9
Manganese (Inorganic Salts)

Raghupathy Ramanathan, Ph.D. NASA-Johnson Space Center Toxicology Group Houston, Texas

OCCURRENCE AND USE

Manganese (Mn) is a component of several minerals in the earth’s crust (rock, soil) and is an abundant element. It is found in most food and in drinking water and is distributed to the environment through dust and industrial emissions during the production of iron alloys and during coal burning. Manganese as methylcyclopentadienyl manganese tricarbonyl (MMT) was used as an additive to gasoline to improve octane rating, to replace tetraethyl lead as an antiknock agent. It has been used in Canada since 1977 (Crump 2000), but it was banned from use as a gasoline additive in the United States because of concerns about neurologic effects from the inhalation of particulate emissions of combustion products of MMT, namely manganese phosphate and manganese sulfate (MnSO4) (see Davis 1999). Manganese exists in several different oxidation states (see Table 9-1). The most common ones are the +2 and +4; the former is the one most commonly found in biologic systems including humans. Manganese chloride (MnCl2), MnSO4, and manganese acetate are the most soluble forms. Manganese oxide, although frequently encountered in the work place, is very insoluble.

Manganese as a metal is primarily used in steel manufacturing. It is also used as a micronutrient in fertilizers and in animal feeds. The sulfate salts are used extensively as nutritional supplements for humans and animals and in dyes and varnishes.

Manganese is an essential element needed for the normal physiologic function of all animal species, including humans. Deficiencies of manganese produce abnormalities in brain function, skeleton and cartilage formation, reproduction, and glucose tolerance and are associated with osteoporosis (see Freeland-Graves 1994). A variety of enzymes



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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 9 Manganese (Inorganic Salts) Raghupathy Ramanathan, Ph.D. NASA-Johnson Space Center Toxicology Group Houston, Texas OCCURRENCE AND USE Manganese (Mn) is a component of several minerals in the earth’s crust (rock, soil) and is an abundant element. It is found in most food and in drinking water and is distributed to the environment through dust and industrial emissions during the production of iron alloys and during coal burning. Manganese as methylcyclopentadienyl manganese tricarbonyl (MMT) was used as an additive to gasoline to improve octane rating, to replace tetraethyl lead as an antiknock agent. It has been used in Canada since 1977 (Crump 2000), but it was banned from use as a gasoline additive in the United States because of concerns about neurologic effects from the inhalation of particulate emissions of combustion products of MMT, namely manganese phosphate and manganese sulfate (MnSO4) (see Davis 1999). Manganese exists in several different oxidation states (see Table 9-1). The most common ones are the +2 and +4; the former is the one most commonly found in biologic systems including humans. Manganese chloride (MnCl2), MnSO4, and manganese acetate are the most soluble forms. Manganese oxide, although frequently encountered in the work place, is very insoluble. Manganese as a metal is primarily used in steel manufacturing. It is also used as a micronutrient in fertilizers and in animal feeds. The sulfate salts are used extensively as nutritional supplements for humans and animals and in dyes and varnishes. Manganese is an essential element needed for the normal physiologic function of all animal species, including humans. Deficiencies of manganese produce abnormalities in brain function, skeleton and cartilage formation, reproduction, and glucose tolerance and are associated with osteoporosis (see Freeland-Graves 1994). A variety of enzymes

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 TABLE 9-1 Physical and Chemical Properties of Some Manganese Compoundsa Chemical Manganese Manganese Chloride Manganese Sulfate Manganese Acetate Manganese Dioxide Formula Mn MnCl2 MnSO4 Mn (CH3COO)2 MnO2 Molecular weight 54.94 125.84 151 173 86.94 Percent manganese 100% 43.66% 36.38% 31.75% 63.19% Solubility in water Decomposes slowly 723 g/L at 25°C 529 g/L at 5°C 970 g/L at 25°C Insoluble General form — MnCl2·4H2O MnSO4·H2O MnAc·4H2O   Molecular weight   197.91 169 245   Percent manganese   27.76% 32.50% 22.40%   aOther common manganese-containing inorganic compounds, such as potassium permanganate (KMnO4), and other compounds, such as the tetraoxides, carbonate, and nitrates of manganese, are not included here. Sources: Data from Aldrich Company 2006; Bingham et al. 2001; Merck 1989. have been reported to interact with Mn+2 or depend on Mn+2 for either catalysis or regulatory properties. Thus, it plays an important role in energy metabolism, bone mineralization, protein and energy metabolism, and the metabolic regulation of several enzymes. Manganese has been reported to activate transferases, decarboxylases, and hydrolases (Wedler 1994). It is also an integral part of mitochondrial superoxide dismutase (thereby playing a role in the protection of free superoxide radical species), carboxylase, and liver arginase (NRC 1989). Food is the major source of manganese, and different foods vary widely in manganese concentration. Nuts and grains contain a high concentration (18-46 parts per million [ppm]) (IOM 2001). For example, Greger (1999) reported that the average intake from Western and vegetarian diets was in the range of 0.7-10.9 mg/d. Milk products contain about 4 ppm. Other investigators have reported various values. The estimated dietary intakes of several nutritional elements for specific age groups have been reported in the U.S. Food and Drug Administration’s (FDA’s) Total Diet Study and updated at various times (1974-1982, 1982-1984, 1982-1986, 1982-1989, 1982-1991, and 1991-1997). Ac-

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 cording to the dietary intake data the from FDA’s Total Diet Study, 1991-1997 (see IOM 2001, Appendix E), the mean daily intakes of manganese for men of age groups 19-30, 31-50, 51-70, and 71+ have been reported to be 3.07, 3.27, 3.07, and 2.82 mg/d, respectively. The corresponding intakes for women of the same age groups are 2.34, 2.43, 2.42, and 2.43 mg/d, respectively. As for the usual amounts of manganese taken as supplements by men and women, according to the National Health and Nutrition Examination Survey (NHANES III, 1988-1994), they are 2.49 mg/d (median or 50th percentile) for men and 2.37 mg/d (median) for women, and the 95th percentile is 5.07 mg/d for both men and women (see IOM 2001, Appendix C-20). Dissolved manganese was detected in surface water in 51% of 1,577 samples, with a mean of 59 micrograms per liter (µg/L) (range of 0.3-3,230 µg/L). A later survey from 286 locations indicated the mean concentration was 24 µg/L and the range was from 11 µg/L (25th percentile) to more than 51 µg/L (75th percentile) (Smith et al. 1987). A 1962 survey of a public drinking water supply reported a concentration of 100 µg/L of manganese (Durfor and Becker 1964). Other reports estimated the values to be very low, between 4 and 32 µg/L (NRC 1980). The U.S. Environmental Protection Agency’s (EPA’s) secondary maximum contaminant limit (SMCL) of 50 µg/mL was exceeded a few times in both the recycled water and in the humidity condensate samples collected from space missions. At least once, a maximum of 150 µg/L was found in the reprocessed water. When a particular component is frequently found in water samples, even if it is at concentrations under the National Aeronautics and Space Administration (NASA) interim levels, a spacecraft water exposure guideline (SWEG) is determined. The main reasons for this are a concern that the component could break through the water processing system and the fact that no real-time monitoring instruments are on board the International Space Station (ISS). PHARMACOKINETICS AND METABOLISM General There are no systematic human studies on the pharmacokinetics of manganese after its ingestion. There are several reports of elimination rates of manganese in human subjects occupationally exposed to manganese via inhalation. In all these studies, the elimination was measured based on the injection of tracer doses of radioactive manganese and elimination based on the injection of tracer doses of radioactive manga-

