5
Cadmium (Inorganic Salts)

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

OCCURRENCE AND USE

Cadmium (Cd) occurs naturally in the earth’s crust. In the environment, it exists as oxides or salts such as cadmium chloride, cadmium sulfate, or cadmium sulfide (see Table 5-1). It also exists as a complex with lead, zinc, and copper ores. In the industrial setting, cadmium is used extensively in smelting, batteries, plastics and metal plating, welding, fabric dyes, glass glazes, and the burning of fossil fuels. In the general population, the sources for cadmium exposure are food and water. There have been numerous reports of the contribution of cadmium to the indoor environment from cigarette smoke, the most important single source of exposure to the general population. Cigarettes and cadmium have been the subject of several investigations, especially using pregnant women who smoke. Depending upon the source of tobacco, a single cigarette may contain from 1 to 2 micrograms (µg) of cadmium (FDA 1993). The average daily intake of 10-20 µg per day (d) of cadmium by adults in the United States has been reported (Reeves and Chaney 2002). There are reports that among food sources, certain vegetables, rice, and meat (kidney and liver) contribute significant concentrations of cadmium. In an FDA survey of fresh clams and oysters from U.S. coastal areas, it was reported that they contain significant amounts of cadmium (Caper and Yess 1996). It has also been stated that the diets in which shellfish constitutes a significant portion contain twice as much cadmium as a more mixed diet. Usually the concentration of cadmium in drinking water in the United States is about 2 µg per liter (L) (below the regulatory level of 5 µg/L). At hazardous waste sites, where cadmium contamination of soil



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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 5 Cadmium (Inorganic Salts) Raghupathy Ramanathan, Ph.D. NASA-Johnson Space Center Toxicology Group Houston, Texas OCCURRENCE AND USE Cadmium (Cd) occurs naturally in the earth’s crust. In the environment, it exists as oxides or salts such as cadmium chloride, cadmium sulfate, or cadmium sulfide (see Table 5-1). It also exists as a complex with lead, zinc, and copper ores. In the industrial setting, cadmium is used extensively in smelting, batteries, plastics and metal plating, welding, fabric dyes, glass glazes, and the burning of fossil fuels. In the general population, the sources for cadmium exposure are food and water. There have been numerous reports of the contribution of cadmium to the indoor environment from cigarette smoke, the most important single source of exposure to the general population. Cigarettes and cadmium have been the subject of several investigations, especially using pregnant women who smoke. Depending upon the source of tobacco, a single cigarette may contain from 1 to 2 micrograms (µg) of cadmium (FDA 1993). The average daily intake of 10-20 µg per day (d) of cadmium by adults in the United States has been reported (Reeves and Chaney 2002). There are reports that among food sources, certain vegetables, rice, and meat (kidney and liver) contribute significant concentrations of cadmium. In an FDA survey of fresh clams and oysters from U.S. coastal areas, it was reported that they contain significant amounts of cadmium (Caper and Yess 1996). It has also been stated that the diets in which shellfish constitutes a significant portion contain twice as much cadmium as a more mixed diet. Usually the concentration of cadmium in drinking water in the United States is about 2 µg per liter (L) (below the regulatory level of 5 µg/L). At hazardous waste sites, where cadmium contamination of soil

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 TABLE 5-1 Physical Properties of Inorganic Cadmium and Cadmium Salts Formula Cda CdCl2b CdSO4c CdCO3d CdOe CdSf Chemical name Cadmium Cadmium chloride Cadmium Sulfate Cadmium carbonate Cadmium oxide Cadmium sulfide Synonyms Cadmium colloidal Cadmium dichloride Cadmium Sulfate Otavite, cadmium monocarbonate Cadmium fume; cadmium monoxide Cadmium yellow; greenockite CAS registry no. 7440–43–9 10108–64–2 10124–36–4 513–78–0 1306–19–0 1306–23–6 Molecular weight 112.41 183.32 208.47 172.42 128.41 144.47 Cadmium (mole %) 100% 61.2% 53.8% 65% 87.5% 77% Solubility Insoluble 140 g/dL 75.5 g/dL Insoluble Insoluble Soluble at 1.3 mg/L aData are from HSDB 2006a. bData are from HSDB 2006b. cData are from HSDB 2006c. dData are from HSDB 2006d. eData are from HSDB 2006e. fData are from HSDB 2006f.

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 is very high because of the disposal of batteries, sewage sludge, and use of phosphate fertilizers, cadmium has the potential to contaminate the water supplies (Elinder 1985). Cadmium can also leach from copper piping in plumbing with nonlead-based solder joints into residential drinking water. A recent survey, the National Human Exposure Assessment Survey in Maryland (NHEXAS-MD), in which 381 water samples were taken from 73 households, indicated only 12 of the households had concentrations of cadmium higher than the method detection limit of 0.1 µg/L (Ryan et al. 2000). Cadmium has been found in the humidity condensate samples collected from several Mir missions at a mean concentration of 27 µg/L, with a maximum concentration of 240 µg/L. In the water processed from humidity condensates, cadmium was not found above 1 µg/L. Once, up to 36 µg/L of cadmium was reported in the crew drinking water collected from the International Space Station (ISS) water-use port in the galley. The problem was isolated. Because cadmium is the most common ingredient in zinc coatings and because of the well-known toxicity of soluble cadmium, the National Aeronautics and Space Administration (NASA) needed to determine the spacecraft water exposure guidelines (SWEGs) for cadmium in case there is a malfunction of the multifiltration beds or other components of the ISS water reclamation system leading to the contamination of ISS crew potable water. TOXICOKINETICS AND METABOLISM The absorption, distribution, and elimination of cadmium have been extensively studied in animals. The route of exposure can greatly affect these parameters and thus the toxic effects. Our discussions will be limited to studies that describe exposure by ingestion of soluble cadmium salts through food and drinking water or gavages only. The data from inhalation exposures, or from intravenous (iv), subcutaneous (sc), or intraperitoneal (ip) injections, may be mentioned but will not be discussed in any detail. Almost all the studies pertaining to ingestion of cadmium have used cadmium chloride (CdCl2). Very few studies have used cadmium acetate, cadmium sulfate, or cadmium iodide. Absorption Whole-body counting after a single oral dose of radiolabeled cadmium has been used for the quantification of whole-body retention and

