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TABLE 1 Dietary Reference Intakes for Manganese by Life Stage Group DRI values (mg/day) AIa ULb males females Life stage group NDc 0 through 6 mo 0.003 0.003 7 through 12 mo 0.6 0.6 ND 1 through 3 y 1.2 1.2 2 4 through 8 y 1.5 1.5 3 9 through 13 y 1.9 1.6 6 14 through 18 y 2.2 1.6 9 19 through 30 y 2.3 1.8 11 31 through 50 y 2.3 1.8 11 51 through 70 y 2.3 1.8 11 > 70 y 2.3 1.8 11 Pregnancy £ 18 y 2.0 9 19 through 50 y 2.0 11 Lactation £ 18 y 2.6 9 19 through 50 y 2.6 11 a AI = Adequate Intake. b UL = Tolerable Upper Intake Level. Unless otherwise specified, the UL represents total intake from food, water, and supplements. c ND = Not determinable. This value is not determinable due to the lack of data of adverse effects in this age group and concern regarding the lack of ability to handle excess amounts. Source of intake should only be from food to prevent high levels of intake.

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PART III: MANGANESE 351 MANGANESE M anganese is involved in the formation of bone and in specific reac- tions related to amino acid, cholesterol, and carbohydrate metabo- lism. Manganese metalloenzymes include arginase, glutamine syn- thetase, phosphoenolpyruvate decarboxylase, and manganese superoxide dismutase. Since data were insufficient to set an Estimated Average Requirement (EAR) and thus calculate a Recommended Dietary Allowance (RDA) for manganese, an Adequate Intake (AI) was instead developed. The AIs for manganese are based on intakes in healthy individuals, using the median manganese intakes reported from the Food and Drug Administration’s (FDA’s) Total Diet Study (1991–1997). The Tolerable Upper Intake Level (UL) is based on elevated blood manganese concentrations and neurotoxicity as the critical adverse effects. DRI values are listed by life stage group in Table 1. The highest contributors of manganese to the diet are grains, beverages (tea), and vegetables. Although a manganese deficiency may contribute to one or more clinical symptoms, a clinical deficiency has not been clearly associated with poor dietary intakes of healthy individuals. Neurotoxicity of orally in- gested manganese at relatively low doses is controversial, but evidence suggests that elevated blood manganese levels and neurotoxicity are possible. MANGANESE AND THE BODY Function Manganese is an essential nutrient involved in the formation of bone and in specific reactions related to amino acid, cholesterol, and carbohydrate metabo- lism. Manganese metalloenzymes include arginase, glutamine synthetase, phos- phoenolpyruvate decarboxylase, and manganese superoxide dismutase. Absorption, Metabolism, Storage, and Excretion Only a small percentage of dietary manganese is absorbed by the body. Some studies indicate that manganese is absorbed via active transport mechanisms, while other studies suggest that passive diffusion via a nonsaturable process occurs. Much of absorbed manganese is excreted very rapidly into the gut via the bile, and only a small amount is retained. Manganese is taken up from the blood by the liver and transported to ex-

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DRIs: THE ESSENTIAL GUIDE TO NUTRIENT REQUIREMENTS 352 trahepatic tissues by transferrin and possibly a2-macroglobulin and albumin. Excretion primarily occurs in the feces. Urinary excretion of manganese is low and has not been found to be sensitive to dietary intake. Therefore, the poten- tial risk for manganese toxicity is highest when bile excretion is low, such as in the neonate or in liver disease. DETERMINING DRIS Determining Requirements Since data were insufficient to set an EAR and thus calculate an RDA for manga- nese, an AI was instead developed. The AIs for manganese are based on intakes in healthy individuals, using the median manganese intake from the FDA’s Total Diet Study (1991–1997). Special Considerations Gender: Men have been shown to absorb significantly less manganese com- pared to women. This may be related to iron status, as men generally have higher serum ferritin concentrations than do women (see “Dietary Interactions”). Criteria for Determining Manganese Requirements, by Life Stage Group Life stage group Criterion 0 through 6 mo Average manganese intake from human milk 7 through 12 mo Extrapolation from adult AI 1 through > 70 y Median manganese intake from the Total Diet Study Pregnancy £ 18 y Extrapolation from adolescent female AI based on body weight 19 through 50 y Extrapolation from adult female AI based on body weight Lactation < 18 y through 50 y Median manganese intake from the Total Diet Study The UL The Tolerable Upper Intake Level (UL) is the highest level of daily nutrient intake that is likely to pose no risk of adverse effects for almost all healthy people. Members of the general population should not routinely exceed the UL. This value is based on elevated blood manganese and neurotoxicity as the critical adverse effects and represents intake from food, water, and supplements.