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 nese and elimination followed via whole-body disappearance of radioactivity over time. One must consider that the metabolic handling of manganese absorbed from the diet is different from that introduced through intravenous (iv) injection (Davidsson et al.1989a) in spite of the fact that in plasma 54Mn is carried by transferrin, regardless of the route, iv or oral, of administration (Davidsson et al.1989c). In a study of five men and six women administered oral loads of elemental manganese at 40 mg per kilogram (kg) of body weight after fasting, the mean T-max (time to reach the peak plasma level) ranged from 1 to 3 hours (h). Then the concentrations gradually decreased to initial levels over the next 4 h. The time to reach the C-max (maximum blood concentration) varied with subjects (Freeland-Graves and Lin 1991). These authors did not calculate any other pharmacokinetic parameters. In a recent study, the toxicokinetics of manganese were investigated in male and female rats following a single iv or oral dose of MnCl2 (6 mg/kg) (Zheng et al. 2000). For the oral dosing, rats were fasted for 12 h before dosing. Upon iv administration of MnCl2, manganese rapidly disappeared from blood, with a terminal elimination half-life (t½) of 1.83 h and plasma clearance (CL) of 0.43 L/h/kg. After oral administration of MnCl2, manganese was rapidly absorbed from the gastrointestinal (GI) tract and entered the systemic circulation (T-max = 0.25 h; C-max = 0.3 µg/mL). The absolute oral bioavailability was about 13% (calculated from the area under the curves from iv and oral dosing). The elimination half-life for the iv dose was 1.83 h compared to 4.6 h for the oral bolus. Plasma concentrations returned to predose levels 12 h after dosing. Absorption Orally ingested manganese is absorbed from the GI tract, but not very efficiently, and the review of literature indicates that only about 3-5% is absorbed in humans and animals. Under normal conditions, the absorption of Mn+2 is low because of poor solubility of the cationic Mn+2 such as in MnCl2 and MnSO4, in the alkaline pH of the intestine. Mn+2 absorption in the GI tract is controlled by homeostatic mechanisms; the absorption rate depends on the amount ingested and the plasma levels of Mn+2. The manganese ion is transported across gut walls by both active transport (based on in vitro studies using the everted intestinal sacs) and by diffusion (Cikrt and Vostal 1969, as cited in WHO 1981), with the diffusion process taking place in iron-overloaded states. However, Garcia-Aranda et al. (1983) using an in vivo perfusion system and perfusing

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 segments of either jejunum or ileum with isotonic solutions containing MnSO4 at 0.0125-0.1 millimoles (mM) concluded that absorption of manganese in rat intestines takes place through a high-affinity, low-capacity, active transport mechanism and suggested that the diffusion-mediated transport plays only a limited role. Manganese absorption (fractional absorption) from diet has been found to vary according to the amount of manganese in the diet. For example, using a rat model and using 54Mn retention method, Davis et al. (1992a, b) found that the absorption of manganese from a manganese-deficient diet was at least two-fold higher than from a manganese-adequate diet or a diet containing higher concentrations of manganese measured after 7 weeks (wk) of feeding. Lee and Johnson (1988) reported that in rats fed diets containing manganese at between 1.3 and 82.4 mg/kg for 7 or 14 d and administered a tracer dose of 54Mn by gavage, increasing dietary manganese reduced manganese absorption and enhanced 54Mn excretion. Absorption of 54Mn by fasted, gavaged rats was four times higher than in unfasted gavaged rats (Lee and Johnson 1988). Mena et al. (1969) found that only about 3% of the administered dose of MnCl2 was absorbed by human subjects, and the difference between the lowest and highest value among the 11 normal subjects was fivefold, as measured by the retention of 54Mn and whole-body counting daily for 2 wk. Similar levels of absorption from oral ingestion have been reported by Davidsson et al. (1988, 1989a). It has to be noted that the estimation of absorption using nutrition-balance studies is confounded by the fact that the GI tract is not only the site of absorption but also the principal site of elimination and where the exsorption of endogenous manganese takes place. Estimated absorption measured using retention of 54Mn in 14 men for 10 d was 5.9% ± 4.8%; however, the range was 0.8-16%. The interindividual variation was large (Davidson et al. 1989b). Using a rat model, Davis et al. (1993) reported that young, growing rats fed manganese at 45 µg/g in their diet absorbed 8.2% of their manganese intake and then lost 37% of this absorbed manganese through gut endogenous losses. The literature indicates the amount of manganese absorbed depends not only on the total amount of it present in food but also on several dietary ingredients that influence the absorption of manganese (Bales et al. 1987; Lee and Johnson 1989; Davidsson et al. 1991). For example, phytate, tannins, oxalates, and fiber inhibit manganese uptake (fractional absorption) from the GI tract. Phytate (myo-inositol hexaphosphate, IP6) is the major storage form of phosphorus in plants, and cereal foods contain large amounts of IP6. IP6 possesses a high potential for chelating