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 the estimation of intestinal cadmium uptake in humans (Newton et al. 1984). The intestinal absorption seems to take place in two steps: first, the trapping of cadmium by the mucosal epithelial cells—this is not considered true absorption; and second, clearance of this trapped cadmium into blood. A large portion of the ingested cadmium is not taken up by the mucosal cells and thus passes through the gastrointestinal (GI) tract without being absorbed, although some is trapped in the intestinal mucosa (Kjellström et al. 1978; Foulkes 1986). Most of the studies on the GI absorption of cadmium have compared the dose given with the amount retained shortly after the dose was administered. This has been measured as whole-body retention by counting a radioactive tracer (109Cd or 115Cd). Because excretion of absorbed cadmium is very slow, wholebody cadmium retention may not be an underestimation of cadmium absorption (at least in the short term). The total retention of cadmium in the bodies of humans has been measured after ingestion of radioactive cadmium. About 25% of a dose of cadmium administered mixed with food to five healthy adults was retained after 3-5 d, but retention decreased to about 6% after 20 d (Rahola et al. 1973 as cited in ATSDR 1999). Similar results were obtained with 14 healthy adults who after 1-2 weeks (wk) retained an average of 4.6% of a dose of CdCl2 in water taken with a meal (McLellan et al. 1978). In a related study, Flanagan et al. (1978) estimated that the average intestinal net uptake of cadmium was 2.6% in males and 7.5% in females. Foulkes (1991) inferred from studies using intestinal segments that mucosal cadmium uptake is a saturable process (see Lehman and Klaassen 1986). Once taken up by the mucosal cells, cadmium is generally believed to be partly bound to intestinal metallothionein (MT). A number of studies indicate that the retention or overall absorption of CdCl2, cadmium nitrate, or cadmium sulfate given orally is 1-2%. Rats (Decker et al. 1958; Moore et al. 1973a, b) and mice (Cotzias et al. 1961; Nordberg 1972; Ogawa et al. 1972; Valberg et al. 1976) exposed to a single oral dose of radioactive CdCl2 retained about 1-2% of it. Nordberg et al. (1985) reported that in monkeys (Saimiri sciureus), the retention of 115CdCl2 administered by stomach tube depended on the dose: about 1% from cadmium at 1 µg per kilogram (kg) and 2.9-3.2% from cadmium at 0.17-1.7 mg/kg. Suzuki and Taguchi (1980), who administered 109Cd by stomach tube to Macaca irus monkeys, observed that after 19 d, 12% of the dose was retained and 50% of this was still in the GI mucosa. They reported a final retention of 6% of administered cadmium in the monkeys. The results of several studies on absorption of cadmium from single oral bolus studies show that monkeys and humans seem to absorb

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 (retain) more cadmium than rodents. Animal studies indicate that absorption of cadmium is complex and depends on the dose rate. Engstrom and Nordberg (1979a) observed that in mice, the absorption was 0.5% from a 1 µg/kg dose, 1.4% from 15 to 750 µg/kg, and 3.25% from 37.5 mg/kg (the highest dose tested). The highest dose caused morphologic changes in the GI mucosa. In a study designed to determine the GI absorption of cadmium, rats were given one oral dose of cadmium (mixed with 109Cd) as CdCl2 (1 or 10,000 µg/kg) and the cadmium content was determined in organs 3 hours (h) later (Lehman and Klaassen 1986). The percent of the dose that was absorbed was dose-dependent (0.35 and 1% at 1 and 10,000 µg/kg, respectively). However, at 3 h, liver cadmium increased 80,000 times between the 1 and 10,000 µg/kg doses. Similar data were obtained for kidney, blood, pancreas, and bone. At the 1 µg/kg dose, 60% of cadmium in intestinal cytosol was bound to MT, whereas at the 10,000 µg/kg dose, 50% of the cadmium was bound to MT. It is also interesting to note that even when cadmium was iv injected into rats (at 0.1, 0.3, 1.0, or 3.0 mg/kg), the biliary excretion percentage of the injected dose measured 2 h after injection was dose dependent, increasing as the dose increased (Gregus and Klaassen 1986). To evaluate the precise nature of cadmium absorption by the intestine and the role of MT in the intestinal absorption of cadmium in rats, a study was conducted by Goon and Klaassen (1989) using an isolated intestinal loop preparation in situ, which allowed direct measurement of intestinal absorption under nearly physiologic conditions. Cadmium (0.1, 10, 100, 1,000, or 10,000 µg/kg) was injected intraluminally into the isolated intestinal loop in situ and all mesenteric venous (portal) blood exiting from the loop was collected for 90 minutes (min). Absorption of cadmium into the portal circulation was low at all doses studied. At low doses (0.1 and 10 µg/kg), little difference was noted in the fractional absorption of cadmium (0.09% and 0.14% of the dose, respectively). However, in rats administered cadmium at 100 µg/kg, the fractional absorption of cadmium was 10-fold greater (1.1% of the dosage). Administration of higher doses of cadmium (1,000 and 10,000 µg/kg) further increased the percentage of the dose absorbed, a nonlinear absorption kinetics (1.8% and 3.4%, respectively) (Goon and Klaassen 1989). This dose-dependent increase in fractional absorption is not because of saturation of intestinal MT at high doses, because this phenomenon was seen even when the intestinal level of MT was experimentally increased (MT induction) by pretreatment of the rats with zinc injections (Goon and Klaassen 1989). In an experiment conducted by Liu et al. (2001) to clar-

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 ify the role of MT in Cd absorption and tissue distribution, single oral doses of 109Cd (1 or 300 micromol/kg) were administered to MT-null mice and their parental wild-type mice. Four hours after Cd administration about 0.15% of the lowest dose (1 micromol/kg) and 0.75% of the highest dose (300 micromol/kg) in the liver, and similarly about 0.05% of the lowest dose and 0.15% of the highest dose in kidneys were found in both MT-null and wild-type mice. This experiment indicated that the absorption and initial distribution of orally administered Cd was dose dependent but was not influenced by MT. Differences between the rodent and human diets may be responsible for the reported differences in absorption rates. Rabar and Kostial (1981) found that retention was at least four times greater when rats were fed bread, meat, or milk that humans consume. Cadmium absorption from the GI tract can be influenced by several factors (for instance, age and dietary constituents such as iron, calcium, zinc, and dietary fiber content [see Wing 1993]). When human volunteers consumed crabmeat into which cadmium was incorporated, the whole-body retention ranged from 1.2% to 7.6% with a mean of 2.7% (Newton et al. 1984). This was only slightly lower than the values of 4.6-6.0% when cadmium salt was ingested as a solution (McLellan et al. 1978). This seems to indicate that complexation of cadmium in the food did not influence the estimated absorption significantly. Cadmium Absorption and Age Consistent with data on absorption of other metals, several animal studies have indicated that in general, absorption of cadmium is higher at younger ages. This appears also partly because of slower excretion from younger animals (Kello and Kostial 1977; Kostial 1984). For example, Engstrom and Nordberg (1979b) reported that absorption from an oral dose of 109Cd in mice of different ages decreased from 5.2% in 1-month (mo)-old mice to 2.9% in 3-mo-olds and 2.1% in 6-mo-old mice. Similar data are not found for rats. No human data could be found. After a single oral administration of 115Cd to albino rats 1-26 wk old, the whole-body cadmium retention (measured 1 or 2 wk after dosing) was higher in sucklings than in weaned rats, and retention of cadmium in the kidneys was 5-7 times higher in the sucklings than in older rats (Kostial 1984).

