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Suggested Citation:"'SELENIUM'." National Research Council. 1974. Geochemistry and the Environment: Volume I: The Relation of Selected Trace Elements to Health and Disease. Washington, DC: The National Academies Press. doi: 10.17226/20136.
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Suggested Citation:"'SELENIUM'." National Research Council. 1974. Geochemistry and the Environment: Volume I: The Relation of Selected Trace Elements to Health and Disease. Washington, DC: The National Academies Press. doi: 10.17226/20136.
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Page 57
Suggested Citation:"'SELENIUM'." National Research Council. 1974. Geochemistry and the Environment: Volume I: The Relation of Selected Trace Elements to Health and Disease. Washington, DC: The National Academies Press. doi: 10.17226/20136.
×
Page 58
Suggested Citation:"'SELENIUM'." National Research Council. 1974. Geochemistry and the Environment: Volume I: The Relation of Selected Trace Elements to Health and Disease. Washington, DC: The National Academies Press. doi: 10.17226/20136.
×
Page 59
Suggested Citation:"'SELENIUM'." National Research Council. 1974. Geochemistry and the Environment: Volume I: The Relation of Selected Trace Elements to Health and Disease. Washington, DC: The National Academies Press. doi: 10.17226/20136.
×
Page 60
Suggested Citation:"'SELENIUM'." National Research Council. 1974. Geochemistry and the Environment: Volume I: The Relation of Selected Trace Elements to Health and Disease. Washington, DC: The National Academies Press. doi: 10.17226/20136.
×
Page 61
Suggested Citation:"'SELENIUM'." National Research Council. 1974. Geochemistry and the Environment: Volume I: The Relation of Selected Trace Elements to Health and Disease. Washington, DC: The National Academies Press. doi: 10.17226/20136.
×
Page 62

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56 THE RELATION OF SELECTED TRACE ELEMENTS TO HEALTH AND DISEASE Tipton, I. H., and P. L. Stewart. 1970. Long-term studies of ele- mental intake and excretion of three adult male subjects. Dev. Appl. Spectrosc. 8:40-50. Underwood, E. J . 1971. Trace elements in human and animal nu- trition (3rd ed.). Academic Press, New York. 543 pp. U.S. Public Health Service. 1962. Public Health Service drinking water standards. PHS Pub!. No. 956. U.S. Government Printing Office, Washington, D.C. Voors, A. W., M.S. Shuman, and P. N. Gallagher. 1973. Zinc and cad- mium autopsy levels for cardiovascular disease in geographical context. In Proceedings of the Sixth Annual Conference on Trace Substances in Environmental Health, June 13-15, 1972, D. D. Hemphill [ed). University of Missouri, Columbia. pp. 215-222. Voors, A. W., M.S. Shuman, and P. N. Gallagher. 1974. Athero- sclerosis and hypertension in relation to some trace elements in tissues. (In press.) World Rev. Nutr. Diet., Vol. 19. Yamagata, N., and I. Shigematsu. 1970. Cadmium pollution in perspective. Bull.lnst. Public Health 19(1):1-27. Zinc Brown, M.A., J. V. Thom, G. L. Orth, P. Cova, and J. Juarez. 1964. Food poisoning involving zinc contamination. Arch. Environ. Health 8:657. Caggiano, V. R., R. Schnitzler, W. Strauss, R. K. Baker, A. C. Carter, A. S. Josephson, and S. Wallach. 1969. Zinc deficiency in a pa- tient with retarded growth, hypogonadism, hypogammaglobu- linemia and chronic infection. Am. J. Med. Sci. 257:305-319. Evans, G. W., C. I. Grace, and H. J. Votava. 1974. A proposed mechanism for zinc absorption in the rat. (In press.) Am. J. Physiol. Halstead, J. A., H. A. Ronaghy, P. Abadi, M. Haghshenass, G. H. Amirhakemi, R. M. Barakat, and J. G. Reinhold. 