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 minerals, such as iron (as Fe+2), zinc (as Zn+2), magnesium (as Mg+2), calcium (as Ca+2), and Mn+2, and, thus, IP6 has a negative influence on the bioavailability of elements from food. Davidsson et al. (1991) studied in humans the effect of adding phytate, phosphate, and ascorbic acid to infant formula and studied manganese absorption using radionuclide techniques. They found no significant differences in manganese absorption, although the addition of calcium to human milk decreased manganese absorption. This seems to contradict the report by Bales et al. (1987) who observed a decrease, apparently caused by the fiber and phytate content of food. In another study by Schwartz et al. (1986) in which adult human males ingested a high-fiber diet containing manganese at 12-17.7 mg/d via wheat bread and bran muffins, there was no net retention, or a negative balance or only a mild positive balance of manganese was observed. Johnson et al. (1991) found that in men and women, absorption of manganese from lettuce was higher than spinach and less so from sunflower seeds compared to that from wheat. Davidsson et al. (1991) reported humans absorbed a higher percentage of manganese from human milk than from cow’s milk or soy formula. Johnson et al. (1991) stated that in humans, manganese absorption tended to be greater from MnCl2 in demineralized water (which ranged from 7.74% to 10.24%) than from foods (vegetables, wheat, and nuts). However, the biologic half-life of manganese from either source is the same. EPA has recommended using an additional factor of at least 3 if an assessment made from the ingestion of manganese from food is extrapolated to drinking water (EPA 1996). One might think, based on the characteristics of other divalent cationic metals, that manganese absorption from water would be much greater than from food. However, no definitive experiments have documented this. Davidsson et al. (1988, 1989a) reported that in humans, the absorption of manganese from these two sources is comparable. If a difference exists, it is masked by vast interindividual variations in (human) absorption of manganese (determined using 54Mn retention with intrinsic and extrinsic labeling of the meal). Mena (1974) reported an absorption of 70% from young rats compared to only 1-2% in adult rats. Similarly, Lonnerdal et al. (1987) reported that in neonatal rats, manganese is absorbed at a very high level (as high as 80%) until 14 d, where it drops to 30% by day 18 and to 3-4% when the animal reaches maturity. The proposed reason that this phenomenon is because of the lack of development of the excretory pathway in the neonates (Miller et al. 1975) has been debated by Ballatori et al. (1987), who in their studies on dose dependency of biliary excretion of intraperitonealy (ip) injected manganese in adult and 14-d-old rats, concluded

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 that at doses higher than tracer doses used in previous studies neonatal rats can excrete as much as adult rats. Manganese Absorption and the Influence of Other Minerals Several minerals have been shown to interact with the absorption of manganese, including iron, calcium, zinc, magnesium, cobalt, and iodine. Interaction of iron with manganese has been the subject of numerous human and animal studies (see Finley and Davis 1999), which have shown metabolic interactions between these metals. Available evidence indicates body stores of iron and manganese inhibit each other’s absorption (Kies 1994), perhaps because of a competition via a common transport protein such as the divalent metal transporter. Diet-induced iron deficiency can increase the GI absorption of manganese, and supplementing the diet with iron suppresses this enhanced manganese absorption (Davis et al. 1992b; Chua and Morgan 1996). Chua and Morgan also observed that the supplementation of manganese via drinking water (manganese acetate at 2 g/L) increased 59Fe uptake from plasma in the brain, liver, and kidneys, which was not seen when iron was loaded in the diet (Chua and Morgan 1996). But a critical observation is that both iron depletion and loading in the diet increased the brain concentrations of manganese. In humans, supplementation of iron decreases not only the absorption of manganese from the diet (Lonnerdal et al. 1987) but also its retention in the body (Kies 1987). Pertinent to the objective of this document, excess manganese will inhibit the intestinal absorption of iron and could lead to iron deficiency and to anemia. However, Davis and Greger (1992) did not find any change in the iron status of 47 women supplemented with manganese at 15 mg/d for 124 d. Recent work by Zheng et al. (1999) on iron homeostasis in rats after chronic exposure to MnCl2 indicates that exposure to manganese alters iron homeostasis, possibly by expediting the influx of iron from the systemic circulation to the cerebral compartment of the brain. It is interesting to note that iron overload in the brain has been thought to be responsible for Parkinson’s disease (PD), causing iron-mediated oxidative stress in the brain and consequent degeneration of neurons. Finley (1999) and Finley et al. (1994) investigated possible gender differences in the influence of iron status (using serum ferritin concentration as the marker), especially on manganese absorption and half-life of manganese (using 54Mn) in men and women. They found that higher ferritin concentrations reduced manganese absorption in young women. Although men absorbed much less manganese than women, manganese had a longer half-life in men (Finley

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 et al. 1994). These findings may be related to the differences in serum ferritin between men and women. In an another study (Finley 1999), it was reported that dietary-manganese concentrations did not affect manganese status, but the absorption of manganese from a low-manganese diet by women with high ferritin concentrations was very low compared to the absorption by women with low ferritin concentrations. In this study, 11-15 women received a diet containing manganese at 0.7 mg/d or 9.5 mg/d for 60 d. Retention of 54Mn, measured after 60 d, indicated that a greater percent of the test dose was retained by women on the low-manganese diet than by those consuming the high-manganese diet. Thus, for manganese absorption and biologic half-life, there was a significant interaction between ferritin status and dietary manganese. The results indicated that dietary manganese intake was not associated with any clinically significant changes, especially at the high dose (9.5 mg/d). It is worth noting that in a population-based study of manganese conducted in southwest Quebec, Baldwin et al. (1999) showed that blood manganese (Mn-B) was negatively correlated with age and serum iron in women, whereas serum iron was negatively correlated with age and not Mn-B in men. Erikson et al. (2002), from their studies on rats fed an iron-deficient diet and groups fed iron-deficient and manganese-supplemented diets (iron-deficient + manganese), concluded that both iron-deficient and iron-deficient + manganese diets significantly increased the concentration of manganese across the brain regions compared to control groups. Based on the concentrations of glutamate, gamma-aminobutyric acid (GABA), and taurin, the authors concluded that iron-deficiency is a significant risk for the central nervous system (CNS) because of increased manganese accumulation and also that the observed changes in the neurochemicals can be attributed to manganese accumulation (Erikson et al. 2002). Recently, Erikson et al. (2004) showed that in 21-d-old male Sprague-Dawley rats given an iron-deficient diet supplemented with manganese (100 mg/kg diet), there was not only an increased overall brain manganese concentration, but this increase was seen in the globus pallidus and substantia nigra in both the groups of rats on an iron-deficient diet and those on an iron-sufficient diet supplemented with manganese compared with controls. In the caudate putamen, the increase was seen only with the manganese-supplemented iron-deficient group (Erikson et al. 2004). An increase in manganese concentration in the globus pallidus, where increased accumulation causes manganism, and observed increased concentrations of divalent metal transporter (DMT-1) protein levels seen in globus pallidus in iron-deficient animals underscores the importance of the interaction of iron and manganese.