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 Cadmium and Iron The body store of iron influences cadmium absorption. Subjects with low iron stores (assessed by serum ferritin concentrations) had an average absorption of 8.9%, and those with adequate iron stores had an average absorption of 2.3% (Flanagan et al. 1978). In 10 human subjects with low body iron stores (serum ferritin less than 20 nanogram (ng)/mL), the average absorption of cadmium labeled with 115mcadmium at 25 µg from a test meal was 8.9 ± 2.0% (mean ± SD), whereas, it was 2.3 ± 0.3% in 12 subjects with normal iron stores (serum ferritin greater than 23 ng/mL). The biologic half-life of 115mcadmium in three of the subjects ranged from 90 to 202 d. Thus, iron deficiency in both experimental animals and human subjects lead to the increased absorption of cadmium (Flanagan et al. 1978). Some of the gender differences in absorption arise from differences in iron status between men and women. Females may absorb a larger fraction of dietary cadmium than men because they have lower body stores of iron (Berglund et al. 1994; Vahter et al. 1996; Choudhury et al. 2001). Increased tissue cadmium concentration in iron deficient rats by increased intestinal absorption and 10-fold higher retention in the body has also been documented (Park et al. 2002). It was proposed that iron depletion upregulates the expression of divalent metal transporter protein (DMT1) in the intestine leading to the increased absorption and transport of cadmium. Cadmium and Calcium Low calcium intake has been shown to increase the whole-body retention of cadmium. Correspondingly, the uptake of calcium decreases when the ingestion of cadmium is high. Female rats on low-calcium diets exposed to cadmium as CdCl2 at 25 mg/L in drinking water for 1 or 2 mo had accumulated about 50% more cadmium than the rats on a high-calcium diet (Larsson and Piscator 1971). Washko and Cousins (1977) showed that when rats were exposed to cadmium as CdCl2 at 25 ppm in drinking water for 8 wk, the groups that were fed a low-calcium diet (0.1%) had enhanced cadmium retention and cadmium toxicity (for example, depressed packed-cell volume and the highest concentrations in lung, liver, and kidneys) compared with groups fed a high-calcium diet (0.6%). In another study, rats on a low-calcium diet or normal-calcium diet were given rice containing cadmium at 0.1-0.6 mg/kg for 74 wk. Liver and kidney cadmium concentrations in the low-calcium-diet group

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 were 1.5-5 times greater than in the normal-calcium-diet group (Kobayashi et al. 1971). Similarly, liver and kidney cadmium concentrations in rats on a low-calcium diet exposed to cadmium at 0-10 mg/L for 1 year (y), were at least two times higher than those on a normal-calcium diet (Piscator and Larsson 1972, as cited in Nordberg et al. 1985). Similar results have been reported by several investigators (Hamilton and Smith 1978). According to Brzoska and Moniuszko-Jakoniuk (1998), large intakes of calcium can protect against absorption, accumulation, and toxicity of cadmium. Cadmium and Zinc Several reports in the literature seem to clearly indicate that zinc plays a critical role in cadmium-induced toxicity and even carcinogenesis (see, for example, Petering et al. 1971; Goering and Klaassen 1984; Waalkes et al. 1989, 1992). Dietary zinc intake has an important effect on the absorption, accumulation, and toxicity of cadmium. Increased zinc supply reduced cadmium absorption. It is beyond the scope of this document to discuss the mechanism of competition between cadmium and zinc. Several studies have been carried out using in vitro systems and should be interpreted carefully because the result can vary depending on whether intraluminally perfused rat intestinal preparations were used or the vascularly perfused system was used. It also depends on the relative concentrations of zinc and cadmium in the perfusion medium (Foulkes and Voner 1981; Hoadley and Cousins 1985; Jaeger 1990). Marginal nutritional status (not a deficient status) with respect to the minerals zinc, iron, or calcium can result from consuming one staple grain such as rice, wheat, sunflower kernels, or maize as a large proportion of the diet. To evaluate the effect of such a diet on the interactions of these minerals with cadmium, Reeves and Chaney (2002) conducted a study in female rats (SAS:VAF [SD] Charles River rats) that were fed a diet containing a high proportion of milled rice that was formulated to give only marginal concentrations of these metals. The diet was supplemented with cadmium (0.25 mg/kg diet), and retention of 109Cd (intrinsically labeled CdCl2) was measured. The rats consumed the rice diet, with or without cadmium, for 5 wk and then were fed 1 g of radiolabeled-cadmium diet for 2 wk. The results were compared with control whose diet contained adequate amounts of these previously mentioned minerals. The authors reported that whole-body retention of cadmium in rats consuming diets low in zinc, iron, or calcium was significantly more than

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 rats consuming a diet adequate in all these minerals. There was a significant interaction of zinc and iron with cadmium; thus, marginal zinc along with marginal iron resulted in greater whole-body retention of (radioactive) cadmium than it did in rats fed adequate zinc and marginal iron. Cadmium concentration in the duodenum was also 10-fold higher in rats fed diets marginally deficient in zinc and iron compared with rats fed diets containing adequate amounts of these minerals. Marginal intake of zinc led to higher concentrations of cadmium in the liver, without any change in concentrations of cadmium in the kidney (Reeves and Chaney 2002). Cadmium and Low Dietary Protein Suzuki et al. (1969) reported that in mice given a low-protein diet 24 h before an oral dose of 115CdCl2, the kidney and liver and the whole body had considerably higher concentrations of cadmium than in mice given a high-protein diet. Whole-body retention of cadmium was 9% (mean of 5-14%) in mice fed a low-protein diet and 4.5% (mean of 3-10%) in mice fed a high-protein diet. On the other hand, a refined diet high in fat and protein increased cadmium absorption in mice, partially because of increased GI-passage time (Schafer et al. 1986). Cadmium and Fasting The acute oral toxicity of cadmium (as CdCl2) was enhanced in rats fasted 24 h, as shown by a markedly decreased LD50 (the dose lethal to 50% of test subjects). Rats were administered cadmium at 75 mg/kg orally 24 h after fasting and euthanized after a further 4 or 24 h for various assays (Shimizu and Morita 1990). Cadmium uptake by the liver (both concentration and content) 24 h after cadmium treatment was higher in fasted rats than in fed rats. Fasting enhanced the focal degenerative and necrotic changes from the midlobular to the pericentral region in the livers. The authors also found changes and shifts in the distribution of liver glutathione (GSH) in the fasted and cadmium-treated rats different from that seen in the control group (Shimizu and Morita 1990, 1992).