1972. Zinc deficiency in man: The Shiraz experiment. Am. J. Med. 53:277. Hambidge, K. M., C. Hambidge, M. Jacobs, and J.D. Baum. 1972. Low levels of zinc in hair, anorexia, poor growth, and hypo- geusia in children. Pediatr. Res. 6:868. Henkin, R. I. 1971. Newer aspects of copper and zinc metabolism. In The newer trace elements in nutrition, W. Mertz and W. E. Cornatzer (eels). Marcel Dekker, New York. pp. 255-312. Henkin, R. 1., P. J. Schechter, R. Hoye, and C. F. T. Mattern. 1971. Idiopathic hypogeusia with dysgeusia, hyposmia, and dysosmia: A new syndrome. J. Am. Med. Assoc. 217 :434-440. Hsu, J. M., W. L. Anthony, and P. J. Buchanan. 1969. Zinc defi- ciency and incorporation of 14C-labeled methionine in to tissue proteins in rats. J. Nutr. 99:425. Kopp, J. F. 1970. The occurrence of trace elements in water. In Proceedings of the Third Annual Conference on Trace Su~ stances in Environmental Health, June 24-26, 1969, D. D. Hemphill [ ed ). University of Missouri, Columbia. pp. 59-73. Ukuski, H. J. A., and R.N. Forbes. 1964. Effects of phytic acid on availability of zinc in amino acid and casein diets fed to chicks. J . Nutr. 84:145. McClain, P. E., E. R. Wiley, G. R. Beecher, W. L. Anthony, and J. M. Hsu. 1973. Influence of zinc defiCiency on synthesis and cross- linking of rat skin collagen. Biochem. Biophys. Acta 304:457- 465. O'Dell, B. L., and J . E. Savage. 1960. Effects of phytic acid on zinc availability. Proc. Soc. Exp. Bioi. Med. 103:304. Papp, J. P. 1968. Metal fume fever. Post Grad. Med. 43:160. Pories, W. J ., J . H. Henzel, C. G. Rob, and W. H. Strain. 1967. Ac- celeration of healing with zinc sulfate. Ann. Swg. 165:432-436. Prasad, A. S., A. Miale, Ir., Z. Farid, H. H. Sandstead, and A. R. Schulert. 1963. Zinc metabolism in patients with the syndrome of iron deficiency anemia, hepatosplenomegaly, dwarfism, and hypogonadism. J. Lab. Clin. Med. 61:537. Sandstead, H. H. 1973. Zinc nutrition in the United States. Am. J . Clin. Nutr. 26:1251-1260. Sandstead, H. H., V. C. Lanier, G. H. Shepard, and D. D. Gillespie. 1970. Zinc and wound healing: effects of zinc deficiency and zinc supplementation. Am. J. Clin. Nutr. 23:514. Sandstead, H. H., A. S. Prasad, A. R. Schulert, Z. Farid, A. Miale, Jr., S. Bassity, and W. J . Darby. 1967. Human zinc deficiency, endo- crine manifestations and response to treatment. Am. J. Clin. Nutr. 20:422. Sandstead, H. H., and R. A. Rinaldi. 1969. Impairment of deoxy- ribonucleic acid synthesis by dietary zinc deficiency in the rat. J. Cell Physiol. 73:81. Schroeder, H. A. 1971. Losses of vitamins and trace minerals result- ing from processing and preservation of foods. Am. J. C1in. Nutr. 24:562-573. Terhune, M. W., and H. H. Sandstead. 1972. Decreased RNA poly- merase activity in mammalian zinc deficiency. Science 177:68. Lead Chisholm, J. J., Jr. 1965. Chronic lead intoxication in children. Dev. Med. Child Neurol 7:529-536. Committee on Biologic Effects of Atmospheric Pollutants. 1972. Lead: airborne lead in perspective. National Academy of Sci- ences, Washington, D.C. 330 pp. Murozumi, M., T. J. Chow, and C. Patterson. 1969. Chemical con- centrations of pollutant lead aerosols, terrestrial dusts, and sea salts in Greenland and Antarctic snow strata. Geochim. Cosmo- chim. Acta 33:1247-1294. Selander, S., and K. Cramer. 1970. Interrelationships between lead in blood, lead in urine, and ALA in urine during lead work. Br. J. Ind. Med. 27:28-39. Snyder, R. N., D. J. Wuebbler, J. E. Pearson, and B. B. Ewing. 1971. A study of environmental pollution by lead. Rept. No. 11EQ71-7. Winois Institute for Environmental Quality. Tepper, L. B. 1971. Seven-city study of air and population lead levels: An interim report. Department of Environmental Health, College of Medicine, University of Cincinnati, Cincinnati, Ohio. II pp.

