk of their daily intake of selenium from food consumption, and to a minor extent, from water intake. According to estimates, the average intake of selenium from food for the majority of individuals range from 71µ to 152µg/d per individual per day. Low levels of selenium can be established in drinking water while individuals may be exposed to higher than usual levels of selenium at hazardous waste sites, or through contact with soils that naturally have high levels of selenium (Lombeck et al. 1984, p.92). Although selenium is a critical trace element, it is toxic when consumed in excess. Exceeding the allowable upper intake level per day may lead to selenosis. A dose of selenium as small as 5mg per day can be fatal for a majority of humans. Selenium toxicity remains mainly reported in livestock grazing in areas where plants contain atypical high levels of the element. Overall, a normal dietary intake of selenium does not necessarily cause any noticeable side effects. Selenium side effects manifest after excess administration of selenium supplements. Consumption of about five times the normal dietary requirements causes certain medical problems since high doses of selenium lead to toxicity (selenosis). Consumption of more than 400mcg selenium per day may yield selenosis. Side effects of selenium, if left untreated, can be fatal (Bratter et al. 1991, p.270). Human toxicity can occur as a result of persistent exposure to high levels of selenium (Koppel et al. 1986, p.22). Sodium selenite is highly toxic at comparatively low levels while amino acid form (selenomethionine) may be safely consumed at levels up to 1,000mcg for adults. There have been reported instances of food supplement companies putting significant doses of sodium selenite into their product. For instance, in 2008, the ingestion of a dietary supplement product in the U.S. labelled as Total Body Formula Mega (TBF) was associated with unusual symptoms such as nail discoloration, hair loss, and joint pain. An analysis of the product indicated that TBF contained selenium far above the amount listed in the product’s label (Sutter at al. 2008, p. 971). Such cases have led to toxicity, especially among children, with reported symptoms such as neurological damage, depigmentation of skin, hair loss, gastrointestinal upsets, irritability, fatigue, mild nerve damage, and deformed nails. A garlic odour on the breath, devoid of garlic ingestion, may be a sign of selenium toxicity. Severe cases of selenosis can lead to cirrhosis of the liver, pulmonary edema, and even death. Elementary selenium and the majority of metallic selenides have comparatively low toxicities due to their low bioavailability. Conversely, selenates and selenite are extremely toxic since they possess an oxidant mode of action equivalent to that of arsenic trioxide. Clinical Manifestations Acute Poisoning Acute selenium toxicity in humans is typified by hyper-salivation, emesis, and a garlic aroma. These effects may be coupled with gastrointestinal effects, hair loss, neurological disturbance, and fatigue (Nante et. al.1985, p.531). Dermal and Ophthalmic Exposure Dermal exposure to selenious acid or selenium dioxide, or selenium oxychloride inflicts significantly painful caustic burns (Koppel et al. 1986, p.21). Similarly, corneal injury with acute pain may result from accidental exposure to selenium dioxide. Inhalation Exposure When inhaled, all selenium compounds can be respiratory irritants. Inhaled elemental selenium dusts can be regarded as less injurious than compounds converted to selenious acid (Sutter et al. 2008, p.970). Hydrogen selenide inhalation toxicity is mainly reported in industry literature. Oral Exposure Acute selenium toxicity manifests after ingestion of inorganic selenium compounds that include sodium selenite, sodium selenate, selenium dioxide, selenic acid, hydrogen selenide, and selenous acid. Elementary selenium and organic selenium compounds do not inflict severe toxicity. Circulatory failure can be considered to be the epitome of severe inorganic selenium toxicity (Spiller 2007, p.67). Other infrequent abnormalities include leukocytosis, hemolysis, and hypokalemia. Chronic selenium toxicity (selenosis) has gained prominence consequent to reports of inappropriately packaged nutritional supplements. For instance, in 2008, close to 200 people were negatively affected by manufacture error in selenium containing dietary supplement, which yielded fatigue, diarrhoea, and nail deformities (Huang et al. 2008, p.139). Selenosis can be compared to arsenic toxicity with the bulk of manifestations being nail and hair abnormalities. Chronic selenium poisoning is linked with changes to the hair and nails, clinical neurological effects such as skin lesions, numbness, convulsions, and