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 Metabolism and Transport Evidence from studies with rats and mice has led investigators to propose a complex mechanism for the transport of cadmium in the intestinal epithelial cells. The mechanism involves the binding of cadmium to membrane proteins involved in the transport of essential metals, such as calcium, iron, and zinc, and endocytosis of the membrane proteins bound to cadmium (Cd-MT) by enterocytes in the small intestine. The transport proteins are DMT1, iron transporter protein (MTP1), and zinc transporter protein (ZTL1). These processes have been described in a recent review by Zalups and Ahmad (2003). Competition by Cd for essential metal transporters could explain the greater gastrointestinal Cd absorption when iron, zinc, and calcium dietary levels are low. Cadmium exists mostly as the Cd2+ ion and is not known to undergo any direct oxidation, reduction, or alkylation. It can avidly bind to sulfhydryl groups in proteins (especially albumin and MT) and other molecules (Nordberg et al. 1978, 1985). In plasma, cadmium is initially and predominantly bound to protein of high molecular weight (albumin) a short time after exposure (in the case of parenteral administration) or 1 d after single oral administration. The cadmium-protein complexes are taken up by the liver. After 2-3 d, when plasma cadmium concentrations are low, plasma cadmium is also bound to a low-molecular-weight protein, MT (Norberg et al. 1985; Foulkes and Blanck 1990). MT is very rich in cysteine and capable of binding as many as seven cadmium atoms per molecule. MT is inducible in most tissues by exposure to cadmium among other metals and agents (Waalkes and Goering 1990). Initially the albumin-bound cadmium is taken up by the liver. In the liver, cadmium induces the synthesis of MT, and a few days after exposure, MT-bound cadmium appears in the blood plasma. MT is ultrafiltrable and taken up by the tubules (Nordberg 1992). Thus, the binding is of interest in relation to kidney function, especially with respect to glomerular filtration and tubular reabsorption of MT-bound cadmium. MT is thought to be a carrier of cadmium from liver to kidney. MT concentrations in urine and plasma of cadmium-exposed workers and in urine samples from cadmium-exposed Japanese farmers and itai-itai disease (a disease resulting from consuming cadmium-contaminated rice in Japan) patients have been extensively reported (Chang et al. 1980; Nordberg et al. 1982; Tohyama et al. 1982; Falck et al. 1983).

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 Distribution Since we will restrict ourselves to discussing the oral route of cadmium exposure, the distribution of cadmium administered via iv, ip, or sc injection will not be discussed here. Upon ingestion of cadmium, a considerable quantity is retained in the intestinal walls. Once transported to blood, it is transported to all the tissues, with a large portion in liver, kidneys, muscle, and bones. The distribution depends on the exposure regimens and the amount of time after exposure. Initially most of the absorbed cadmium will go to the liver, with small amounts going to the kidneys. With increasing time after exposure, cadmium will be redistributed and concentrations in the kidneys will increase. The time-dependent changes in the distribution to kidneys and liver have been the subject of numerous investigations because these organs are considered storage organs (Kotsonis and Klaassen 1978; Weigel et al. 1984; Andersen et al. 1988; Jonah and Bhattacharya 1989). In the liver and kidneys of cadmium-exposed animals, more than 80% of the cadmium is bound to MT. The concentration of cadmium is higher in the kidney cortex than in the medulla. Renal damage initially occurs in the proximal tubules located in the renal cortex. Livingston (1972) analyzed the concentrations in serial sections of the cortex and found that cadmium decreased from the outer layer to the inner medulla. A ratio of 2:1 between the outer cortex and inner medulla has been reported. In humans, 65-75% of the whole kidney is cortex and 25-35% is the medullar collection system, and this ratio is usually taken into consideration when calculating the cadmium concentration in cortex and the whole kidney concentration (Kjellström and Nordberg 1978; Kjellström et al. 1984; Svartengren et al. 1986). A number of studies have confirmed the selection distribution of cadmium to the cortex of the kidney in preference to the medulla for different routes of exposure, exposure types, and animal species. The cadmium concentration in kidney and liver tissues is very low at birth but markedly increases with age. In humans with normal exposures, liver accumulation reaches near steady-state at age 30, and kidney accumulation reaches a maximum at 40-50 y of age (Bernard and Lauwerys 1986). In muscles, accumulation of cadmium continues throughout life (Elinder 1985; Satarug et al. 2000). Decker et al. (1958) gave 115Cd nitrate to rats (cadmium at 6.6 mg/kg) by gavage. After 8 h, the largest total amount was in the liver, although the highest concentration was in the kidney. The maximum concentration in both tissues was reached at 72 h after exposure. Kotsonis and Klaassen (1977) administered a single oral bolus dose of

