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13
Arsenic, Boron, Nickel, Silicon, and Vanadium

SUMMARY

An Estimated Average Requirement (EAR) or Adequate Intake (AI) was not set for arsenic, boron, nickel, silicon, or vanadium. In the case of the vitamins and other minerals reviewed in this report, there are well-established studies typically based on observations from several laboratories. The data currently available for these vitamins and other minerals provide an understanding of the metabolic role of each and describe the consequences of their restriction in the diets of both laboratory animals and humans. There are also clearly defined, readily reproducible indicators in humans for these vitamins and other minerals that can be used to determine an EAR and calculate a Recommended Dietary Allowance, or to establish an AI. At present, such data do not exist for arsenic, boron, nickel, silicon, and vanadium.

In the case of arsenic, boron, nickel, silicon, and vanadium, there is evidence that they have a beneficial role in some physiological processes in some species. For boron, silicon, and vanadium, measurable responses of human subjects to variations in dietary intake have also been demonstrated. However, the available data are not as extensive (e.g., dose-response data are absent) and the responses are not as consistently observed as they are for the vitamins and other minerals. Thus, data are insufficient to determine an EAR for any of these minerals.

Estimates of dietary intakes of arsenic, boron, nickel, silicon, and vanadium by the North American adult population are available



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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc 13 Arsenic, Boron, Nickel, Silicon, and Vanadium SUMMARY An Estimated Average Requirement (EAR) or Adequate Intake (AI) was not set for arsenic, boron, nickel, silicon, or vanadium. In the case of the vitamins and other minerals reviewed in this report, there are well-established studies typically based on observations from several laboratories. The data currently available for these vitamins and other minerals provide an understanding of the metabolic role of each and describe the consequences of their restriction in the diets of both laboratory animals and humans. There are also clearly defined, readily reproducible indicators in humans for these vitamins and other minerals that can be used to determine an EAR and calculate a Recommended Dietary Allowance, or to establish an AI. At present, such data do not exist for arsenic, boron, nickel, silicon, and vanadium. In the case of arsenic, boron, nickel, silicon, and vanadium, there is evidence that they have a beneficial role in some physiological processes in some species. For boron, silicon, and vanadium, measurable responses of human subjects to variations in dietary intake have also been demonstrated. However, the available data are not as extensive (e.g., dose-response data are absent) and the responses are not as consistently observed as they are for the vitamins and other minerals. Thus, data are insufficient to determine an EAR for any of these minerals. Estimates of dietary intakes of arsenic, boron, nickel, silicon, and vanadium by the North American adult population are available

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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc and could have been used to establish an AI. However, establishing an AI also requires a clearly defined, reproducible indicator in humans sensitive to a range of intakes. Indicators that meet this criterion for establishing an AI are not currently available for any of these minerals, and therefore no AI was set. Notwithstanding, observations of deficiency effects (e.g., on growth and development) in multiple animal species and data from limited human studies suggest beneficial roles for arsenic, boron, nickel, silicon, and vanadium in human health. These data clearly indicate a need for continued study of these elements to determine their metabolic role, identify sensitive indicators, and more fully characterize specific functions in human health. Estimates of Tolerable Upper Intake Levels (UL) were set for boron, nickel, and vanadium. The ULs for boron and vanadium are based on animal data and have been set for adults at 20 mg/day and 1.8 mg/day, respectively. The UL for nickel is 1 mg/day. There were insufficient data using the model described in Chapter 3 to set a UL for arsenic and silicon. ARSENIC BACKGROUND INFORMATION Function There have been no studies to determine the nutritional importance of arsenic for humans. Although the metabolic function of arsenic is not well understood, one study in rats suggests that arsenic may have a role in the metabolism of methionine (Uthus and Poellot, 1992). Arsenic deprivation was associated with an increase in hepatic S-adenosyl-homocystine concentrations and a decrease in hepatic S-adenosyl-methionine concentrations. Arsenic deprivation has also been associated with impaired growth and abnormal reproduction in rats, hamsters, chicks, goats, and miniature pigs (Anke, 1986; Uthus, 1994). Arsenic has also been suggested to be involved with the regulation of gene expression (Meng and Meng, 1994). Arsenite is associated with changes in the methylation of core histones and therefore is active at the transcriptional level (Desrosiers and Tanguay, 1986).

