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vl Toxicity of Selected Inorganic Contaminants in Drinking Water SELECTION OF CONTAMINANTS In 1977, the Safe Drinking Water Committee examined health effects associated with microbiological, radioactive, particulate, inorganic, and organic chemical contaminants found in drinking water (National Acad- emy of Sciences, 1977~. Additional selected chemical contaminants were considered in a subsequent study (National Academy of Sciences, 1980b). The health effects of the organic and inorganic contaminants evaluated in Chapters VI and VII of this volume were selected for one or more of the following reasons: They are contaminants that have been identified in drinking water since the previous studies were conducted by the Safe Drinking Water Committee. Sufficient new data have become available to justify further attention to contaminants evaluated in the earlier studies. Several compounds were judged to be of concern because of potential spill situations. They are contamintants associated with the drinking water distribu- tion system. They are structurally related to known toxic chemicals. 152

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Toxicity of Selected Inorganic Contaminants in Drinking Water 153 ACUTE AND CHRON IC EXPOSURE The committee has evaluated the data concerning both acute and chronic exposures to selected chemicals. Information derived from studies of acute exposure provides a basis for judging health effects resulting from accidental spills of chemicals into drinking water supplies. A suggested no-adverse-response level (SNARL) for acute exposures of 24 hours or 7 days has been calculated for these compounds for which suf- ficient data were available. These values were based on the assumption that 100% of the exposure to the chemical was supplied by drinking water during either the 24-hour or 7-day period. When the chemical was a known or suspected carcinogen, the potential for carcinogenicity after acute exposure was not considered. Acute SNARL's were calculated only when there were data on human exposures or data from oral tests in animals. LD50's were not used as a basis for calculation. If no-effect levels were not known, the lowest level producing an observed effect was used with an appropriate safety factor. Some 7-day values were derived by dividing the 24-hour SNARL by 7. The converse was not done, nor were data obtained from studies of lifetime exposures used to establish acute SNARL's. The calculated acute SNARL's should not be used to estimate hazards from exposures exceeding 7 days. They are not a guarantee of absolute safety. Furthermore, SNARL's are based on exposure to a single agent and do not take into account possible interactions with other con- taminants. In all cases, the safety or uncertainty factor used in the calculations of the SNARL's reflect the degree of confidence in the data as well as the combined judgment of the committee members. As in the previous reports, the following assumptions were used when assigning an uncertainty factor to calculate either the acute or chronic SNARL's: An uncertainty (safety) factor of 10 was used when data on both human exposure and extensive chronic exposures of animals were avail- able. A factor of 100 was used when chronic and acute toxicity data were available for one or more species. A factor of 1,000 was used when the acute or chronic toxicity data were limited or incomplete. SNARL's for chronic exposure were calculated for chemicals that were not known or suspected to be carcinogens on the basis of data obtained

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154 DRINKING WATER AND HEALTH TABLE VI-1 Summation of Acute and Chronic Exposure Levels for Inorganic Chemicals Reviewed in this Chapter Suggested No-Adverse-Response Level (SNARL), mg/liter, by Exposure Perioda Chemical 24-Hour 7-Day Chronic Aluminum 35.0 5.0 Barium 6.0 4. 7 Cadmium 0.15 0.021 0.005 Chlorate 0.125 0.125 Chlorite 0.125 0.125 Chlorine dioxide 1.2 0.125 Chloramine 1.2 0.125 Strontium 8.4 aSee text for details on individual compounds. during a major portion of the lifetime of the laboratory animals. An ar- bitrary assumption was made that 20% of the intake of the chemical of concern was derived from drinking water. Therefore, it would be inap- propriate to use these values as though they were maximum contaminant intakes. Table VI-1 summarizes the acute and chronic SNARL's for the inorganic chemicals reviewed in this chapter. The 1977 Amendments to the Safe Drinking Water Act of 1974 (PL 93- 523) authorized the committee to revise the earlier studies to reflect "new information which has become available since the most recent previous report [and which shall be reported to Congress each two years thereafter)." Thus, the descriptions of some contaminants in Chapters VI and VII are limited to data generated since the last three volumes of Drinking Water and Health were published. Other contaminants and their health effects are evaluated for the first time in this series of reports. This is one reason why no significance should be attached to the length of the discus- sion devoted to each contaminant. Included in this chapter is information on the toxicity of several metallic ions associated generally with drinking water distribution systems. Other contaminants, such as barium, lead, and strontium, pose problems only in certain local areas. The chlorine derivatives were evaluated because of their possible use as alternatives to chlorine in the disinfection of drinking water.