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 Kjellström, T., C.G. Elinder, and L. Friberg. 1984. Conceptual problems in establishing the critical concentration of cadmium in human kidney cortex. Environ. Res. 33:284-295. Kjellström, T., L. Friberg, and B. Rahnster. 1979. Mortality and cancer morbidity among cadmium-exposed workers. Environ. Health Perspect. 28:199-204. Kjellström, T., and G.F. Nordberg. 1978. A kinetic model of cadmium metabolism in the human being. Environ. Res. 16:248-269. Kjellström, T., and G.F. Nordberg. 1986. Kinetic model of cadmium metabolism. Pp. 179-197 in Cadmium and Health: A Toxicological and Epidemiological Appraisal, Vol. I, Exposure, Dose and Metabolism, L. Friberg, C.G. Elinder, G.F. Nordberg, and T. Kjellström, eds. Cleveland, OH: CRC Press. Kobayashi, J., H. Nakahara, and T. Hasegawa. 1971. Accumulation of cadmium in organs of mice fed on cadmium-polluted rice [in Japanese]. Nippon Eiseigaku Zasshi 26(5):401-407. Koller, L.D. 1980. Immunotoxicology of heavy metals. Int. J. Immunopharmacol. 2:269-279. Koller, L.D. 1996. Profiling immunotoxicology: Past, present and future. Pp. 301-310 in Modulators of Immune Response: The Evolutionary Trail, J.S. Stolen, T.C. Fletcher, and C.J. Bayne, eds. Fair Haven, NJ: SOS Publications. Koller, L.D. 1998. Cadmium. Pp. 41-61 in Immunotoxicology of Environmental and Occupational Metals, J.T. Zelicoff, ed. Bristol, PA: Taylor and Francis. Koller, L.D., J.H. Exon, and J.G. Roan. 1975. Antibody suppression by cadmium. Arch. Environ. Health 30:598-601. Kopp, S.J., T. Glonek, M. Erlanger, E.F. Perry, H.M. Perry, Jr., and M. Barany. 1980. Cadmium and lead effects on myocardial function and metabolism. J. Environ. Pathol. Toxicol. 4:205-227. Kostial, K. 1984. Effect of age and diet on renal cadmium retention in rats. Environ. Health Perspect. 54:51-56. 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. Kotsonis, F.N., and C.D. Klaassen. 1977. Toxicity and distribution of cadmium administered to rats at sublethal doses. Toxicol. Appl. Pharmacol. 41:667-680. Kotsonis, F.N., and C.D. Klaassen. 1978. The relationship of metallothionein to the toxicity of cadmium after prolonged oral administration to rats. Tox. Appl. Pharmacol. 46:39-54. Lafuente, A., A. Gonzalez-Carracedo, A. Romero, and A.I. Esquifino. 2003. Effect of cadmium on lymphocyte subsets distribution in thymus and spleen. J. Physiol. Biochem. 59:43-48.

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 Lang, T., A. LeBlanc, H. Evans, Y. Lu, H. Genant, and A. Yu. 2004. Cortical and trabecular bone mineral loss from the spine and hip in long-duration spaceflight. J. Bone Miner. Res. 19:1006-1012. Larsson, S.E., and M. Piscator. 1971. Effect of cadmium on skeletal tissue in normal and calcium-deficient rats. Isr. J. Med. Sci. 7:495-498. Laskey, J.W., G.L. Rehnberg, S.C. Laws, and J.F. Hein. 1984. Reproductive effects of low acute doses of cadmium chloride in adult male rats. Toxicol. Appl. Pharmacol. 73:250-255. Lauwers, R., and P. De Wals. 1981. Environmental pollution by cadmium and mortality from renal diseases. Lancet 1:383. Lauwerys, R.R., A. Bernard, H.A. Roels, J.P. Buchet, and C. Viau. 1984. Characterization of cadmium proteinuria in man and rat. Environ. Health Perspect. 54:147-152. Leffel, E.K., C. Wolf, A. Poklis, and K.L. White, Jr. 2003. Drinking water exposure to cadmium, an environmental contaminant, results in the exacerbation of autoimmune disease in the murine model. Toxicology 188:233-250. Lehman, L.D., and C.D. Klaassen. 1986. Dosage-dependent disposition of cadmium administered orally to rats. Toxicol. Appl. Pharmacol. 84:159-167. LeBlanc, A. 1998. Summary of research issues in human studies. Bone 22(Suppl. 5):117S-118S. LeBlanc, A., V. Schneider, L. Shackelford, S. West, V. Oganov, A. Bakulin, and L. Voronin. 2000. Bone mineral and lean tissue loss after long duration space flight. J. Musculoskelet. Neuronal Interact. 1(2):157-160. Levy, L.S., and J. Clack. 1975. Further studies on the effect of cadmium on the prostate gland. I. Absence of prostatic changes in rats given oral cadmium sulfate for two years. Ann. Occup. Hyg. 17:205-211. Levy, L.S., J. Clack, and F.J. Roe. 1975. Further studies on the effect of cadmium on the prostate gland. II. Absence of prostatic changes in mice given oral cadmium sulfate for eighteen months. Ann. Occup. Hyg. 17:213-220. Levy, L.S., F.J. Roe, D. Malcolm, G. Kazantzis, J. Clack, and H.S. Platt. 1973. Absence of prostatic changes in rats exposed to cadmium. Ann. Occup. Hyg. 16:111-118. Liu, J., and C.D. Klaassen. 1996. Absorption and distribution of cadmium in metallothionein-I transgenic mice. Fundam. Appl. Toxicol. 29:294-300. Liu, Y., J. Liu, S.M. Habeebu, M.P. Waalkes, and C.D. Klaassen. 2000. Metallothionein-I/II null mice are sensitive to chronic oral cadmium-induced nephrotoxicity. Toxicol. Sci. 57:167-176. Liu, Y., J. Liu, and C.D. Klaassen. 2001. Metallothionein-null and wild-type mice show similar cadmium absorption and tissue distribution following oral cadmium administration. Toxicol. Appl. Pharmacol. 175:253-259. Livingston, H.D. 1972. Measurement and distribution of zinc, cadmium, and mercury in human kidney tissue. Clin. Chem. 18(1):67-72. Loeser, E., and D. Lorke. 1977a. Semichronic oral toxicity of cadmium. I. Studies on rats. Toxicology 7:215-224.