VII Selenium JAMES E. OLDFIELD, Chairman William H. Allaway, Herbert A. Laitinen, Hubert W. Lakin, 0. H. Muth During the last decade, a voluminous scientific literature has accumulated on selenium and has been reviewed by a number of authors (Rosenfeld and Beath, 1964; Muth et aL, 1961; and Committee on Animal Nutrition, 1971). It is generally accepted that health problems associated with selenium in animals exist at both ends of the nutritional spectrum-because of both deficiency and excess. Histori- cally, selenium has been recognized as a toxicant, asso- ciated with animal diseases referred to as "alkali disease" or"blind staggers." Symptoms, lesions, and the choice of designation depend on the concentrations ingested and the time span of exposure. These two terms originated about a century ago when "blind staggers" was associated with severe abdominal pain in cattle. The animal seeks re- lief from constant abdominal discomfort by continual walking. The condition worsens; there is central-nervous- system involvement, impairment of vision, and staggering in attempts to avoid objects not seen clearly. Weakness, dyspnea, cyanosis, and death follow-primarily from res- piratory failure. "Alkali disease," the chronic form of selenium poisoning, was originally considered to result from excessive ingestion of soil alkali. It is characterized by loss of hair and abnor- malities of the hooves. In both "blind staggers" and "alkali disease" there is focal myocardial necrosis, cerebral edema, and liver and kidney damage. Within the last 20 years, the existence of deficiency dis- 57 eases involving selenium have been recorded, and selenium has been added to the list of essential nutrients. The two areas of selenium research in regard to man that have received most attention relate to the correlation of excess selenium with periodontal disease and dental caries. In animals, research on the effect of excess selenium on carcinogenicity and teratogenicity has been of greatest interest. Effects on the two latter conditions are contro- versial, and great difficulty or failure has resulted from attempts to repeat original work. Recent investigations into the essential role of selenium as a nutrient for poultry and domestic animals have created considerable interest. SOURCES AND OCCURRENCE Selenium has atomic number 34, an atomic weight of 78.96, and percentage isotopic composition of 14Se 0.87, 76Se 9.02, 77Se 7.58, 78Se 23.52, 80Se 49.82, and 82Se 9.19. It forms naturally occurring compounds of valence 2-, 4+, and 6+; in the reduced divalent state, its ionic radius is 1.91 A, and it replaces S2 - in many sulfides. The commercial source of selenium is the anodic slime from electrolytic copper refming. Selenium is erratically dispersed in geologic materials. Goldschmidt and Strock (1935) estimated that the sulfur/ selenium ratio in sulfides is about 6,000, and the abundance of sulfur in igneous rocks is 520 ppm. A ftgure of 0.09 ppm

58 THE RELATION OF SELECTED TRACE ELEMENTS TO HEALTH AND DISEASE for the estimated abundance of selenium in igneous rocks was obtained by dividing 520 by 6,000. This f~gure was used as the crustal abundance of selenium until 1961, when Tureldan and Wedepohl (1961) revised the sulfur content of igneous rocks downward to 300 ppm and divided that f~gure by Goldschmidt's sulfur/selenium ratio of 6,000 to obtain an estimated abundance of 0.05 ppm selenium in the earth's crust. Relatively few igneous rocks have been analyzed for selenium. Volcanic-ash flows and lava from New Zealand are rich in selenium (Wells, 1967). We can conclude that the selenium content of igneous rocks ranges from 0.004 to 1.5 ppm, that some andesitic-ash flows contain unusually high amounts of selenium, and that lavas are usually higher in selenium than intrusives. The selenium content of sedimentary rocks often ex- ceeds by one or more orders of magnitude the content of intrusive igneous rocks because of the selenium added to surficial deposits by volcanic emanations. Biological pro- . .. . . ·:: :: . . .. : .. . .. . :-. ·.