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Toxicity of Selected Inorganic Contaminants in Drinking Water 155 Recently, the EPA Criteria and Standards Division of the Office of Water Planning and Standards released a series of documents on Ambient Water Quality Criteria. Although the committee does not endorse all of the conclusions (e.g., numerical criterion formulations) reached in those documents it does believe that they are a valuable source of general tox- icological information. Several of the contamintants that are examined in Chapters VI and VII of this report were previously evaluated in one of these criteria documents. This committee agrees with the following statement from Drinking Water and Health, Volume 3 (National Academy of Sciences, 1980, p. 68~: It was the belief of this subcommittee that it could perform a more valuable service to the Environmental Protection Agency (EPA) in the future if it evaluated criteria documents that were prepared by the EPA or other groups contracted to conduct these tasks. It will be necessary for the EPA to develop a mechanism for a com- prehensive search and review of the literature in order to make in-depth hazard assessments for these chemicals. It is the consensus of this subcommittee that this cannot be done appropriately by the National Academy of Sciences because time and staff requirements far exceed those available. Neither can it be expected that the scientists who donate their services on these subcommittees will have the resources or time to carry out the routine aspects of this task. In keeping with this philosophy, the committee drew heavily from criteria documents when one had already been prepared for the contami- nant being studied. In such cases, the document was reviewed for ac- curacy and updated when additional information was available. For some of the contaminants reviewed here, appropriate parts of the criteria documents were condensed and included in the final report. The committee commends the EPA for making this valuable material available for study and evaluation. It hopes that future committees with a similar mission will have the opportunity to review documents of this type prior to their general release. Because of the tremendous volume of data to evaluate for the hundreds of potential drinking water contaminants, this type of collaboration is beneficial to all concerned. Aluminum (Al) Aluminum, a silver-white, malleable, and ductile metal, is the third most abundant element in the earth's crust, comprising 8.3% of its volume. In nature, it is generally found in a combined state with various silicates, the most important of which are bauxite and cryolite (Norseth, 1979~. The world production of aluminum in 1974 was estimated to be approx- imately 14 million tons (Norseth, 1979~. There are more than 4,000 ter

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156 DRINKING WATER AND HEALTH minal uses of this element in such fields as electrical engineering and the transport and air traffic industries and in such products as building materials, home furnishings, kitchen appliances, farm implements, con- tainers for packaging material, and building structures. In powder form, aluminum is a component of paints, pigments, missile fuel, and chemical explosives. Medicinally, aluminum and its salts are used in antacids, an- tidiarrheals, and protective dermatological pastes. It is also found in cosmetics and deodorants. Aluminum compounds are applied in the pro- cessing, packaging, and preservation of foods. It is also used to line water storage vessels and in the purification of drinking water (Gilman et al., 1980; Norseth, 1979; Sorenson et al., 1974~. Concentrations of aluminum in soils vats widely, and its solubility is determined by pH. Concentrations of aluminum in water also vary. Since large amounts (> 100 ,ug/ml) occur only when the pH is less than 5, the concentration of aluminum in most natural waters is negligible (Sorenson et al., 1974~. In analyses of 1,577 U.S. water samples, Kopp and Korner (1970) found 456 samples positive for aluminum. Concentrations of soluble aluminum were as high as 2.76 ,ug/ml (mean, 0.074~. Aluminum compounds such as aluminum sulfate and potash aluminum and certain aluminum-bearing minerals are commonly used as major coagulants in the treatment of drinking water supplies. The principal coagulants are aluminum sulfate and potash aluminum. Aluminum sulfate is the principal coagulant and bentonite is a coagulating aid. Aluminum ammonium sulfate is used as a dechlorinating agent (Sorenson et al., 1974~. Sodium aluminate is added sometimes to remove fine turbidity. In modern purification practice, aluminum-based coagulants usually result in the presence of lower concentrations of aluminum in the drinking water than in the raw water (Sorenson et al.' 19741. The major sources of aluminum in the normal human diet include plants and processed foods (Crapper and DeBoni, 1980~. The concentrations in foods and beverages vary widely, depending upon the product, the type of processing, and the geographical areas in which the plants are raised (Sorenson et al., 19741. The daily intake of aluminum has been estimated in several studies. In general, the data pertaining to natural dietary intake indicate that concen- trations range from approximately 10 to 50 mg/day (Sorenson et al., 1974~. The use of aluminum in the processing and storing of food increases the aluminum content, but not enough to contribute significantly either to total body burden or the toxic effects (Norseth, 1979; Underwood, 1971~. In general, aluminum has largely been regarded as nontoxic. Neither the international nor the European standards for drinking water (World Health Organization 1970, 1973) lists aluminum among those substances for which