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 Several animal investigations suggested that a high intake of calcium can affect manganese balance and vice versa. This has prompted several studies evaluating this interaction in humans because of concerns over increased use of calcium supplements for osteoporosis, particularly among postmenopausal women. Mixed results have been reported. Variations such as the chemical form of calcium, the concentration of calcium, and/or its ratio to manganese may be a reason. An inhibitory effect of calcium on manganese absorption in humans was found in women consuming calcium at 400 and 6.3 mg/d, and manganese negative balance was found in men who took supplements of calcium at 916 mg either as lactate or as milk (McDermott and Kies 1987). Freeland-Graves and Lin (1991) observed that the addition of calcium as calcium carbonate CaCO3 or 2% milk, which provided calcium at 800 mg and manganese at 40 mg, given to adult subjects essentially blocked the plasma uptake of manganese (indicating inhibition of absorption). Similar results were obtained by Davidsson et al. (1991). However, no effect was found by Johnson et al. (1991). The differences may be accounted for by the relative amounts of manganese and calcium. In the study by Johnson et al. (1991), the human subjects were fed conventional diets containing manganese at 1 or 5.6 mg/d with calcium at 587 or 1,336 mg/d in a 2 × 2 factorial design. 54Mn was used to study the absorption of manganese. Biologic half-life was unaffected by calcium concentration. Spencer et al. (1979) found little effect on the excretion or the retention of manganese in adults when 200 or 800 or 1,500 mg/d of calcium was provided as a supplement. Transport of Manganese Absorbed from Oral Ingestion Considerable speculation exists in the literature about the oxidation state of manganese that binds to the manganese transport protein in the plasma and is speculated to be responsible for manganese toxicity. Several carrier/transfer proteins have been proposed for manganese, including serum albumin, transferrin (Scheuhammer and Cherian 1985), transmanganin (Cotzias 1962), and beta-1-globulin (Foradori et al. 1967). The finding of significantly different turnover rates of manganese in humans (as measured by the whole-body retention of 54Mn) after iv and oral administration of 54Mn seems to indicate that humans have at least two different Mn+ binding proteins. Davidsson et al. (1989c) identified transferrin as the only major plasma carrier protein when manganese is administered orally or by iv. It has been proposed that after ingestion of Mn+2 and after absorption from the gut, manganese binds to alpha-2-macro-

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 globulin in the plasma (Gibbons et al. 1976) and reaches the liver. While Mn+2 is traversing the liver, a major amount of it is secreted into the bile while a small amount is oxidized by liver ceruloplasmin to Mn+3. Transferrin has a high binding affinity for Mn+3. This enters the circulation as Mn+3-transferrin conjugate and is transported to tissues (Aisen et al. 1969; Aschner and Aschner 1991). That transferrin is the only transport mechanism of manganese from liver to the brain through the systemic circulation has been questioned by other investigators. For example, in the transferrin knock-out mice, the uptake of injected 54Mn in the brain (and other tissues) was comparable to that found in wild mice (Dickinson et al. 1996). In the last few years, a significant amount of research has been carried out to delineate the complex diffusion-mediated and transporter-mediated processes by which manganese is taken up and transported into the brain and the dependence of these mechanisms on the route of administration. In short, the results indicate that the transport of manganese into the brain takes place in three different ways, and some of these are more relevant to inhaled manganese than to exposure by other routes. One of them is the uptake and transport of manganese via primary and secondary olfactory neurons in pike and has received significant attention by researchers (see Tjalve and Henriksson 1999). Because systemically absorbed manganese enters the brain through the blood brain barrier, olfactory transport through olfactory neurons, relevant to transport of inhaled manganese, will not be relevant here. The other proposed routes are a saturable, transferrin-independent transport across the blood brain barrier, the transferrin-dependent transferring receptor, and DMT-1, which is also an iron-transporter protein in the brain. There is a considerable amount of speculation as to which of these is most important (see Aschner and Gannon 1994; Aschner et al. 1999; Malecki et al. 1999; Aschner 2000; Crossgrove and Yokel 2004) and whether the distribution of manganese among the target brain regions are different depending on the transport system. Distribution Normal human and animal tissues contain manganese. Human tissues contain manganese at 0.1-1 µg/g tissue (Tipton and Cook 1963; Sumino et al. 1975), with the highest concentrations in the liver, pancreas, and kidney. Tissue manganese concentrations are controlled by the homeostatic control mechanism through absorption and elimination; thus, the liver and intestines play important roles in maintaining manga-

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 nese status (see, for example, Bertinchamps et al. 1966; Papavasiliou et al. 1966; Abrams et al. 1976). The profile of tissue distribution of manganese seems to vary with the routes of administration and various salt forms of manganese (see Davis et al. 1993 and Roels et al. 1997). Therefore, descriptions of studies on other routes of administration will be limited. Maximal concentration depends on time, due to different rates of uptake by the tissues, and different rates of tissue elimination half-lives for manganese. For example, after a single dose, it takes several days for the brain to reach the maximum concentrations (see Newland et al. 1987). Rats given a single, oral dose of manganese as MnCl2 at 416 mg/kg had little tissue accumulation of manganese 14 d later (Holbrook et al. 1975). This pattern is thought to result from a homeostatic mechanism that leads to decreased absorption and/or increased excretion of manganese when the intake of manganese is high (Mena et al. 1967; Abrams et al. 1976; Ballatori et al. 1987). A study in which the retention of a single oral dose of radiolabeled manganese was measured in adult and neonatal rats indicated that 6 d after exposure, tissue retention of the label was much greater in pups (67%) than in adults (0.18%) (Kostial et al. 1989). A study by Lai et al. (1991) confirmed that chronic exposure to MnCl2 (1 and 10 mg/mL) in drinking water increased brain manganese concentrations; rats exposed to manganese from conception to 120 d had much higher concentrations than controls. Lai et al. (1992) determined several neurochemical parameters in brain regions of rats chronically treated with MnCl2·4H2O at 20 mg/mL drinking water throughout development until adulthood. The highest increases of manganese accumulation in manganese-treated rats were found in the hypothalamus, (increase of 530%) and striatum (an increase of 479%), and the increase in other regions were between 152% and 250%. Chronic MnCl2 exposure in drinking water (20 mg/mL) throughout development until adulthood was found to alter brain regional manganese concentrations in neonatal rats. However, the regional manganese differences were less pronounced in weanling and adult rats (Chan et al. 1992). These results indicate that manganese accumulates in the brain particularly during neonatal exposure. Manganese content as a function of the salt form of various tissues was reported in a dietary study (Komura and Sakamoto 1991). Elevated manganese concentrations were found in the organs of male mice fed MnCl2, manganese acetate, manganese carbonate (MnCO3), or manganese dioxide (MnO2) at about 200 mg/kg/day for 100 d. Concentrations of manganese in the tissues were generally higher from MnCO3 and