· .... .. . . . . .. . ... ···:· ....... cesses also result in local concentration of selenium, for instance, in coals and in present-day swamps in Ireland. The selenium content of streams is a function of the available selenium of the drainage basin and the pH of the water. A map is included (Figure 7) to indicate selenium con- centrations in forage and grain and to show where selenium deficiencies and excesses are known to occur in animals. Rocks and Soils The primary sources of selenium are volcanic emanations and metallic sulfides associated with igneous activity; sec· ondary sources are biological sinks in which the selenium has accumulated. The selenium content of black shales and coal is 10-20-times the crustal abundance of the element. Shales containirJg unusually high amounts of selenium, which may have resulted from volcanic-ash ~ • D Low-approximately 80 percent of all forage and grain contains < 0.05 ppm of selenium . Variable-approximately 50 percent of all forage and grain contains> 0.1 ppm. Adequate-SO percent of all forage and grain contains > 0.1 ppm of selenium. Local areas where selenium accumulator plants contain > 50 ppm. FIGURE 7 Map showing concentration of selenium in plants in the United States (Kubota and Allaway, 1972).

falls, are widespread and form the parent material of many soils. Particularly well known are the western shales of Cretaceous age. Selenium also accompanies uranium and vanadium in the sandstone ores of the Colorado Plateau. The presence of above-average amounts of selenium in soils does not always affect the uptake of selenium by all plants or, consequently, its presence in the diet of animals. How- ever, the relatively widespread occurrence of selenium- accumulator plants on western shales and in uranium dis- tricts of the Colorado Plateau has been hazardous to the raising of livestock. Water Selenium concentration in river water in the United States is normally less than 0.5 ppb. Certain alkaline streams drain· ing seleniferous lands in the western United States may, however, contain as much as0.5 ppm (Kharkar etaL, 1968; and Scott and Voegeli, Sr., 1961). P/Jmts Selenium has not been generally established as essential for food or feed-crop plants. Plants are more tolerant of exces- sive levels of selenium than are animals, but this is not nec· essarily true of microorganisms. The availability to plants of selenium in soils is governed by the chemical form of the selenium in the soil. The chemical form is a function of the pH and Eh of the soil. Gissel-Nielsen and Bisbjerg ( 1970) added selenium in its metallic forms to soils as K2 Se03 , K2Se04, and BaSe04. In a 2-year study, they found that for mustard plants the total uptake as a percentage of the added selenium was 0.01 percent of metallic selenium, 4 percent ofK2Se03 , and 30 percent of K2Se04 and BaSe04. For alfalfa, barley, and sugar beets, uptake was one-third less than that obtained in mustard. Elemental selenium in soils (Geering et aL, 1968) is a moderately stable form, and as such is not appreciably available to plants. In acid soils (pH 4.5-6.5) selenium is usually bound as a basic ferric selenite of extremely low solubility and is essentially unavailable to plants. In alka- line soils (pH 7 .5-8.5), selenium may be oxidized to selenate ions and become water-soluble; this form is readily available to plants. The chemistry of selenium in soils in relation to its availability to plants has been reviewed by Moxon et al. (1950) and Allaway (1968) and summarized in a 1971 pub- lication by the National Academy of Sciences-National Re- search Council (Committee on Animal Nutrition, 1971 ). There is not necessarily a direct relation between the total selenium concentration in the soil and its concentra- tion in plants. Where the parent rock contains selenium and weathers to form alkaline soil, plants may contain from 0.1 to 10 ppm (dry wt). Selenate is present and generally available to plants in these alkaline soils. Where the rocks Selenium 59 weather to form acid soils, selenium concentrations in plants are generally from 0.02 to 0.2 ppm (dry wt). In- soluble compounds or complexes of selenite and iron are present in acid soils. At the present time, there is no widely accepted chemical procedure for measuring plant-available selenium in soils. Striking differences in uptake of selenium from selenif· erous soils have been noticed among plant species. A group of plants referred to as selenium indicators or selenium ac· cumulators may contain 50-1,000 ppm (dry wt) whereas nearby