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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc Physiology of Absorption, Metabolism, and Excretion The absorption of inorganic arsenic is related to the solubility of the compound ingested (Vahter, 1983). In humans, more than 90 percent of inorganic arsenite and arsenate from water is absorbed (Vahter, 1983), and approximately 60 to 70 percent of dietary arsenic is absorbed (Hopenhayn-Rich et al., 1993). Once absorbed, inorganic arsenic is transported to the liver where it is reduced to arsenite and then methylated. The majority of ingested arsenic is rapidly excreted in the urine. The proportion of the various forms of arsenic in urine can vary; however, the common forms present are inorganic arsenic, monomethylarsonic acid, dimethylarsinic acid, and trimethylated arsenic (Yamato, 1988). FINDINGS BY LIFE STAGE AND GENDER GROUP Because of the lack of human data to identify a biological role of arsenic in humans, neither an Estimated Average Requirement, Recommended Dietary Allowance, nor Adequate Intake were established. INTAKE OF ARSENIC Food Sources Dairy products can contribute as much as 31 percent of arsenic in the diet; meat, poultry, fish, grains and cereal products collectively contribute approximately 56 percent (Mahaffey et al., 1975). Based on a national survey conducted in six Canadian cities from 1985 to 1988, it was reported that foods containing the highest concentrations of arsenic were fish (1,662 ng/g), meat and poultry (24.3 ng/g), bakery goods and cereals (24.5 ng/g), and fats and oils (19 ng/g) (Dabeka et al., 1993). The substantial portion of arsenic present in fish is in the organic form. The major contributors of inorganic arsenic are raw rice (74 ng/g), flour (11 ng/g), grape juice (9 ng/ g), and cooked spinach (6 ng/g) (Schoof et al., 1999). Dietary Intake Results of the analysis of 265 core foods conducted by the Food and Drug Administration (1991–1997), and analysis of foods and intake data from the U.S. Department of Agriculture Continuing Survey of Food Intakes by Individuals (1994–1996), indicate that

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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc the intakes of arsenic for all age groups ranged from 0.5 to 0.81 μg/ kg/day (Gunderson, 1995) and that the median intake of arsenic by adult men and by women was approximately 2.0 to 2.9 μg/day and 1.7 to 2.1 μg/day, respectively (Appendix Table E-2). Adams and coworkers (1994) reported lower intakes for adults (23 to 58 μg/day) from 1982 to 1991. There was not a marked difference in the arsenic consumption between various age groups. Gartrell and coworkers (1985) reported a similar mean U.S. intake of arsenic of 62 μg/day, and Tao and Bolger (1999) reported intakes ranging from 28 to 72 μg/day for adults from 1987 to 1988. Data on the concentration of arsenic in human milk are limited; however, studies have reported mean concentrations ranging from 0.2 to 6 μg/kg wet weight (Byrne et al., 1983; Dang et al., 1983; Grimanis et al., 1979). TOLERABLE UPPER INTAKE LEVELS The Tolerable Upper Intake Level (UL) is the highest level of daily nutrient intake that is likely to pose no risk of adverse health effects for almost all individuals. Although members of the general population should be advised not to routinely exceed the UL, intake above the UL may be appropriate for investigation within well-controlled clinical trials. Clinical trials of doses above the UL should not be discouraged, as long as subjects participating in these trials have signed informed consent documents regarding possible toxicity and as long as these trials employ appropriate safety monitoring of trial subjects. Arsenic is currently under investigation for the treatment of leukemia (Look, 1998). Arsenic occurs in both inorganic and organic forms, with the inorganic forms that contain trivalent arsenite (III) or pentavalent arsenate (V) being of the greatest toxicological significance (Chan and Huff, 1997). No data on the possible adverse effects of organic arsenic compounds in food were found. Because the organic forms are usually less toxic than the inorganic (ATSDR, 1998), adverse effects of inorganic forms are described. It is unclear whether risk assessments should be developed for specific groups of inorganic arsenic compounds. Adverse Effects The adverse effects of arsenic in humans have been identified with exposure to inorganic arsenic, although in animals higher exposures to organic arsenic produces some of the same effects as