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 Bonilla, E. 1978. Increased GABA content in caudate nucleus of rats after chronic manganese chloride administration. J. Neurochem. 31:551-552. Bonilla, E. 1980. L-tyrosine hydroxylase activity in the rat brain after chronic oral administration of manganese chloride. Neurobehav. Toxicol. 2:37-41. Bonilla, E. 1984. Chronic manganese intake induces changes in the motor activity of rats. Exp. Neurol. 84:696-700. Bonilla, E., and M. Diez-Ewald. 1974. Effect of L-DOPA on brain concentration of dopamine and homovanillic acid in rats after chronic manganese chloride administration. J. Neurochem. 22:297-299. Bonilla, E., and A.L. Prasad. 1984. Effects of chronic manganese intake on the levels of biogenic amines in rat brain regions. Neurobehav. Toxicol. Teratol. 6:341-344. Brenneman, K.A., R.C. Cattley, S.F. Ali, and D.C. Dorman. 1999. Manganese-induced developmental neurotoxicity in the CD rat: Is oxidative damage a mechanism of action? Neurotoxicology 20:477-487. Britton, A.A., and G.C. Cotzias. 1966. Dependence of manganese turnover on intake. Am. J. Physiol. 211:203-206. Calabresi, P., M. Ammassari-Teule, P. Gubellini, G. Sancesario, M. Morello, D. Centonze, G.A. Marfia, E. Saulle, E. Passino, B. Picconi, and G. Bernardi. 2001. A synaptic mechanism underlying the behavioral abnormalities induced by manganese intoxication. Neurobiol. Dis. 8:419-432. Calne, D.B., N.S. Chu, C.C. Huang, C.S. Lu, and W. Olanow. 1994. Manganism and idiopathic parkinsonism: similarities and differences. Neurology 44:1583-1586. Casto, B.C., J. Meyers, and J.A. DiPaslo. 1979. Enhancement of viral transformation for evaluation of the carcinogenic or mutagenic potential of inorganic metal salts. Cancer Res. 39:193-198. Chan, A.W., M.J. Minski, L. Lim, and J.C. Lai. 1992. Changes in brain regional manganese and magnesium levels during postnatal development: Modulations by chronic manganese administration. Metab. Brain Dis. 7:21-33. Chandra, S.V. 1983. Psychiatric illness due to manganese poisoning. Acta. Psychiatr. Scand. (Suppl. 303):49-54. Chandra, S.V., and G.S. Shukla. 1981. Concentrations of striatal catecholamines in rats given manganese chloride through drinking water. J. Neurochem. 36:683-687. Chua, A.C., and E.H. Morgan. 1996. Effects of iron deficiency and iron overload on manganese uptake and deposition in the brain and other organs of the rat. Biol. Trace Elem. Res. 55:39-54. Cikrt, M, and J. Vostal. 1969. Study of manganese resportion in vitro through intestinal wall. Int. Z. Klin. Pharmakol. Ther. Toxikol. 3:280-285. Cotzias, G.C. 1962. Manganese. Pp. 403-442 in Mineral Metabolism: An Advanced Treatise, Vol. 2, C.L. Comar and F. Bronner, eds. New York: Academic Press. Cotzias, G.C. 1966. Manganese, melanins and the extrapyramidal system. J. Neurosurg. 24(Suppl.):170-180.

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 Cotzias, G.C., K. Horiuchi, S. Fuenzalida, and I. Mena. 1968. Chronic manganese poisoning. Clearance of tissue manganese concentrations with persistance of the neurological picture. Neurology 18:376-382. Cotzias, G.C., S.T. Miller, P.S. Papavasiliou, and L.C. Tang. 1976. Interactions between manganese and brain dopamine. Med. Clin. North Am. 60:729-738. Crossgrove, J.S., and R.A. Yokel. 2004. Manganese distribution across the blood-brain barrier III. The divalent metal transporter-1 is not the major mechanism mediating brain manganese uptake. Neurotoxicology 25:451-460. Crump, K.S. 2000. Manganese exposures in Toronto during use of the gasoline additive, methylcyclopentadienyl manganese tricarbonyl. J. Expo. Anal. Environ. Epidemiol. 10:227-239. Dastur, D.K., D.K. Manghani, and K.V. Raghavendran. 1971. Distribution and fate of 54Mn in the monkey: Studies of different parts of the central nervous system and other organs. J. Clin. Invest. 50:9-20. Davidsson, L., A. Cederblad, E. Hagebo, B. Lonnerdal, and B. Sandstrom. 1988. Intrinsic and extrinsic labeling for studies of manganese absorption in humans. J. Nutr. 118:1517-1521. Davidsson, L., A. Cederblad, B. Lonnerdal, and B. Sandstrom. 1989a. Manganese absorption from human milk, cow's milk, and infant formulas in humans. Am. J. Dis. Child 143:823-827. Davidsson, L., A. Cederblad, B. Lonnerdal, and B. Sandstrom. 1989b. Manganese retention in man: a method for estimating manganese absorption in man. Am. J. Clin. Nutr. 49:170-179. Davidsson, L., A. Cederblad, B. Lonnerdal, and B. Sandstrom. 1991. The effect of individual dietary components on manganese absorption in humans. Am. J. Clin. Nutr. 54:1065-1070. Davidsson, L., B. Lonnerdal, B. Sandstrom, C. Kunz, and C.L. Keen. 1989c. Identification of transferrin as the major plasma carrier protein for manganese introduced orally or intravenously or after in vitro addition in the rat. J. Nutr. 119:1461-1464. Davis, C.D., and J.L. Greger. 1992. Longitudinal changes of manganese-dependent superoxide dismutase and other indexes of manganese and iron status in women. Am. J. Clin. Nutr. 55:747-752. Davis, C.D., E.A. Malecki, and J.L. Greger. 1992a. Interactions among dietary manganese, heme iron, and nonheme iron in women. Am. J. Clin. Nutr. 56:926-932. Davis, C.D., D.M. Ney, and J.L. Greger. 1990. Manganese, iron and lipid interactions in rats. J. Nutr. 120:507-513. Davis, C.D., T.L. Wolf, and J.L. Greger. 1992b. Varying levels of manganese and iron affect absorption and gut endogenous losses of manganese by rats. J. Nutr. 122:1300-1308.