nonaccumulators may contain only 1-5 ppm. The accumulators include a number of Astragalus species, Stannleya (Ap/opappus), and some of the asters. None of the common food and feed crops is a selenium accumulator. Selenium taken up by accumulators is metabolized to methylselenocysteine and selenocystathionine and remains in the soluble fraction of the plant. In nonaccumulator spe- cies the selenium is primarily in protein-bound selena- methionine. As shown in the map by Kubota and Allaway ( 1972) (Figure 7), the concentration of selenium in nonaccumula- tor plants in the United States varies markedly from one part of the country to another. Concentrations of less than 0.05 ppm selenium (dry wt) are common in plants from the Pacific Northwest, the northeastern United States and Florida. Plants grown in the west central states generally contain from 0.10-1.0 ppm (dry wt ). It is interesting to note that small amounts of selenium enter the atmosphere from biological processes within some plants. Dimethyldiselenide is a volatile product of Astragalus racemosus (Evans eta/., 1968), and volatile selenium is also released by such nonaccumulator plants as alfalfa. The amounts of selenium released are related to the amounts of volatile compounds within the plant (Lewis eta/., 1966). Animals From existing information, it is possible to trace the geo- chemical-biological movement of selenium from rocks and soils through plants and animals to man (Allaway eta/., 1966). The total amount of selenium moving from soils to food and feed crops appears to be substantially greater than the amount extracted from ores used for industrial purposes. Animals retain 25-75 percent of the dietary selenium consumed. Factors influencing retention include body stores of selenium as well as the chemical form of selenium present in the diet. Several investigations indicate that when the diet dry matter contains from 0.5 to 1.5 ppm selenium, selenium from selenomethionine or seleniferous feed crops is retained by the animal to a greater extent than is these- lenium from inorganic selenite or selenate. Relationships between the level of dietary selenium and its concentration in animal tissues have been summarized (Committee on Ani·

60 THE RELATION OF SELECTED TRACE ELEMENTS TO HEALTH AND DISEASE mal Nutrition, 1971 ). Concentrations of selenium in milk tend to correlate with concentrations in the cow's diet. EFFECTS OF SELENIUM ON ANIMAL AND HUMAN HEALTH A multitude of factors bears on the relationship between environmental supplies of selenium and animal and human health: Included are influences of various forces (such as volcanic eruption) on the formation of soils, weathering, effects of wind and water, presence of ions or organic sub- stances that enhance or depress the availability of selenium to plants and animals, and the interplay of physiological forces within the host. It is important also to consider the effects of man-made contamination. In farm animals, selenium deficiency is currently recog- nized more often than selenium toxicity. Deficiency symp- toms appear at diet dry-matter levels as low as 0.02-0.04 ppm; levels of 2-4 ppm or more are toxic. Although the absolute levels are small, the hundredfold difference be- tween essentiality and toxicity is comparable to that for other dietary trace elements. Positive relations have been established between the geo- chemical environment and selenium deficiency or toxicity in animals. Although similar relations have been ascribed to humans, the situation needs more study. Soils supporting plants with toxic levels of selenium are confined to small areas, but the plants may be dispersed worldwide (Rosen- feld and Death, 1964; and Muth eta/., 1967). Feeds are shipped from high-selenium areas to low-selenium areas and vice versa, as well as similar transfers of animals. Deficiency of Selenium in the Diet of Animals During the past two decades, selenium has been recognized as an essential element for several animal species (Schwarz, 1967; and Thompson and Scott, 1970). A deficiency of dietary selenium results in degenerative changes that vary somewhat according to the species of animal. In ruminants, these changes consist primarily of myopathy, especially of the heart and skeletal muscles. Exercising a selenium- deficient animal can