Publisher Summary This chapter reviews the geomedical aspects of selenium (Se), ranging from the soil through the plants to animal and human nutrition. Selenium has several essential functions in the animal and human body, and interactions occur with other elements and compounds. The beneficial effects of Se are obtained at different concentration levels, depending on the functions of Se and on interacting factors such as vitamin E, fatty acids, and sulfur. The nutritional minimum level for animals and humans is about 0.05–0.10 ppm Se in dry fodder/food, and intake below that cause severe deficiency diseases. At somewhat higher levels of Se intake, there are indications of a protective effect toward a number of human diseases, and toxic effects of Se occur with exposure to levels of 2–5 ppm Se or more, depending on the chemical form of the Se. Selenium toxicity in livestock is known in a few areas around the world, but Se deficiency has turned out to be much more common than Se toxicity. The Se deficiency problem is severe in New Zealand, in parts of China, in parts of North America, and in the Scandinavian countries.

Selenium in Soils and Plants and its Importance in Livestock and Human Nutrition

SELENIUM ii DISCLAIMER The use of company or product name(s) is for identification only and does not imply endorsement by the Agency for Toxic Substances and Disease Registry. A Toxicological Profile for selenium, Draft for Public Comment was released in September, 2001. This edition supersedes any previously released draft or final profile. Toxicological profiles are revised and republished as necessary, but no less than once every three years. For information regarding the update status of previously released profiles, contact ATSDR at: Toxicological Profiles are a unique compilation of toxicological information on a given hazardous substance. Each profile reflects a comprehensive and extensive evaluation, summary, and interpretation of available toxicologic and epidemiologic information on a substance. Health care providers treating patients potentially exposed to hazardous substances will find the following information helpful for fast answers to often-asked questions. Chapter 1: Public Health Statement: The Public Health Statement can be a useful tool for educating patients about possible exposure to a hazardous substance. It explains a substance's relevant toxicologic properties in a nontechnical, question-and-answer format, and it includes a review of the general health effects observed following exposure. Chapter 3: Health Effects: Specific health effects of a given hazardous compound are reported by type of health effect (death, systemic, immunologic, reproductive), by route of exposure, and by length of exposure (acute, intermediate, and chronic). In addition, both human and animal studies are reported in this section. NOTE: Not all health effects reported in this section are necessarily observed in the clinical setting. Please refer to the Public Health Statement to identify general health effects observed following exposure. The following additional material can be ordered through the ATSDR Information Center: Case Studies in Environmental Medicine: Taking an Exposure History—The importance of taking an exposure history and how to conduct one are described, and an example of a thorough exposure history is provided. Other case studies of interest include Reproductive and Developmental Hazards; Skin Lesions and Environmental Exposures; Cholinesterase-Inhibiting Pesticide Toxicity; and numerous chemical-specific case studies. SELENIUM viii Managing Hazardous Materials Incidents is a three-volume set of recommendations for on-scene (prehospital) and hospital medical management of patients exposed during a hazardous materials incident. Volumes I and II are planning guides to assist first responders and hospital emergency department personnel in planning for incidents that involve hazardous materials. Volume III— Medical Management Guidelines for Acute Chemical Exposures—is a guide for health care professionals treating patients …

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Toxicological profile for selenium

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Toxicological profile for malathion

Excess consumption of selenium (Se) accumulator plants can result in selenium intoxication. The objective of the study reported here was to compare the acute toxicosis caused by organic selenium (selenomethionine) found in plants with that caused by the supplemental, inorganic form of selenium (sodium selenite). Lambs were orally administered a single dose of selenium as either sodium selenite or selenomethionine and were monitored for 7 days, after which they were euthanized and necropsied. Twelve randomly assigned treatment groups consisted of animals given 0, 1, 2, 3, or 4 mg of Se/kg of body weight as sodium selenite, or 0, 1, 2, 3, 4, 6, or 8 mg of Se/kg as selenomethionine. Sodium selenite at dosages of 2, 3, and 4 mg/kg, as well as selenomethionine at dosages of 4, 6, and 8 mg/kg resulted in tachypnea and/or respiratory distress following minimal exercise. Severity and time to recovery varied, and were dose dependent. Major histopathologic findings in animals of the high-dose groups included multifocal myocardial necrosis and pulmonary alveolar vasculitis with pulmonary edema and hemorrhage. Analysis of liver, kidney cortex, heart, blood, and serum revealed linear, dose-dependent increases in selenium concentration. However, tissue selenium concentration in selenomethionine-treated lambs were significantly greater than that in lambs treated with equivalent doses of sodium selenite. To estimate the oxidative effects of these selenium compounds in vivo, liver vitamin E concentration also was measured. Sodium selenite, but not selenomethionine administration resulted in decreased liver vitamin E concentration. Results of this study indicate that the chemical form of the ingested Se must be known to adequately interpret tissue, blood, and serum Se concentrations.

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Comparative toxicosis of sodium selenite and selenomethionine in lambs.

Male weanling rats were raised on diets based on torula yeast which were deficient in vitamin E and selenium, or supplemented with these substances. They were injected intraperitoneally with sodium selenite at 2 mg Se/kg or with sodium sulfite to give the same level of sodium. Following injection, lipid peroxidation in vivo was estimated by monitoring the production of ethane, a volatile product formed on the peroxidation of ω-3-unsaturated fatty acids. In the hour following injection, vitamin E- and selenium-deficient rats injected with selenite produced 15 times as much ethane as did controls injected with sulfite. All rats in this group died from 1 to 4 hr after injection. Rats fed diets supplemented with selenite showed only a two- to threefold stimulation of ethane production by selenite and 3/4 survived. Rats fed diets supplemented with vitamin E did not produce more ethane in response to selenite injection and 3/4 survived. All four rats supplemented with both vitamin E and selenium survive...

F.L. Clark

Papers

Acute selenium toxicity in lambs following intramuscular injection of sodium selenite.

Experimental acute toxicity of orally administered sodium selenite in lambs.