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 Davis, C.D., L. Zech, and J.L. Greger. 1993. Manganese metabolism in rats: an improved methodology for assessing gut endogenous losses. Proc. Soc. Exp. Biol. Med. 202:103-108. De Meo, M., M. Laget, M. Castegnaro, and G. Dumenil. 1991. Genotoxic activity of potassium permanganate in acidic solutions. Mutat. Res. 260:295-306. Dickinson, T.K., A.G. Devenyi, and J.R. Connor. 1996. Distribution of injected iron 59 and manganese 54 in hypotransferrinemic mice. J. Lab. Clin. Med. 128:270-278. Dietz, M.C., W. Wrazidlo, A. Ihrig, M. Bader, and G. Triebig. 2000. Magnetic resonance tomography of the brain in workers with chronic occupational manganese dioxide exposure [in German]. Rofo 172:514-520. DiPaolo, J.A. 1964. The potentiation of lymphosarcomas in the mouse by manganous chloride. Fed. Proc. 23. Dorman, D.C., M.F. Struve, D. Vitarella, F.L. Byerly, J. Goetz, and R. Miller. 2000. Neurotoxicity of manganese chloride in neonatal and adult CD rats following subchronic (21-day) high-dose oral exposure. J. Appl. Toxicol. 20:179-187. Durfor, C.N., and E. Becker. 1964. Public water supplies of the 100 largest cities in the United States, 1962. U.S. Geological Survey Paper 1812. Washington, DC: U.S. Government Printing Office. Ejima, A., T. Imamura, S. Nakamura, H. Saito, K. Matsumoto, and S. Momono. 1992. Manganese intoxication during total parenteral nutrition. Lancet 339:426. Elbetieha, A., H. Bataineh, H. Darmani, and M.H. Al-Hamood. 2001. Effects of long-term exposure to manganese chloride on fertility of male and female mice. Toxicol. Lett. 119:193-201. EPA (U.S. Environmental Protection Agency). 1996. Manganese. Integrated Risk Information System on-line. U.S. Environmental Protection Agency, Washington, DC. Erikson, K.M., Z.K. Shihabi, J.L. Aschner, and M. Aschner. 2002. Manganese accumulates in iron-deficient rat brain regions in a heterogeneous fashion and is associated with neurochemical alterations. Biol. Trace Elem. Res. 87:143-156. Erikson, K.M., T. Syversen, E. Steinnes, and M. Aschner. 2004. Globus pallidus: a target brain region for divalent metal accumulation associated with dietary iron deficiency. J. Nutr. Biochem. 15:335-341. Eriksson, H., S. Lenngren, and E. Heilbronn. 1987a. Effect of long-term administration of manganese on biogenic amine levels in discrete striatal regions of rat brain. Arch. Toxicol. 59:426-431. Eriksson, H., K. Magiste, L.O. Plantin, F. Fonnum, K.G. Hedstrom, E. Theodorsson-Norheim, K. Kristensson, E. Stalberg, and E. Heilbronn. 1987b. Effects of manganese oxide on monkeys as revealed by a combined neurochemical, histological and neurophysiological evaluation. Arch. Toxicol. 61:46-52.

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 Eriksson, H., J. Tedroff, K.A. Thuomas, S.M. Aquilonius, P. Hartvig, K.J. Fasth, P. Bjurling, B. Langstrom, K.G. Hedstrom, and E. Heilbronn. 1992. Manganese induced brain lesions in Macaca fascicularis as revealed by positron emission tomography and magnetic resonance imaging. Arch. Toxicol. 66:403-407. Finley, J.W. 1999. Manganese absorption and retention by young women is associated with serum ferritin concentration. Am. J. Clin. Nutr. 70:37-43. Finley, J.W., and C.D. Davis. 1999. Manganese deficiency and toxicity: are high or low dietary amounts of manganese cause for concern? Biofactors 10:15-24. Finley, J.W., P.E. Johnson, and L.K. Johnson. 1994. Sex affects manganese absorption and retention by humans from a diet adequate in manganese. Am. J. Clin. Nutr. 60:949-955. Finley, J.W., J.G. Penland, R.E. Pettit, and C.D. Davis. 2003. Dietary manganese intake and type of lipid do not affect clinical or neuropsychological measures in healthy young women. J. Nutr. 133:2849-2856. Foradori, A.C., A. Bertinchamps, J.M. Gulibon, and G.C. Cotzias. 1967. The discrimination between magnesium and manganese by serum proteins. J. Gen. Physiol. 50:2255-2266. Freeland-Graves, J.H. 1994. Derivation of Manganese estimated safe and adequate daily dietary intakes. Pp. 237-252 in Risk Assessment of Essential Elements, W. Mertz, C.O. Abernathy, and S.O. Olin, eds. Washington, DC: ILSI Press. Freeland-Graves, J.H., and P.H. Lin. 1991. Plasma uptake of manganese as affected by oral loads of manganese, calcium, milk, phosphorus, copper, and zinc. J. Am. Coll. Nutr. 10:38-43. Galloway, S.M., M.J. Armstrong, C. Reuben, S. Colman, B. Brown, C. Cannon, A.D. Bloom, F. Nakamura, M. Ahmed, S. Duk, J. Rimpo, B.H. Margolin, M.A. Resnick, B. Anderson, and E. Zeiger. 1987. Chromosome aberrations and sister chromatid exchanges in Chinese hamster ovary cells: evaluations of 108 chemicals. Environ. Mol. Mutagen. 10(Suppl. 10):1-175. Garcia-Aranda, J.A., R.A. Wapnir, and F. Lifshitz1983. In vivo intestinal absorption of manganese in the rat. J. Nutr. 113:2601-2607. Gennart, J.P., J.P. Buchet, H. Roels, P. Ghyselen, E. Ceulemans, and R. Lauwerys. 1992. Fertility of male workers exposed to cadmium, lead, or manganese. Am. J. Epidemiol. 135:1208-1219. Gianutsos, G., and M.T. Murray. 1982. Alterations in brain dopamine and GABA following inorganic or organic manganese administration. Neurotoxicology 3:75-81. Gibbons, R.A., S.N. Dixon, K. Hallis, A.M. Russell, B.F. Sansom, and H.W. Symonds. 1976. Manganese metabolism in cows and goats. Biochim. Biophys. Acta 444(1):1-10.