precipitate an acute myocardial defi- cit and death. Other species, including rats and swine, respond to se- lenium deficiency with hepatic degeneration, although other organs and tissues are also affected to varying degrees. In the mouse and squirrel monkey (Muth eta/., 1971), sele- nium deficiency is associated with loss of hair, emaciation, and severe lesions in liver and muscles. Both chronic and acute forms of myopathy have been reported in horses. In addition to the deficiency lesions noted in ruminants, periodontal disease and impaired reproduction have been reported in New Zealand sheep. Another lesion that may prove significant in future investigations of selenium de· ficiency is the development of cataracts in rats (Sprinker eta/., 1971 ). Although diets imposed on domestic ani· mals by man may contribute to the frequency of selenium deficiency, wild deer also suffer similar lesions. Effects of selenium deficiency are more frequent in ruminants than in monogastric animals. Among animals of the same species, there is sufficient difference in selenium utilization to warrant an assumption of individual varia- tion in metabolism (Blaxter, 1962). Factors in natural foods can inhibit or enhance the metabolism of selenium (Thompson and Scott, 1968, 1970). A dietary deficiency of selenium in poultry is associated with exudative diathesis, poor growth, poor feathering, and fibrotic degeneration of the pancreas (Committee on Ani· mal Nutrition, 1971). By implication, it has been assumed that such selenium deficiency results from peculiar geo- chemical conditions in specific crop-producing areas. Soils deficient in, or with unavailable, selenium produce plants deficient in selenium, and can induce deficiency disease in the animals eating the plants. Bruins et aL (1966) con- fll111ed this by preparing animal feeds from identical plant species grown in areas where soil selenium contents were known to be either adequate or low. Signs of selenium deficiency occurred in turkeys fed materials from Ohio and New York (dietary selenium 0.08 ppm), but not in birds fed the same feeds from plants grown in western Iowa (dietary selenium 0.37 ppm). Selenate, selenite, selenomethionine, and natural or- ganic selenium in grains and forages have all been found to be effective in prevention of selenium deficiency diseases in animals. Elemental selenium has been effective in cattle and sheep only when used in a heavy pellet retained in the rumen for long periods (Handreck and Godwin, 1970). Toxicity in Animals Chronic selenium poisoning in livestock occurs in many parts of the world and is usually the result of feeding on seleniferous plants. Toxic effects of selenium in animals have been reported from dietary concentrations of about 3-5 ppm. The attendant signs of selenium toxicity in af- fected animals are weight loss, general deterioration of physical well-being, and alopecia. There is also a distur- bance in growth pattern of hooves and horns. In the higher animals, excessive amounts of selenium apparently have a direct effect on the myocardium, resulting in progressive cardiac failure and sudden death. This is attended by pul- monary changes characteristic of circulatory impairment (Muth and Binns, 1964). Selenium and Human Health The relationship between selenium and human health is not as well understood. Hadjimarkos (1965) has indicated that

the incidence of caries may increase in seleniferous areas. Conversely, Ludwig and Bibby (1969) suggested that there was no consistent relationship between seleniferous regions and the incidence of caries in school children. However, Schwarz (I 967) has pointed out that such surveys may be deceptive because they do not include all variables, some of which-like economic status and concern for dental hygiene-may be important influences on dental disease. Possible relationships between dietary selenium levels and incidence of cancer provide an intensely interesting and potentially valuable field for study. Concern over pos- sible carcinogenic effects from excess selenium stems from the work of Nelson et aL ( 1943), who fed highly selenif- erous wheat to rats on low-protein diets: Of 53 rats, II developed tumors of the liver. Results of this study are difficult to interpret because of the low concentration and poor quality of