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Chronic toxicity, selenium

Ward, G.S., T.A. Hollister, P.T. Heitmuller, and P.R. Parrish. 1981. Acute and chronic toxicity of selenium to estuarine organisms. Northeast Gulf Sci. 4 73-78. [Pg.1634]

Variations in the use pattern of industrial and agricultural chemicals throughout the world preclude standardization by international organizations such as OECD. Despite this fact, common dietary constituents, which are known to influence toxicity are antioxidants, unsaturated fatty acids, and selenium. These must be present in interfering concentrations. The potential impact of several common dietary contaminants on chronic toxicity assessment therefore, necessitates that special attention be given to their presence. In this respect, substances of concern include pesticide residues, chlorinated and polycyclic aromatic hydrocarbons, estrogens, heavy metals, nitrosamines, and mycotoxins. [Pg.497]

McAdam, P.A. and Levander, O.A. 1987. Chronic toxicity of dietary selenium fed to rats as D- or L-selenomethionine, selenite or selenate. Nutr. Res. 7, 601-610. [Pg.107]

Although chronic toxicity due to inhalation or absorption of selenium is usually seen only in industry, cases of chronic poisoning in seleniferous areas (for instance, the Enshi region in China) have been studied and attributed to consumption of food contaminated with selenium (NAS 1976, Glover et al. 1979, Newland 1982, Olson 1986, Einbrodt and Michels 1984, WHO... [Pg.1388]

Several lab studies have examined effects from single metal exposure to birds. Eggs from adults dosed with arsenic have been examined for accumulation and effects 109). Eggs have been dosed with lead followed by embryo examination for effects 101). Although Beyer et al. 42) did not examine multiple metals, they did examine the uptake and biological effects of six avian species dosed with lead. The dose dependent distributions and effects of lead, selenium and cadmium have been examined in several species 72, 98, 110). Scheiihammer 83) reviews numerous studies examining chronic toxicity of several metals. [Pg.332]

Laboratory animals show similar symptoms, and a dietary level of 5 to 10 ppm has been found to induce chronic toxicity in rats [32]. The vascular system and liver are the most affected by long term exposure to selenium. [Pg.55]

Schrauzer, G.N., Effects of selenium antagonists on cancer susceptibility New aspects of chronic heavy metal toxicity, J UOEH 9, 208, 1987. [Pg.223]

Toxicology. Selenium is an essential trace element that can be toxic in excessive amounts. Elemental selenium and selenium compounds as dusts, vapors, and fumes are irritants of the eyes, mucous membranes, and skin. Chronic exposure may cause central nervous system effects, gastrointestinal disturbances, and loss of hair and fingernails. [Pg.623]

Larger particles (several micrometers in size) are deposited in the ciliated portion and are cleared from the respiratory system by muco-ciliary action into the gastronomical tract, but may produce systemic toxic effects by absorption in body fluids. Finer particles reach the lower non-ciliated portion of the lungs, are cleared very slowly, and are responsible for diseases such as pneumoconiosis and lung cancer. Metallic lead (Pb), tellurium ( ), selenium (Se), and platinum (Pt) are known to cause both systemic and respiratory toxicity in laboratory animals and several cases of acute and chronic poisoning among metal workers have also been documented. [Pg.95]

Selenium is mostly found in arid environments under irrigated agriculture. Selenium has toxic effects at high dose levels, but at low dose levels is an essential nutrient. It is classified in the EPA s Group D (not classifiable), and because of its potential chronic health effects, it is regulated by the U.S. government. [Pg.487]

Extremely small amounts of Se are required by warm-blooded animals, but Se is also highly toxic in larger amounts. Two livestock diseases known as blind staggers and alkali disease were identified as manifestations of acute and chronic Se poisoning (Robinson, 1933). New Zealand scientists McLean et al. (1959) discovered that muscular dystrophy in lambs and calves could be prevented by Se therapy. Selenium-deficiency areas were later identified in many other countries and it soon became apparent that these areas were of far greater extent than those affected by excessive Se levels. [Pg.547]

Selenium is an essential element but is toxic when excessive quantities are ingested. Exposure of horses is usually through consumption of seleniferous (accumulator or indicator) plants (e.g.. Astragalus spp.). Exposure to high quantities of selenium over a short time causes diarrhea (which is often foul smelling and contains air bubbles), neurological and cardiovascular effects, and respiratory difficulty. Death in these horses is due to respiratory failure. Chronic exposure to low levels of excessive selenium is characterized by hoof abnormalities at the coronary bands and by discoloration and loss of hair. The hoof deformities are painful and cause lameness. [Pg.2823]

Similarly, in most studies, the simultaneous administration of mercury and selenium in equimolar doses to animals has resulted in decreased toxicity of both elements in acute and chronic exposure studies. [Pg.355]


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