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 Loeser, E., and D. Lorke. 1977b. Semichronic oral toxicity of cadmium. II. Studies on dogs. Toxicology 7:225-232. Loeser, E. 1980. A 2 year oral carcinogenicity study with cadmium on rats. Cancer Lett. 9:191-198. Machemer, L., and D. Lorke. 1981. Embryotoxic effect of cadmium on rats upon oral administration. Toxicol. Appl. Pharmacol. 58:438-443. Malave, I., and D.T. de Ruffino. 1984. Altered immune response during cadmium administration in mice. Toxicol. Appl. Pharmacol. 74:46-56. Masaoka, T., F. Akahori, S. Arai, K. Nomiyama, H. Nomiyama, K. Kobayashi, Y. Nomura, and T. Suzuki. 1994. A nine-year chronic toxicity study of cadmium ingestion in monkeys. I. Effects of dietary cadmium on the general health of monkeys. Vet. Hum. Toxicol. 36:189-194. McLellan, J.S., P.R. Flanagan, M.J. Chamberlain, and L.S. Valberg. 1978. Measurement of dietary cadmium absorption in humans. J. Toxicol. Environ. Health 4:131-138. Mitsumori, K., M. Shibutani, S. Sato, H. Onodera, J. Nakagawa, Y. Hayashi, and M. Ando, 1998. Relationship between the development of hepatorenal toxicity and cadmium accumulation in rats given minimum to large amounts of cadmium chloride in the long-term: Preliminary study. Arch. Toxicol. 72:545-552. Moore, W., Jr., J. F. Stara, and W.C. Crocker. 1973a. Gastrointestinal absorption of different compounds of 115m cadmium and the effect of different concentrations in the rat. Environ. Res. 6, 159-164. Moore, W., Jr., J.F. Stara, W.C. Crocker, M. Malanchuk, and R. Iltis. 1973b. Comparison of 115m cadmium retention in rats following different routes of administration. Environ. Res. 6:473-478. Mukherjee, A., A.K. Giri, A. Sharma, and G. Talukder. 1988. Relative efficacy of short-term tests in detecting genotoxic effects of cadmium chloride in mice in vivo. Mutat. Res. 206:285-295. Muller, S., K.E. Gillert, C. Krause, G. Jautzke, U. Gross, and T. Diamantstein. 1979. Effects of cadmium on the immune system of mice. Experientia 35:909-910. Nakagawa, H., S. Kawano, Y. Okumura, T. Fujita, and M. Nishi. 1987. Mortality study of inhabitants in a cadmium-polluted area. Bull. Environ. Contam. Toxicol. 38:553-560. Nakagawa, H., M. Nishijo, Y. Morikawa, M. Tabata, M. Senma, Y. Kitagawa, S. Kawano, M. Ishizaki, N. Sugita, and M. Nishi. 1993. Urinary beta 2-microglobulin concentration and mortality in a cadmium-polluted area. Arch. Environ. Health 48:428-435. NAS (National Academy of Sciences). 1980. Toxicity of selected drinking water contaminants. Pp. 91-96 in Drinking Water and Health, Vol. 3. Washington, DC: National Academy Press. Nation, J.R., A.E. Bourgeois, D.E. Clark, D.M. Baker, and M.F. Hare. 1984. The effects of oral cadmium exposure on passive avoidance performance in the adult rat. Toxicol. Lett. 20:41-47.

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 Nation, J.R., C.A. Grover, G.R. Bratton, and J.A. Salinas. 1990. Behavioral antagonism between lead and cadmium. Neurotoxicol. Teratol. 12:99-104. Newton, D., P. Johnson, A. Lally, R.J. Pentreath, and D.J. Swift. 1984. The uptake by man of cadmium ingested in crab meat. Hum. Toxicol. 3:23-28. Nishijo, M., H. Nakagawa, Y. Morikawa, M. Tabata, M. Senma, K. Miura, H. Takahara, H., S. Kawano, M. Nishi, K. Mizukoshi, T. Kido, and K. Nogawa. 1995. Mortality of inhabitants in an area polluted by cadmium: 15 year follow up. Occup. Environ. Med. 52:181-184. Nishiyama, S., N. Itoh, S. Onosaka, M. Okudaira, H. Yamamoto, and K. Tanaka. 2003. Dietary cadmium inhibits spontaneous hepatocarcinogenesis in C3H/HeN mice and hepatitis in A/J/ mice, but not in C57BL/6 mice. Toxicol. Appl. Pharmacol. 186(1):1-6. Noble, R.L. 1982. Prostate carcinoma of the Nb rat in relation to hormones. Int. Rev. Exp. Pathol. 23:113-159. Noda, M., and M. Kitagawa. 1990. A quantitative study of iliac bone histopathology on 62 cases with itai-itai disease. Calcif. Tissue Int. 47:66-74. Nogawa, K., R. Honda, T. Kido, I. Tsuritani, Y. Yamada, M. Ishizaki, and H. Yamaya. 1989. A dose-response analysis of cadmium in the general environment with special reference to total cadmium intake limit. Environ. Res. 48:7-16. Nogawa, K., and T. Kido. 1993. Biological monitoring of cadmium exposure in itai-itai disease epidemiology. Int. Arch. Occup. Environ. Health 65:S43-46. Nogawa, K., I. Tsuritani, T. Kido, R. Honda, M. Ishizaki, and Y. Yamada. 1990. Serum vitamin D metabolites in cadmium-exposed persons with renal damage. Int. Arch. Occup. Environ. Health 62:189-193. Nogawa, K., I. Tsuritani, T. Kido, R. Honda, Y. Yamada, and M. Ishizaki. 1987. Mechanism for bone disease found in inhabitants environmentally exposed to cadmium: Decreased serum 1 alpha, 25-dihydroxyvitamin D level. Int. Arch. Occup. Environ. Health 59:21-30. Nordberg, G.F. 1972. Cadmium metabolism and toxicity. Environ. Physiol. Biochem. 2:7-36. Nordberg, G.F. 1992. Application of the ‘critical effect’ and ‘critical concentration’ concept to human risk assessment for cadmium. IARC Sci. Publ. (118):3-14. Review. Nordberg, G.F., J.S. Garvey, and C.C. Change. 1982. Metallothionein in plasma and urine of cadmium workers. Environ. Res. 28(1):179-182. Nordberg, G.F., T. Jin, A. Bernard, S. Fierens, J.P. Buchet, T. Ye, Q. Kong, and H. Wang. 2002. Low bone density and renal dysfunction following environmental cadmium exposure in China. Ambio 31:478-481. Nordberg, G.F., Kjellström, T., and M. Nordberg. 1985. Kinetics and Metabolism. Pp. 103-178 in Cadmium and Health: A Toxicological and Epidemiological Appraisal, Vol. I, Exposure, Dose, and Metabolism, L. Friberg, C.G. Elinder, T. Kjellström, and G.F. Nordberg, eds. Boca Raton, FL: CRC Press.