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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc lower exposures to inorganic arsenic (ATSDR, 1998). There is some evidence that arsenic III may be more toxic than arsenic V (Byron et al., 1967; Maitani et al., 1987). Animals do not appear to be good quantitative models for inorganic arsenic toxicity in humans (ATSDR, 1998), perhaps because of the species diversity of erythrocyte-binding of arsenic and inorganic arsenic methyltransferase activity, a detoxification mechanism (Aposhian, 1997; Goering et al., 1999). Acute Effects Inorganic arsenic is an established human poison. Ingestion of doses greater than 10 mg/kg/day leads to encephalopathy and gastrointestinal symptoms (Civantos et al., 1995; Levin-Scherz et al., 1987; Quatrehomme et al., 1992). Poisoning also occurs with arsenic doses of 1 mg/kg/day or greater and can be accompanied by anemia and hepatotoxicity (Armstrong et al., 1984; Fincher and Koerker, 1987). Arsenicism Chronic intake of 10 μg/kg/day or greater of inorganic arsenic produces arsenicism, a condition characterized by alteration of skin pigmentation and keratosis (NRC, 1999). In some regions, an occlusive peripheral vascular disease also occurs resulting in gangrene of the extremities, especially of the feet, thus termed blackfoot disease (Engel and Receveur, 1993; Tseng, 1977). It has been hypothesized that zinc deficiency may exacerbate the toxicity of arsenic (Engel and Receveur, 1993). Malnutrition has been associated with an increased risk of blackfoot disease (Yang and Blackwell, 1961). Because arsenicism may be associated with arsenic intakes higher than those causing other adverse effects (see “Carcinogenicity”), it was not selected as a critical adverse effect to set a UL. Peripheral Neuropathy Intermediate and chronic exposures of arsenic up to levels of 11 mg/L of water are associated with symmetrical peripheral neuropathy (Franzblau and Lilis, 1989; Huang et al., 1985; Wagner et al., 1979). However, in some populations exposures of 5 mg/L of water did not result in clinical or subclinical neuropathy (Kreiss et al., 1983).

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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc Developmental Toxicity Developmental effects in humans have not been demonstrated (ATSDR, 1998; NRC, 1999). In the hamster, single intragastric doses of 1.4 mg of arsenic/kg to pregnant females led to fetal mortality (Hood and Harrison, 1982). In the mouse, fetal mortality and teratogenicity were produced by single intragastric doses of 6 to 7 mg/kg (Hood, 1972) and 11 mg/kg (Hood and Bishop, 1972); oral doses of 23 mg/kg (Baxley et al., 1981) had the same effects. In the rat, an intraperitoneal dose of 5 to 10 mg/kg produced a high percentage of malformed fetuses (Beaudoin, 1974). Genotoxicity Sodium arsenite induced point mutations in two strains of Escherichia coli WP2; negative results were obtained in a recA strain. Arsenic trichloride and sodium arsenite gave positive results in a rec assay in Bacillus subtilis (Nishioka, 1975). Positive results were also obtained in this assay with arsenic trioxide and arsenic pentoxide (Kanematsu et al., 1980). Sodium methanearsonates were negative in this assay (Shirasu et al., 1976). Potassium and sodium arsenite caused mitotic arrest and chromosomal aberrations, including chromatid gaps, breaks, translocations, dicentrics, and rings in cultured human peripheral leukocytes and human diploid fibroblast WI.38 and MRC5 lines (Oppenheim and Fishbein, 1965; Paton and Allison, 1972). Some of the mutagenic effects of arsenic may be a consequence of the formation of reactive oxygen species (Hei et al., 1998). Carcinogenicity Ingestion of inorganic arsenic is associated with risk of cancers of the skin, bladder, and lung (IARC, 1980, 1987; NRC, 1999). Increased risks of other cancers such as kidney and liver have also been reported, but the strength of the association is not great (NRC, 1999). There are no studies of cancer in humans after exposure to organic arsenicals (ATSDR, 1998). Most studies of a positive association with cancer involve intake of inorganic arsenic in drinking water. A large-scale survey of 40,421 inhabitants (19,269 men and 21,152 women) of an area on the southwest coast of Taiwan, where artesian well water with a high concentration of arsenic was consumed for more than 45 years, found that the overall prevalence rates for skin cancer, hyper-