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 Goldsmith, J.R., Y. Herishanu, J.M. Abarbanel, and Z. Weinbaum. 1990. Clustering of Parkinson’s disease points to environmental etiology. Arch. Environ. Health 45:88-94. Gottschalk, L.A., T. Rebello, M.S. Buchsbaum, H.G. Tucker, and E.L. Hodges. 1991. Abnormalities in hair trace elements as indicators of aberrant behavior. Compr. Psychiatry 32:229-237. Gray, L., Jr., and J.W. Laskey. 1980. Multivariate analysis of the effects of manganese on the reproductive physiology and behavior of the male house mouse. J. Toxicol. Environ. Health 6:861-867. Greger, J.L. 1999. Nutrition versus toxicology of manganese in humans: evaluation of potential biomarkers. Neurotoxicology 20:205-212. Gupta, S.K., R.C. Murthy, and S.V. Chandra. 1980. Neuromelanin in manganese-exposed primates. Toxicol. Lett. 6:17-20. Hamilton-Koch, W., R.D. Snyder, and J.M. Lavelle. 1986. Metal-induced DNA damage and repair in human diploid fibroblasts and Chinese hamster ovary cells. Chem. Biol. Interact. 59:17-28. Hauser, R.A., T.A. Zesiewicz, C. Martinez, A.S. Rosemurgy, and C.W. Olanow. 1996. Blood manganese correlates with brain magnetic resonance imaging changes in patients with liver disease. Can. J. Neurol. Sci. 23:95-98. Herishanu, Y.O., M. Medvedovski, J.R. Goldsmith, and E. Kordysh. 2001. A case-control study of Parkinson's disease in urban population of southern Israel. Can. J. Neurol. Sci. 28:144-147. Holbrook, D.J., Jr., M.E. Washington, H.B. Leake, and P.E. Brubaker. 1975. Studies on the evaluation of the toxicity of various salts of lead, manganese, platinum, and palladium. Environ. Health Perspect. 10:95-101. Holzgraefe, M., W. Poser, H. Kijewski, and W. Beuche. 1986. Chronic enteral poisoning caused by potassium permanganate: a case report. J. Toxicol. Clin. Toxicol. 24:235-244. IOM (Institute of Medicine). 2001. Manganese. Pp. 394-419 in Dietary Reference Intakes for Vitamin A, Molybdenum, Nickel, Silicon, Vanadium and Zinc. Washington, DC: National Academy Press. Joardar, M., and A. Sharma. 1990. Comparison of clastogenicity of inorganic Mn administered in cationic and anionic forms in vivo. Mutat. Res. 240:159-163. Johnson, P.E., G.I. Lykken, and E.D. Korynta. 1991. Absorption and biological half-life in humans of intrinsic and extrinsic 54Mn tracers from foods of plant origin. J. Nutr. 121:711-717. Kanematsu, N., M. Hara, and T. Kada. 1980. Rec assay and mutagenicity studies on metal compounds. Mutat. Res. 77:109-116. Kawamura, R., H. Ikuta, S. Fukuzumi, R. Yamada, S. Tsubaki, T. Kodama, and S. Kurata. 1941. Intoxication of manganese in well water. Kitasato Arch. Exp. Med. 18:145-169. Kies, C. 1987 Manganese bioavailability overview. In Nutritional Bioavailability of Manganese, C. Kies, ed. Washington, DC: American Chemical Society.

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 Kies, C. 1994. Bioavailability of Manganese. Pp. 39-58 in Manganese in Health and Disease, D.J. Klimis-Tzvatzis, ed. Boca Raton, FL: CRC Press. Kilburn, C.J. 1987. Manganese, malformations and motor disorders: findings in a manganese-exposed population. Neurotoxicology 8:421-429. Klaassen, C.D. 1974. Biliary excretion of manganese in rats, rabbits, and dogs. Toxicol. Appl. Pharmacol. 29:458-468. Klaassen, C.D. 1976. Biliary excretion of metals. Drug Metab. Rev. 5:165-196. Komura, J., and M. Sakamoto. 1991. Short-term oral administration of several manganese compounds in mice: physiological and behavioral alterations caused by different forms of manganese. Bull. Environ. Contam. Toxicol. 46:921-928. Komura, J., and M. Sakamoto. 1992. Effects of manganese forms on biogenic amines in the brain and behavioral alterations in the mouse: long-term oral administration of several manganese compounds. Environ. Res. 57:34-44. Kondakis, X.G., N. Makris, M. Leotsinidis, M. Prinou, and T. Papapetropoulos. 1989. Possible health effects of high manganese concentration in drinking water. Arch. Environ. Health 44:175-178. Kontur, P.J., and L.D. Fechter. 1985. Brain manganese, catecholamine turnover, and the development of startle in rats prenatally exposed to manganese. Teratology 32:1-11. Kontur, P.J., and L.D. Fechter. 1988. Brain regional manganese levels and monoamine metabolism in manganese-treated neonatal rats. Neurotoxicol. Teratol. 10:295-303. Kostial, K., M. Blanusa, T. Maljkovic, D. Kello, I. Rabar, and J.F. Stara. 1989. Effect of a metal mixture in diet on the toxicokinetics and toxicity of cadmium, mercury and manganese in rats. Toxicol. Ind. Health 5:685-698. Kostial, K., D. Kello, S. Jugo, I. Rabar, and T. Maljkovic. 1978. Influence of age on metal metabolism and toxicity. Environ. Health Perspect. 25:81-86. Lai, J.C., A.W. Chan, T.K. Leung, M.J. Minski, and L. Lim. 1992. Neurochemical changes in rats chronically treated with a high concentration of manganese chloride. Neurochem. Res. 17:841-847. Lai, J.C., T.K. Leung, L. Lim, A.W. Chan, and M.J. Minski. 1991. Effects of chronic manganese treatment on rat brain regional sodium-potassium-activated and magnesium-activated adenosine triphosphatase activities during development. Metab. Brain Dis. 6:165-174. Lai, J.C., M.J. Minski, A.W.K. Chan, T.K.C. Leung, and L. Lim. 1999. Manganese mineral interactions in brain. Neurotoxicology 20:433-444. Laskey, J.W., G.L. Rehnberg, J.F. Hein, and S.D. Carter. 1982. Effects of chronic manganese (Mn3O4 exposure on selected reproductive parameters in rats. J. Toxicol. Environ. Health 9:677-687. Lauwerys, R., H. Roels, P. Genet, G. Toussaint, A. Bouckaert, and S. De Cooman. 1985. Fertility of male workers exposed to mercury vapor or to manganese dust: a questionnaire study. Am. J. Ind. Med. 7:171-176.