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 Nordberg, G.F., S. Slorach, and T. Stenstrom. 1973. Cadmium poisoning caused by a cooled-soft-drink machine [in Swedish]. Läkartidningen 70(7):601-604. NRC (National Research Council). 2000. Methods for Developing Spacecraft Water Exposure Guidelines. Washington, DC: National Academy Press NTP (National Toxicology Program). 2005. 11th report on carcinogenesis. National Toxicology Program, U.S. Department of Health and Human Services, Research Triangle Park, NC. Oberdorster, G. 1990. Equivalent oral and inhalation exposure to cadmium compounds: Risk estimation based on route-to-route extrapolation. Pp. 217-235 in Principles of Route-to-Route Extrapolation for Risk Assessment, T.R. Gerrity, and C.J. Henry, eds. New York: Elsevier Science Publishing Co., Inc. Oberly, T.J., C.E. Piper, and D.S. Mcadmiumonald. 1982. Mutagenicity of metal salts in the L5178Y mouse lymphoma assay. J. Toxicol. Environ. Health 9:367-376. Ochi, T., and M. Ohsawa. 1983. Induction of 6-thioguanine-resistant mutants and single-strand scission of DNA by cadmium chloride in cultured Chinese hamster cells. Mutat. Res. 111:69-78. Ogawa, E., S. Suzuki, and H. Tsuzuki. 1972. Radiopharmacological studies on the cadmium poisoning. Jpn. J. Pharmacol. 22:275-281. Ogoshi, K., T. Moriyama, and Y. Nanzai. 1989. Decrease in the mechanical strength of bones of rats administered cadmium. Arch. Toxicol. 63:320-324. Ogoshi, K., Y. Nanzai, and T. Moriyama. 1992. Decrease in bone strength of cadmium-treated young and old rats. Arch. Toxicol. 66:315-320. Ohsawa, M., K. Sato, K. Takahashi, and T. Ochi. 1983. Modified distribution of lymphocyte subpopulation in blood and spleen from mice exposed to cadmium. Toxicol. Lett. 19:29-35. Ohsawa, M., K. Takahashi, and F. Otsuka. 1988. Induction of anti-nuclear antibodies in mice orally exposed to cadmium at low concentrations. Clin. Exp. Immunol. 73:98-102. Ohta, H., Y. Yamauchi, M. Nakakita, H. Tanaka, S. Asami, Y. Seki, and H. Yoshikawa. 2000. Relationship between renal dysfunction and bone metabolism disorder in male rats after long-term oral quantitative cadmium administration. Ind. Health 38:339-355. Olsson, I.M., I. Bensryd, T. Lundh, H. Ottosson, S. Skerfving, and A. Oskarsson. 2002. Cadmium in blood and urine—impact of sex, age, dietary intake, iron status, and former smoking—association of renal effects. Environ. Health Perspect. 110(12):1185-1190. Park, J.D., N.J. Cherrington, and C.D. Klaassen. 2002. Intestinal absorption of cadmium is associated with divalent metal trasporter 1 in rats. Toxicol. Sci. 68:288-294. Paton, G.R., and A.C. Allison. 1972. Chromosome damage in human cell cultures induced by metal salts. Mutat. Res. 16(3):332-336.

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 Pennington, J.A., B.E. Young, D.B. Wilson, R.D. Johnson, and J.E. Vanderveen. 1986. Mineral content of foods and total diets: The Selected Minerals in Foods Survey, 1982 to 1984. J. Am. Diet Assoc. 86:876-891. Petering, H.G., H. Choudhury, and K.L. Stemmer. 1979. Some effects of oral ingestion of cadmium on zinc, copper, and iron metabolism. Environ. Health Perspect. 28:97-106. Petering, H.G., M.A. Johnson, and K.L. Stemmer. 1971. Studies of zinc metabolism in the rat. I. Dose-response effects of cadmium. Arch. Environ. Health. 23:93-101. Piscator, M., L. Bjorck, and M. Nordberg. 1981. Beta 2-microglobulin levels in serum and urine of cadmium exposed rabbits. Acta Pharmacol. Toxicol. (Copenh.) 49:1-7. Piscator, M., and S.E. Larsson. 1972. Retention and toxicity of cadmium in calcium deficient rats. In Proceedings of the 17th International Congress on Occupational Health, Buenos Aires. Pleasants, W., M.E. Sandow, S. DeCandido, C. Waslien, and B.A. Naughton. 1992. The effect of vitamin D3 and 1,25-dihydroxyvitamin D3 on the toxic symptoms of cadmium exposed rats. Nutr. Res. 12:1392-1403. Pleasants, W., C. Waslien, and B. Naughton. 1993. Dietary modulation of the symptoms of cadmium toxicity in rats: Effects of vitamins A, C, D, DD hormone and fluoride. Nutrition. Res. 13:839-850. Prigge, E. 1978. Early signs of oral and inhalative cadmium uptake in rats. Arch. Toxicol. 40:231-247. Rabar, I., and K. Kostial. 1981. Bioavailability of cadmium in rats fed various diets. Arch Toxicol. 47:63-66. Rahola , T., R-K Aaran, and J.K. Miettenen. 1973. Retention and elimination of 115mCd in man. In Health Physics Problem in Internal Contamination. Budapest: Akademia 213-128. Reeves, P.G., and R.L. Chaney. 2002. Nutritional status affects the absorption and whole-body and organ retention of cadmium in rats fed rice-based diets. Environ. Sci. Technol. 36:2684-2692. Reeves, P.G., and R.L. Chaney. 2004. Marginal nutritional status of zinc, iron, and calcium increases cadmium retention in the duodenum and other organs of rats fed rice-based diets. Environ. Res. 96:311-322. Rimbach, G., J. Pallauf, K. Brandt, and E. Most. 1995. Effect of phytic acid and microbial phytase on Cd accumulation, zinc status, and apparent absorption of Ca, P, Mg, Fe, Zn, Cu, and Mn in growing rats. Ann. Nutr. Metab. 39:361-370. Roels, H.A., R.R. Lauwerys, J.P. Buchet, and A. Bernard. 1981. Environmental exposure to cadmium and renal function of aged women in three areas of Belgium. Environ. Res. 24:117-130. Rohr, G., and M. Bauchinger. 1976. Chromosome analyses in cell cultures of the Chinese hamster after application of cadmiumsulphate. Mutat. Res. 40:125-130.