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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc pigmentation, and keratosis were 10.6, 183.5, and 71.0/1,000, respectively (Tseng et al., 1968). They also found that the male-to-female ratio for skin cancer was 2.9:1 and 1.1:1 for hyperpigmentation and keratosis. The prevalence appeared to increase progressively with age for all three conditions, although there was a decline in cancer and hyperpigmentation in women older than 69 years of age. The prevalence rates for skin cancer, hyperpigmentation, and keratosis showed an ascending gradient which correlated with the arsenic content of the well water. Blackfoot disease had an overall prevalence rate of 8.9/1,000 and, similar to skin cancer, displayed a dose-response relationship with the amount of arsenic in the well water. There was a significantly high association of blackfoot disease with hyperpigmentation, keratosis, and skin cancer. The risk of bladder cancer in Taiwan was increased with intake of arsenic from water of 10 μg/kg/day (Chen et al., 1992). This increased risk has been confirmed in studies from Japan (Tsuda et al., 1995), Argentina (Hopenhayn-Rich et al., 1996), and Chile (Smith et al., 1998). Studies in U.S. populations exposed to arsenic in drinking water have not identified cancer increases (Morton et al., 1976; Southwick et al., 1981; Valentine et al., 1992). These epidemiological associations have to some extent been replicated in animal experiments (Simeonova et al., 2000; Yamamoto et al., 1995). However, the mechanisms of arsenic carcinogenesis are not established, but may involve genetic effects (Goering et al., 1999) or perturbation of cellular signaling pathways (Simeonova et al., 2000). Summary Clearly, high intakes of inorganic arsenic are associated with various toxicities, including increased risks of several cancers with chronic exposure to high levels in drinking water. There is no evidence linking organic arsenic in food to any adverse effect, including cancer. Since there is no evidence available to define the mechanisms of arsenic carcinogenesis and no data to support a threshold, it is not possible to establish a health-based level of inorganic arsenic in drinking water and food. It should be noted that a recent report of the National Research Council recommended a downward revision from the current maximum contaminant level for arsenic in drinking water of 50 μg/L (NRC, 1999). Because organic forms of arsenic are less toxic than inorganic forms, any increased health risk from intake of organic arsenic from food products such as fish is unlikely.

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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc Intake Assessment The highest concentrations of arsenic in food are found in marine products, but these are in the organic form, usually arsenobetaine, which is not toxic. Various sources of exposure to inorganic arsenic, as arsenates or arsenites, exist. Occupational exposure to inorganic forms of arsenic occurs primarily by inhalation. Arsenic in drinking water is predominantly the trivalent and pentavalent forms as salts (EPA, 1988). Arsenic is also being used in the treatment of leukemias (Konig et al., 1997; Look, 1998). The median intake of arsenic by men and by women was approximately 2.0 to 2.9 μg/day and 1.7 to 2.1 μg/day, respectively (Appendix Table E-2). Adams and coworkers (1994) reported lower intakes for adults (23 to 58 μg/day) from 1982 to 1991. The level of inorganic arsenic in water was about 2 μg/L (ATSDR, 1998). The drinking water for about 98 percent of the U.S. population was below 10 μg/L (Chappell et al., 1997). The U.S. Environmental Protection Agency (EPA) has a maximum contaminant level (MCL) of 50 μg/L for water supplies in the United States (EPA, 1975). However, the agency recently proposed a much lower MCL of 5 μg/ L for arsenic in drinking water and is seeking comments on MCLs ranging from 3 to 20 μg/L (EPA, 2000). The EPA expects to promulgate a new, lower MCL in the near future. The average arsenic content of mineral drinking water in European countries is 21 μg/L (Zielhuis and Wibomo, 1984). Risk Characterization Although no UL was set for arsenic, there is no justification for adding arsenic to food and there may be a risk of adverse effects with consumption of organic arsenic in food or with intake of inorganic arsenic in water supplies at the current MCL of 50 μg/L in the United States. Substantial numbers of individuals in North America, however, are exposed to arsenic levels exceeding the MCL (Chappell et al., 1997; Grantham and Jones, 1977; Kreiss et al., 1983). Inhalation exposure occurs in occupational settings such as smelters and chemical plants, where the predominant form of airborne arsenic is arsenic trioxide dust (ATSDR, 1998). RESEARCH RECOMMENDATIONS FOR ARSENIC A better understanding of species differences in biotransformation of arsenic and toxicity.