protein in the diet and the open ques- tion of whether mycotoxins were present in the wheat and corn used in the diet. Liver injury from some other cause, such as deficiency in lipotropic factors, may relate to se- lenium carcinogenesis. Schroeder and Mitchener ( 1971 a) describe a carcinogenic effect on rats given 3 ppm sele- nium in drinking water, but this is approximately !50- times the required dietary level. Other investigators report conflicting experiences. Harr et al. (1967) found no malig- nancies attributable to selenium in studies over the life- time of rats, although the actual length of the study was not as long as Schroeder and Mitchener's ( 1971a). Shamberger and Rudolph ( 1966) demonstrated inhibi- tion of dimethylbenzanthracene-croton oil cocarcinogenesis by selenium, and subsequently Shamberger and Frost ( 1969) and Shamberger and Willis (1971) reported geo- graphic studies suggesting lower cancer death rates in human populations living in high-selenium areas. Harr et al. (1972) found that the addition of 0.5 ppm selenium as selenite to a vitamin E-supplemented diet decreased the incidence of N-2-fluorenylacetamide-induced cancer in rats. The relationship of selenium to cancer in man needs to be resolved through carefully controlled biomedical studies. It was first suggested nearly 20 years ago that selenium might be teratogenic, because hens in seleniferous regions either produced sterile eggs or a high percentage of chicks with anomalies (Moxon and Rhian, 1943). Schroeder and Mitchener ( 1971 b) note that selenium is teratogenic in mice given it by mouth. The teratogenic nature of sele- nium requires further study. Robertson (1970) cited cases of anomalies in infants born to women employed in weighing powders containing selenite for culture media, suggesting a teratogenic effect from selenium. Shamberger (1971), however, presented op- posing evidence in material published on laboratory experi- ments conducted by Holmberg and Ferm (1969), who showed that selenium protected hamsters against the tera- togenic effects of cadmium and arsenic. Shamberger also Selenium 61 cited statistics showing lower human neonatal death rates in states where selenium content of the soil is higher, in contrast to death rates in states with less selenium. This situation also requires clarification. Selenium and Sudden Infant Death or Crib Death A deficiency of selenium or vitamin E has been suggested as a possible factor in the sudden infant death (SID) prob- lem. This suggestion was fust made by Money ( 1970) on the basis of similarities between the postmortem findings in infants who died unexpectedly and necropsy material in young pigs that died of selenium-vitamin E deficiency in New Zealand. Levels of selenium and vitamin E in whole blood and blood plasma from infants whose deaths were diagnosed as SID have been compared with those found in fetal cord blood or in blood of infants hospitalized for various causes (Rhead et al., 1972). Plasma vitamin-E levels in SID infants were not significantly different from those previously re- ported for normal or premature infants. Plasma vitarnin-E levels of all infants were about half those characteristic of normal adults. Selenium levels in the plasma and whole blood of SID infants were not significantly different from those in fetal cord blood or in blood from hospitalized in- fants. Infants have lower plasma and whole-blood selenium levels than those obtained from normal adults. Although the data do not show an association between SID and low plasma selenium-vitamin E levels when com- parisons are made among infants dying before the age of 2 months, comparisons of infant and adult plasma indicate that the selenium-vitamin E status of many infants may be too low to prevent damage from stresses of varied origin. SELENIUM POLLUTION The amount of selenium entering the atmosphere from the burning of fossil fuel is approximately 6-times greater than that derived from mined ores. Preliminary estimates of se- lenium in rainfall indicate that regions of high fossil-fuel use have higher rates of deposition by rain. On the other hand, the fact that selenium deficiencies in livestock are prevalent in the northeastern United States, where fossil fuel con- sumption is high, indicates that airborne selenium may not be a major factor in environmental concentration of this element. RECOMMENDATIONS FOR RESEARCH 1. Easier and more rapid analytical methods should be developed. Current methods that meet acceptable criteria for accuracy and sensitivity are, however, available for se- lenium measurements. 2. Baseline data should be established with reference to