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 Layrargues, G.P., C. Rose, L. Spahr, J. Zayed, L. Normandin, and R.F. Butterworth. 1998. Role of manganese in the pathogenesis of portal-systemic encephalopathy. Metab. Brain Dis. 13:311-317. Lee, D.Y., and P.E. Johnson. 1988. Factors affecting absorption and excretion of 54Mn in rats. J. Nutr. 118:1509-1516. Lee, D.Y., and P.E. Johnson. 1989. 54Mn absorption and excretion in rats fed soy protein and casein diets. Proc. Soc. Exp. Biol. Med. 190:211-216. Lonnerdal, B., C.L. Keen, J.G. Bell, and B. Sandstrom. 1987. Manganese uptake and retention: Expermental animal and human studies. Pp. 9-20 in Nutritional Bioavailability of Manganese: ACS Symposium Series 354, C. Kies, ed. Washington, DC: American Chemical Society. Lucchini, R., E. Albini, D. Placidi, R. Gasparotti, M.G. Pigozzi, G. Montani, and L. Alessio. 2000. Brain magnetic resonance imaging and manganese exposure. Neurotoxicology 21:769-775. Lucchini, R., L. Selis, D. Folli, P. Apostoli, A. Mutti, O. Vanoni, A. Iregren, and L. Alessio. 1995. Neurobehavioral effects of manganese in workers from a ferroalloy plant after temporary cessation of exposure. Scand. J. Work Environ. Health 21:143-149. Mahoney, J.P., and W.J. Small. 1968. Studies on manganese. 3. The biological half-life of radiomanganese in man and factors which affect this half-life. J. Clin. Invest. 47(3):643-653. Malecki, E.A., A.G. Devenyi, J.L. Beard, and J.R. Connor. 1999. Existing and emerging mechanisms for transport of iron and manganese to the brain. J. Neurosci. Res. 56:113-122. McDermott, S.D., and C. Kies. 1987. Manganese usage in humans as affected by use of calcium supplements. Pp. 146-151 in Nutritional Bioavailability of Manganese, C. Kies, ed. Washington, DC: American Chemical Society. McLeod, B.E., and M.F. Robinson. 1972. Metabolic balance of manganese in young women. Br. J. Nutr. 27:221-227. McMillan, D.E. 1999. A brief history of the neurobehavioral toxicity of manganese: some unanswered questions. Neurotoxicology 20:499-507. Mena, I. 1974. The role of manganese in human disease. Ann. Clin. Lab. Sci. 4:487-491. Mena, I., K. Horiuchi, K. Burke, and G.C. Cotzias. 1969. Chronic manganese poisoning. Individual susceptibility and absorption of iron. Neurology 19:1000-1006. Mena, I., O. Marin, S. Fuenzalida, and G.C. Cotzias. 1967. Chronic manganese poisoning. Clinical picture and manganese turnover. Neurology 17:128-136. Merck. 1989. The Merck Index, An Encyclopedia of Chemicals, Drugs, and Biologicals, 11th Edition, S. Budavari, M.J. O’Neil, A. Smith, and P.E. Heckelman, eds. Rathway, NJ: Merck and Co. Mergler, D. 1999. Neurotoxic effects of low level exposure to manganese in human populations. Environ. Res. 80:99-102.

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 Mergler, D., M. Baldwin, S. Belanger, F. Larribe, A. Beuter, R. Bowler, M. Panisset, R. Edwards, A. de Geoffroy, M.P. Sassine, and K. Hudnell. 1999. Manganese neurotoxicity, a continuum of dysfunction: results from a community based study. Neurotoxicology 20:327-342. Miller, S.T., G.C. Cotzias, and H.A. Evert. 1975. Control of tissue manganese: initial absence and sudden emergence of excretion in the neonatal mouse. Am. J. Physiol. 229:1080-1084. Mortelmans, K., S. Haworth, T. Lawlor, W. Speck, B. Tainer, and E. Zeiger. 1986. Salmonella mutagenicity tests: II. Results from the testing of 270 chemicals. Environ. Mutagen. 8(Suppl. 7):1-119. Nachtman, J.P., R.E. Tubben, and R.L. Commissaris. 1986. Behavioral effects of chronic manganese administration in rats: locomotor activity studies. Neurobehav. Toxicol. Teratol. 8:711-715. Newell, G.W., T.A. Jorgenson, and V.F. Simmon. 1974. Study of mutagenic effects manganese sulfate (FDA No. 71-71 compound report No.3. U.S. Food and Drug Administration, Rockville, MD. Newland, M.C. 1999. Animal models of manganese's neurotoxicity. Neurotoxicology 20:415-432. Newland, M.C., T.L. Ceckler, J.H. Kordower, and B. Weiss. 1989. Visualizing manganese in the primate basal ganglia with magnetic resonance imaging. Exp. Neurol. 106:251-258. Newland, M.C., C. Cox, R. Hamada, G. Oberdorster, and B. Weiss. 1987. The clearance of manganese chloride in the primate. Fundam. Appl. Toxicol. 9:314-328. Newland, M.C., and B. Weiss. 1992. Persistent effects of manganese on effortful responding and their relationship to manganese accumulation in the primate globus pallidus. Toxicol. Appl. Pharmacol. 113:87-97. Nishioka, H. 1975. Mutagenic activities of metal compounds in bacteria. Mutat. Res. 31:185-189. Normandin, L., and A.S. Hazell. 2002. Manganese neurotoxicity: an update of pathophysiologic mechanisms. Metab. Brain Dis. 17:375-387. Normandin, L., M. Panisset, and J. Zayed. 2002. Manganese neurotoxicity: behavioral, pathological, and biochemical effects following various routes of exposure. Rev. Environ. Health 17:189-217. NRC (National Research Council). 1980. V. The contribution of drinking water to mineral nutrition in humans. Pp. 265-404 in Drinking Water and Health. Washington, DC: National Academy Press. NRC (National Research Council). 1989. Recommended Dietary Allowances, pp. 231-235. Washington, DC: National Academy Press. NRC (National Research Council) 2000. Methods for Developing Spacecraft Water Exposure Guidelines. Washington, DC: National Academy Press. NTIS (National Technical Information Service). 1973. Teratological evaluation of FDA-71-71 (Manganese Sulfate.monohydrate). Springfield, VA: National Technical Information Service.

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