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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc The role of arsenic in methyl metabolism and genetic expression; identification of a reliable indicator of arsenic status in humans. Because relatively low serum arsenic concentrations have been associated with vascular diseases and central nervous system injury, more systematic investigation of the possible role of arsenic in these disorders. BORON BACKGROUND INFORMATION Function Of the five minerals discussed in this chapter, boron has received the most extensive study of its possible nutritional importance for animals and humans. Still, the collective body of evidence has yet to establish a clear biological function for boron in humans. There is evidence that boron is required by vascular plants and some microorganisms. The only known boron-containing compounds in nature are organoboron complexes from plants, some of which may have antibiotic properties (Hunt, 1998; Nielsen, 1997). Principles of bioinorganic chemistry predict that boron, which is primarily in the form of boric acid, B(OH)3, at physiological pH, binds to cis-diols, perhaps with some specifically, and forms condensation products that are moderately labile in aqueous solutions (da Silva and Williams, 1991). The latter could theoretically provide stability to diol-rich molecules such as polysaccharides or steroids. Boron can act as an inhibitor of activity for a wide variety of enzymes in vitro (Hunt, 1998). However, no boron-containing enzyme has been identified. In higher animals, boron has not been shown to have a sufficiently definitive pattern of effects to establish a function. Embryonic defects related to boron depletion have been reported for zebra fish (Rowe and Eckhert, 1999), frogs (Fort et al., 1998, 1999), and trout (Eckhert, 1998), and they suggest a function for boron in reproduction and development. However, boron-related developmental defects have not been found consistently in rodent models (Lanoue et al., 1998, 1999). Physiological effects, including changes in blood glucose and triglyceride concentrations and abnormal calcitriol (1,25,OH2D3) metabolism or function have been reported in boron-deficient chicks that have a concomitant vitamin D deficiency (Hunt, 1996). Higher insulin secretion from the pancreas of boron-deprived chicks has also been reported (Bakken, 1995). How-

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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc ever, many of these studies found effects of boron only in the presence of secondary nutritional stressors, such as vitamin D deficiency. Metabolism of vitamin D and estrogen, as measured by plasma metabolites, macromineral (especially calcium) metabolism, and immune function have been proposed as related to a function for boron in humans (Nielsen, 1998; Nielsen and Penland, 1999; Samman et al., 1998). Findings supporting these possible functions also have come from studies where another nutritional stressor was present or effects have not been consistently demonstrated. In one laboratory, several dietary boron deprivation studies in both rats and humans have consistently found an effect of boron intake on brain electrophysiology and, in humans, on performance of tasks measuring eye-hand coordination, attention, and short-term memory (Penland, 1998). However, these possible functions of boron have yet to be studied and confirmed by other laboratories. Physiology of Absorption, Metabolism, and Excretion Studies with animals and humans indicate that about 90 percent of boron is absorbed in the normal intake range (Hunt and Stoecker, 1996; Sutherland et al., 1998). Most dietary boron is hydrolyzed within the gut to yield B(OH)3 which, as a neutral compound, is easily absorbed. The mechanism of boron absorption has not been studied, but a passive, nonmediated diffusion process involving B(OH)3 is likely (da Silva and Williams, 1991). Some evidence for boron homeostasis exists. In a 42-day study in men with a boron intake average of 3.73 mg/day, urinary loss was 3.20 mg/day (86 percent of intake), whereas urinary boron loss was less when the boron intake was less than 3.20 mg/day and loss was more when the intake was more than that amount (Sutherland et al., 1998). In a study with postmenopausal women, 89 percent of boron from a low-boron diet (0.36 mg/day from food and 2.87 μg/day from a supplement) was excreted in the urine and 3 percent in the feces (Hunt and Stoecker, 1996). Other metabolic studies do not support homeostatic control. For example, urinary excretion was 86 and 84 percent when boron intake was 2.2 and 10 mg/day, respectively (Samman et al., 1998). Boron chemistry suggests it is transported in the blood as B(OH)3. Specifically, because boron forms labile complexes in aqueous solution, transport is probably as free boric acid rather than a complex (da Silva and Williams, 1991). The blood boron concentration is dependent on dietary intake as primarily shown by animal studies (Price et al., 1998; Samman et al., 1998). This reflects the relatively