62 THE RELATION OF SELECTED TRACE ELEMENTS TO HEALTH AND DISEASE selenium levels in humans in health and disease. Much more extensive sampling of human material, such as blood, urine, and hair, might be done in attempts to correlate concentra- tions of selenium with disease incidence. Autopsy material from human cadavers might be valuable also, as would ma- terial from domestic and wild animals. 3. Data on selenium concentrations in rain, surface waters, and natural plant exudations are needed. 4. Relative availability of selenium and plant and animal response to different forms of selenium need further evalua- tion. 5. Substances that interact with and modify the effects of selenium on animals need identification and study (e.g., vitamin E, vanadium). 6. An understanding of the precise metabolic role of selenium in biological systems is needed. 7. Cause-effect relations between dietary selenium, malignant tumors, and teratogeny in animals need further study. Gaps are apparent in available knowledge of the transfer of selenium from soil through plants and animals to man. Answers are needed for immediate needs and may also have long-range implications for future agricultural production, and ultimately, for the health and well-being of mankind. Two examples lend emphasis to this observation. As human population increases on earth, cropping of land areas now considered to be of marginal value for agriculture seems likely. Some of the most dramatic exhibitions of selenium deficiency have occurred when such lands have been sub- jected to intensive farming. Moreover, the continuing de· velopment of agricultural and industrial technology will create effects on the environment that may have important implications for the removal and utilization of nutrient sub- stances in it. Several facets of the geobiological cycle for selenium need to be examined carefully with these pos- sibilities in mind. REFERENCES Allaway, W. H. 1968. Control of the environmental levels of selenium. In Proceedings of the Second Annual Conference on Trace Sub- stances In Environmental Health, July 16-18, 1968, D. D. Hemp- hill (ed). University of Missouri, Columbia. pp. 181-206. Allaway, W. H., D.P. Moore, J. E. Oldfield, and 0. H. Muth. 1966. Movement of physiological levels from soils through plants to animals. J. Nutr. 88:411-418. Blaxter, K. L. 1962. The effect of selenium on lamb growth: Coop- erative experiments on Scottish fums. Proc. Nutr. Soc. 21:xix. Brulns, H. W., L. E. Osterhout, M. L. Scott, E. E. Cary, and W. H. Allaway. 1966.1s selenium deficiency a practical problem In poultry? Feedstuffs 38:66-67. Committee on Animal Nutrition. 1971. Selenium In nutrition: a report of the Subcommittee on Selenium. National Academy of Sciences, Waahlnaton, D.C. 79 pp. Evans, C. S., C. J. Asher, and C. M. Johnson. 1968. Isolation of eli- methyl diselenide and other volatile selenium compounds from A1tragalu1 racemoms (Pursh.). Aust. J. Bioi. Sci. 21:13-20. Geerlns, H. R., E. E. Cary, L. H. P. Jones, and W. H. Allaway. 1968. Solubility and redox criteria for the possible forms of selenium in soils. Soil Sci. Soc. Am. Proc. 32(1):35-40. Gissel-Nielsen, G., and B. Bisbjeig. 1970. The uptalce of applied se- lenium by agricultural plants-(2) the utilization of various se- lenium compounds. Plant and SoU 32(2):382-396. Goldschmidt, V. M., and L. W. Strock. 1935. Zur Geochemie des Selens II. Nechr. Ges. Wiss. Gottingen Math.-Phys. Kl. IV. 1:123-143. Hadjimukos, D. M. 1965. Effect of selenium on dental caries. Arch. Environ. Health 10:893-899. Handreck, K. A., and K. D. Godwin. 1970. Distribution in the sheep of selenium derived from 75Se-labelled ruminal pellets. J. Nutr. 79:493-502. Hur, J. R., J. F. Bone, I. J. Tinsley, P. H. Weswig, and R. S. Yama- moto. 1967. Selenium toxicity in rats: II, Histopathology. In Symposium: Selenium in biomedicine, 0. H. Muth, J. E. Oldfield, and P. H. Weswig (eds). 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