paralysis (Pentel, Fketcher and Jentzen1985, p.556). How Can Selenium Affect Children Selenium has potential health effects on children right from conception to maturity. Children living close to selenium waste sites such as coal burning plants are likely to be exposed to increased environmental levels of selenium through breathing, eating contaminated soil, and touching soil. For instance, children living in areas of China with high selenium in soil manifested higher levels of selenium in the blood than adults from that area. Children require small amounts of selenium to aid normal growth and development (Collip and Chen 1981, p. 1304). Children manifest similar health effects from selenium exposure as adults; however, some studies imply that children may be less susceptible to health impacts of selenium compared to adults (Rossipal and Tiran 1995, p.573). Presently, it is unknown whether selenium toxicity could lead to birth defects, in children. Selenium compounds have not been linked to birth defects. Indeed, there is no information to suggest that there are any disparities between children and adults regarding where selenium is found in the body, or the rate of intake. Studies in humans indicate that infants are supplied with selenium via breast milk, which means that women exposed to high levels of selenium might transfer selenium to their children, subsequently risking them to selenium poisoning. Conclusion Selenium is a critical trace element and is necessitated in the diet of both animals and humans. Nevertheless, in overdose or with excessive, chronic exposure, toxicity may result. Some instances such as ingestion of selenious acid may be lethal. Selenium intake should be closely supervised to prevent an overdose as this may yield negative effects on the subject. The best means of attaining the daily requirement of essential vitamins are to consume a balanced diet that contains diverse foods. It is highly advisable to prevent selenium toxicity from occurring as there is no verified antidote or curative treatment for selenium toxicity exposure; rather, treatment focuses on stopping the exposure and availing supportive care for symptoms. References List Arthur, J.R. & Beckett, G.J. (1994). Neometabolic roles for selenium, Proceedings of the Nutrition Society 53 (1). pp.615-624. Barceloux D. G. (1999). Selenium, Journal of Toxicology Clinical Toxicology 37 (2). pp.145-172. Bratter, P., et al. (1991). Selenium status of children living in seleniferous areas of Venezuela, Journal of Trace Elements Electrolytes Health Dis 5 (4). pp.269-270. Collip, P.J. & Chen, S.Y. (1981). Cardiomyopathy and selenium deficiency in a two year old girl, The New England Journal of Medicine, 304 (21). pp.1304-1305. Ge, K. & Yang, G. (1993). The epidemiology of selenium deficiency in the etiological study of endemic diseases in China, The American Journal of Clinical Nutrition 57 (2). pp.259-263. Huang, Z., et al. (2008). Low selenium status affects arsenic metabolites in an arsenic exposed population with skin lesions, Clinica Chimica Acta 387 (1-2). pp.139-144. Koppel, C., et al. (1986). Fatal poisoning with selenium dioxide. Journal of Toxicology Clinical 24 (1). pp.21-35. Levander, O.A. (1986). Selenium in Trace elements in human and animal nutrition, 5th ed. Mertz, W. ed., Orlando, Academic Press Inc. pp.209-279. Lombeck, I., et al. (1984). Selenium intake of infants and young children, healthy children and dietetically treated patients with phenylketonnria, European Journal Paediatric 143 (2). pp. 91-102. Mairrino, M., Thomas, J.P., Girotti, A.W. & Ursini, F. (1991). Reactivity of phospholipd hydroperoxide glutathione peroxidase with membrane and lipoprotein lipid hydroperoxides, Free Radical Research Communications 12 (1). pp.131-135. Nantel, A. J., et al. (1985). Acute poisoning by selenious acid, Veterinary & Human Toxicology 27 (6). pp.531-533. Rossipal, E. & Tiran, B. (1995). Selenium and glutathione peroxidase levels in healthy infants and children in Austria and the influence of nutrition regimens on these levels, Nutrition 11 (5). pp. 573-575. Pentel, P., Fketcher, D., & Jentzen, J. (1985). Fatal acute selenium toxicity, Journal of Forensic Sciences 30 (2), pp.556-562. Spiller, H. A. (2007). Two fatal cases of selenium toxicity, Forensic Science International Journal 171 (1). pp.67-72. Sutter, M. E. et al. (2008). Selenium toxicity: a case of selenosis caused by a nutritional supplement, Annals of Internal Medicine 148 (12). pp.970-971. Watts, D. (1994). The nutritional relationships of selenium, Journal of Orthomolecular Medicine 9 (2). pp.111-117. Yang, G., et al. (1983). Endemic selenium intoxication of humans in China, American Journal of Clinical Nutrition 37 (5). pp. 872-881. Read More