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 Ruoff, W.L., G.L. Diamond, S.F. Velazquez, W.M. Stiteler, and D.J. Gefell. 1994. Bioavailability of cadmium in food and water: A case study on the derivation of relative bioavailability factors for inorganics and their relevance to the reference dose. Regul. Toxicol. Pharmacol. 20:139-160. Ryan, P.B., N. Huet, and D.L. MacIntosh. 2000. Longitudinal investigation of exposure to arsenic, cadmium, and lead in drinking water. Environ. Health Perspect. 108:731-735. Sakata, S., K. Iwami, Y. Enoki, H. Kohzuki, S. Shimizu, M. Matsuda, and T. Moriyama. 1988. Effects of cadmium on in vitro and in vivo erythropoiesis: erythroid progenitor cells (CFU-E), iron, and erythropoietin in cadmium-induced iron deficiency anemia. Exp. Hematol. 16:581-587. Salvatori, F., C.B. Talassi, S.A. Salzgeber, H.S. Spinosa, and M.M. Bernardi. 2004. Embryotoxic and long-term effects of cadmium exposure during embryogenesis in rats. Neurotoxicol. Teratol. 26:673-680. Saplakoglu, U., and M. Iscan. 1998. Sister chromatid exchanges in human lymphocytes treated in vitro with cadmium in G(o) and S phase of their cell cycles. Mutat. Res. 412:109-114. Sasser, L.B., and G.E. Jarboe. 1977. Intestinal absorption and retention of cadmium in neonatal rat. Toxicol. Appl. Pharmacol. 41:423-431. Satarug, S., M.R. Haswell-Elkins, and M.R. Moore. 2000. Safe levels of cadmium intake to prevent renal toxicity in human subjects. Br. J. Nutr. 84:791-802. Satarug, S., P. Ujjin, Y. Vanavanitkun, J.R. Baker, and M.R. Moore. 2004. Influence of body iron store status and cigarette smoking on cadmium body burden of healthy Thai women and men. Toxicol. Lett. 148:177-185. Saxena, D.K., R.C. Murthy, C. Singh, and S.V. Chandra. 1989. Zinc protects testicular injury induced by concurrent exposure to cadmium and lead in rats. Res. Commun. Chem. Pathol. Pharmacol. 64:317-329. Schafer, L., O. Andersen, and J.B. Nielsen. 1986. Effects of dietary factors on g.i. Cd absorption in mice. Acta Pharmacol. Toxicol. (Copenh.) 59(Suppl. 7):549-552. Schroeder, H.A., J.J Balassa, and W.H. Vinton, Jr. 1965. Chromium, cadmium and lead in rats: Effects on life span, tumors and tissue levels. J. Nutr. 86:51-66. Schroeder, H.A., and M. Mitchener. 1971. Toxic effects of trace elements on the reproduction of mice and rats. Arch. Environ. Health 23:102-106. Schulte, S., K. Mengel, U. Gatke, and K.D. Friedberg. 1994. No influence of cadmium on the production of specific antibodies in mice. Toxicology 93:263-268. Seth, P., M.M. Husain, P. Gupta, A. Schoneboom, B.F. Grieder, H. Mani, and R.K. Maheshwari. 2003. Early onset of virus infection and up-regulation of cytokines in mice treated with cadmium and manganese. Biometals 16:359-368. Shaikh, Z.A., and J.C. Smith. 1980. Metabolism of orally ingested cadmium in humans. Dev. Toxicol. Environ. Sci. 8:569-574.

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Spacecraft Water Exposure Guidelines: For Selected Contaminants, Volume 2 Shibutani, M., K. Mitsumori, N. Niho, S. Satoh, H. Hiratsuka, M. Satoh, M. Sumiyoshi, M. Nishijima, Y. Katsuki, J. Suzuki, J. Nakagawa, and M. Ando. 2000. Assessment of renal toxicity by analysis of regeneration of tubular epithelium in rats given low-dose cadmium chloride or cadmium-polluted rice for 22 mo. Arch. Toxicol. 74:571-577. Shigematsu, I. 1984. The epidemiological approach to cadmium pollution in Japan. Ann. Acad. Med. Singapore 13:231-236. Shimizu, M., and S. Morita. 1990. Effects of fasting on cadmium toxicity, glutathione metabolism, and metallothionein synthesis in rats. Toxicol. Appl. Pharmacol. 103:28-39. Shimizu, M., and S. Morita. 1992. Effects of feeding and fasting on hepatolobular distribution of glutathione and cadmium-induced hepatotoxicity. Toxicology 75:97-107. Shiraishi, Y. 1975. Cytogenetic studies in 12 patients with itai-itai disease. Humangenetik 27:31-44. Shiraishi, Y.H. Kurahashi, and T.H. Yoshida. 1972. Chromosomal aberrations in cultured human leukocytes induced by cadmium sulphide. Proc. Jpn. Acad. 48:133-137. Shiraishi, Y., and T.H. Yoshida. 1972. Chromosomal abnormalities in cultured leukocyte cells from itai-itai patients. Proc. Jpn. Acad. 48:248-251. Siemiatycki, J., R. Dewar, L. Nadon, and M. Gerin. 1994. Occupational risk factors for bladder cancer: Results from a case-control study in Montreal, Quebec, Canada. Am. J. Epidemiol. 140:1061-1080. Smith, S.M., and M. Heer. 2002. Calcium and bone metabolism during space flight. Nutrition 18:849-852. Smith, S. M., J.L. Nillen, A. Leblanc, A. Lipton, L.M. Demers, H.W. Lane, and C.S. Leach. 1998. Collagen cross-link excretion during space flight and bed rest. J. Clin. Endocrinol. Metab. 83:3584-3591. Smith, S.M., M.E. Wastney, B.V. Morukov, I.M. Larina, L.E. Nyquist, S.A. Abrams, E.N. Taran, C.Y. Shih, J.L. Nillen, J.E. Davis-Street, B.L. Rice, and H.W. Lane. 1999. Calcium metabolism before, during, and after a 3-month spaceflight: Kinetic and biochemical changes. Am. J. Physiol. 277:R1-10. Sorahan, T., and N.A. Esmen. 2004. Lung cancer mortality in UK nickelcadmium battery workers, 1947-2000. Occup. Environ. Med. 61:108-116. Sorahan, T., and R. Lancashire. 1994. Lung cancer findings from the NIOSH study of United States cadmium recovery workers: A cautionary note. Occup. Environ. Med. 51:139-140. Sorahan, T., and R.J. Lancashire. 1997. Lung cancer mortality in a cohort of workers employed at a cadmium recovery plant in the United States: An analysis with detailed job histories. Occup. Environ. Med. 54:194-201. Stacey, N.H., G. Craig, and L. Muller. 1988. Effects of cadmium on natural killer and killer cell functions in vivo. Environ. Res. 45:71-77. Staessen, J., and R. Lauwerys. 1993. Health effects of environmental exposure to cadmium in a population study. J. Hum. Hypertens. 7:195-199.

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