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PART III: MANGANESE 353 Based on the Total Diet Study, the highest dietary manganese intake at the 95th percentile was 6.3 mg/day, which was the level consumed by men aged 31 to 50 years. Data from the Third National Health and Nutrition Examination Survey (NHANES III, 1988–1994) indicated that the highest supplemental in- take of manganese at the 95th percentile was approximately 5 mg/day, which was consumed by adults, including pregnant women. The risk of an adverse effect resulting from excess intake of manganese from food and supplements appears to be low at these intakes. DIETARY SOURCES Foods Based on the Total Diet Study, grain products contributed 37 percent of dietary manganese, while beverages (tea) and vegetables contributed 20 and 18 per- cent, respectively, to the adult male diet. Dietary Supplements According to U.S. data from the 1986 National Health Interview Survey (NHIS), 12 percent of adults consumed supplements that contained manganese. Based on data from NHANES III, the median supplemental intake of manganese was 2.4 mg/day for those adults who took supplements, an amount similar to the average dietary manganese intake. Bioavailability Several factors may affect the bioavailability of manganese (see “Dietary Interac- tions”). Dietary Interactions There is evidence that manganese may interact with certain other nutrients and dietary substances (see Table 2). INADEQUATE INTAKE AND DEFICIENCY Although a manganese deficiency may contribute to one or more clinical symp- toms, a clinical deficiency has not been clearly associated with poor dietary intakes of healthy individuals. In limited studies on induced manganese deple- tion in humans, subjects developed scaly dermatitis and hypocholesterolemia. Studies in various animal species observed signs and symptoms of deficiency, including impaired growth and skeletal development, impaired reproductive

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DRIs: THE ESSENTIAL GUIDE TO NUTRIENT REQUIREMENTS 354 TABLE 2 Potential Interactions with Other Dietary Substances Substance Potential Interaction Notes SUBSTANCES THAT AFFECT MANGANESE Calcium Calcium may reduce In one study, adding calcium to human milk reduced manganese absorption. the absorption of manganese from 4.9 percent to 3.0 percent. Iron Iron status may affect Low ferritin concentrations are associated with manganese absorption: low increased manganese absorption, thereby having a serum ferritin concentration gender effect on manganese bioavailability (because may increase manganese women tend to have lower ferritin concentrations absorption. compared with men). Phytate Phytate may decrease In a study of infant formula, the soy-based formula manganese absorption. without phytate produced manganese absorption of 1.6 percent, whereas a formula with phytate produced an absorption of 0.7 percent. function, impaired glucose tolerance, and alterations in carbohydrate and lipid metabolism. EXCESS INTAKE Manganese toxicity, which causes central nervous system effects similar to those of Parkinson’s disease, is a well-recognized occupational hazard for people who inhale manganese dust. The totality of evidence in animals and humans sup- ports a causal association between elevated blood manganese concentrations and neurotoxicity. Special Considerations Individuals susceptible to adverse effects: People with chronic liver disease may be distinctly susceptible to the adverse effects of excess manganese intake, probably because elimination of manganese in bile is impaired. Also, manga- nese in drinking water and supplements may be more bioavailable than food manganese. Therefore, individuals who take manganese supplements, particu- larly those who already consume large amounts of manganese from diets high in plant products, should take extra caution. Plasma manganese concentrations can become elevated in infants with choleostatic liver disease who are given supplemental manganese in total parenteral nutrition (TPN).

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PART III: MANGANESE 355 KEY POINTS FOR MANGANESE Manganese is an essential nutrient involved in the formation of 3 bone and in specific reactions related to amino acid, cholesterol, and carbohydrate metabolism. Since data were insufficient to set an EAR and thus calculate 3 an RDA for manganese, an AI was instead developed. The AIs for manganese are based on the intakes of healthy 3 individuals, using median manganese intakes reported from the FDA’s Total Diet Study. The UL is based on elevated blood manganese concentrations and neurotoxicity as the critical adverse effects. The risk of an adverse effect resulting from excess intake of 3 manganese from food and supplements appears to be low. The highest contributors of manganese to the diet are grain 3 products, beverages (tea), and vegetables. Although a manganese deficiency may contribute to one or 3 more clinical symptoms, a clinical deficiency has not been clearly associated with poor dietary intakes of healthy individuals. In limited studies on induced manganese depletion in humans, subjects developed scaly dermatitis and hypocholesterolemia. Manganese toxicity, which causes central nervous system 3 effects similar to those of Parkinson’s disease, is a well- recognized occupational hazard for people who inhale manganese dust. Neurotoxicity of orally ingested manganese at relatively low doses is more controversial, but evidence suggests that elevated blood manganese levels and neurotoxicity are possible. Plasma manganese concentrations can become elevated in 3 infants with choleostatic liver disease who are given supplemental manganese in total parenteral nutrition.