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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc small boron pool that blood represents as well as efficient absorption and excretion. The excretory form of boron has not been studied. As a neutral molecule, blood borate should have high fractional renal clearance and easily enter the glomerular filtrate. FINDINGS BY LIFE STAGE AND GENDER GROUP There is evidence supporting a biological role of boron in some microroganisms. In higher animals, boron has been shown to have a role in reproduction and development. The collective body of evidence, however, has yet to establish a clear biological function for boron in humans. Therefore, neither an Estimated Average Requirement, Recommended Dietary Allowance, nor Adequate Intake was established for boron. INTAKE OF BORON Food Sources Hunt and coworkers (1991) reported that the highest concentrations of boron were found in fruit-based beverages and products, tubers, and legumes. Depending on the geographic location, water could contribute a major portion of the dietary boron. Negligible or minimal amounts (less than 0.100 μg/g) were found in animal products, certain grain products, condiments, and confections. Similar findings were reported by Anderson and coworkers (1994). Meacham and Hunt (1998) reported that the ten foods with the highest concentration of boron were avocado, peanut butter, peanuts, prune and grape juice, chocolate powder, wine, pecans, and granola raisin and raisin bran cereals. Rainey and coworkers (1999), however, examined both the content and total food consumption (amount and frequency), reporting that the five major contributors of boron were coffee, milk, apples, dried beans, and potatoes, which collectively accounted for 27 percent of the dietary boron consumption. Although coffee and milk are low in boron, they were the top contributors due to the volumes consumed. Dietary Intake U.S. boron consumption was assessed by use of the Boron Nutrient Data Base linked to 2-day food records from respondents to the Third National Health and Nutrition Examination Survey (NHANES III) (Appendix Table C-12) and the Continuing Survey

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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc RESEARCH RECOMMENDATIONS FOR VANADIUM Determination of the biochemical role of vanadium in both higher animals and humans and a reliable status indicator of vanadium for further work in humans. The efficacy and safety of the use of vanadium as a nutritional supplement. REFERENCES ABC (American Biogenics Corporation). 1988. Ninety Day Gavage Study in Albino Rats Using Nickel. Study 410-2520. Final report submitted to the U.S. Environmental Protection Agency, Office of Solid Waste, by Research Triangle Institute and American Biogenics Corporation under contract 68-01-7075. Adams MA, Bolger PM, Gunderson EL. 1994. Dietary intake and hazards of arsenic. In: Chappell WR, Abernathy CO, Cothern CR, eds. Arsenic: Exposure and Health. Northwood, UK: Science and Technology Letters. Pp. 41–49. Allen HE, Halley-Henderson MA, Hass CN. 1989. Chemical composition of bottled mineral water. Arch Environ Health 44:102–116. Ambrose AM, Larson PS, Borzelleca JF, Hennigar GR. 1976. Long term toxicologic assessment of nickel in rats and dogs. J Food Sci Technol 13:181–187. Anderson DL, Cunningham WC, Lindstrom TR. 1994. Concentrations and intakes of H, B, S, K, Na, Cl, and NaCl in foods. J Food Comp Anal 7:59–82. Anderson RR. 1992. Comparison of trace elements in milk of four species. J Dairy Sci 75:3050–3055. Andrews RK, Blakeley RL, Zerner B. 1988. Nickel in proteins and enzymes. In: Sigel H, Sigel A, eds. Metal Ions in Biological Systems, Vol. 23. New York: Marcel Dekker. Pp. 165–284. Anke M. 1986. Arsenic. In: Mertz W, ed. Trace Elements in Human and Animal Nutrition, Vol. 2, 5th ed. Orlando, FL: Academic Press. Pp. 347–372. Anke M, Groppel B, Gruhn K, Langer M, Arnhold W. 1989. The essentiality of vanadium for animals. In: Anke M, Bauman W, Braunlich H, eds. 6th International Trace Element Symposium, Vol. 1. Jena, Germany: Friedrich-Schiller-Universitat. Pp. 17–27. Aposhian HV. 1997. Enzymatic methylation of arsenic species and other new approaches to arsenic toxicity. Annu Rev Pharmacol Toxicol 37:397–419. Armstrong CW, Stroube RB, Rubio T, Siudyla EA, Miller GB Jr. 1984. Outbreak of fatal arsenic poisoning caused by contaminated drinking water. Arch Environ Health 39:276–279. ATSDR (Agency for Toxic Substances and Disease Registry). 1992. Toxicological Profile for Boron. Atlanta: U.S. Public Health Service, ATSDR. ATSDR. 1998. Toxicological Profile for Arsenic. Atlanta: U.S. Public Health Service, ATSDR. Bakken N. 1995. Dietary Boron Modifies the Effects of Vitamin D Nutriture on Energy Metabolism and Bone Morphology in the Chick . Masters of Science thesis, University of North Dakota, Grand Forks. Barceloux DG. 1999. Vanadium. J Toxicol Clin Toxicol 37:265–278. Baxley MN, Hood RD, Vedel GC, Harrison WP, Szczech GM. 1981. Prenatal toxicity of orally administered sodium arsenite in mice. Bull Environ Contam Toxicol 26:749–756.

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