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Toxicity of Selected Inorganic Contaminants in Drinking Water 157 limits are specified. The National Academy of Sciences' Committee on Water Quality Criteria recommended the following maximum concentra- tions of aluminum in agricultural and irrigation waters: 5.0 ,ug/ml for waters used continuously on all soil and 20 ,ug/ml for waters used not more than 20 years on fine textured neutral to alkaline soils (National Academy of Sciences, 1973~. Although the question of the essentiality of aluminum for biological func- tion was raised as early as 1915, its function remains unknown (Sorenson et al., 1974~. Failure to demonstrate this essentiality probably results from the difficulty of finding a diet that is deficient in the metal (Norseth, 1979; Underwood, 1971~. METAB OLISM The dynamics of absorption, distribution, and excretion of aluminum are poorly understood. Furthermore, little is known about its metabolism or the factors that determine burdens of aluminum in specific tissues. This is par- tially due to a lack of detection methodology and the universal contamina- tion of laboratory reagents and chemicals with the metal (Crapper and DeBoni, 1980; Norseth, 1979; Sorenson et al., 1974~. The human body burden of aluminum is estimated to range from 50 to 150 ma, most soft tissues containing approximately 0.2 to 0.6 Agog (Underwood, 1971~. Contrary to former opinion, studies by Kaehuy et al. (1977a) have shown that aluminum is readily absorbed from the gastrointestinal tract by normal persons who consume one of several aluminum salts (e.g., hydroxide or car- bonate) or dihydroxy aluminum aminoacetate, but not aluminum phosphate. In earlier studies, Clarkson et al. (1972) found a net gastrointestinal absorption of aluminum ranging from 100 to 568 mg/day in dialysis patients taking antacids containing 2 to 3.4 mg of aluminum daily for 20 to 32 days. In another study, Cam et al. (1976) studied the absorption of aluminum in both normal patients and patients suffering from chronic renal failure. Both groups of patients received approximately 2.5 g of aluminum daily for 23 to 27 days. In the normal group, the maximum ab- sorption of aluminum was approximately 97 mg/day, while in the renal failure patients it was 256 mg/day. In balance studies conducted by Gorsky et al. (1979), the aluminum balance was usually negative in those patients receiving less than 5 mg of aluminum per day. However, when the diet was supplemented with antacids that contributed from 1 to 3 g of aluminum daily, an average positive balance of 23 to 313 mg of aluminum per day was observed over an 18- to 30-day period. Studies by Mayor et al. (1977a,b) strongly suggest that aluminum in the gastrointestinal tract and its subsequent distribution in tissue can be in

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158 DRINKING WATER AND HEALTH fluenced by increasing the concentration of parathyroid hormone (PTH). They fed male rats aluminum as 0.1 To of their diet for 2S days. The ready absorption of aluminum from the gastrointestinal tract of these normal rats was enhanced by injections of PTH (17 U twice weekly). There was also increased deposition of the metal in the kidney, muscle, bone, and the gray matter of the brain, but not in the liver or in the white matter of the brain. Thus, the PTH exerted a specific effect on the absorption and distribution of aluminum. In 1977, these same investigators had found a positive correlation between increased serum PTH and serum aluminum levels in dialysis patients. The increase in serum PTH in these patients had been reported earlier by Kleeman and Better (1973~. In patients on dialysis, there are apparently two sources of extraneous aluminum: via the gastrointestinal tract from aluminum antacids, which are used to bind phosphate, and via the dialysate solution. Kaehny et al. (1977b) have shown that aluminum can also be transferred across the dialysis membranes. This transfer can occur even if the levels of aluminum in plasma are much higher than the levels of aluminum in the dialysate solution. Thus, aluminum has been shown to accumulate in the serum and in the tissues of chronic renal failure patients either after ab- sorption from the gastrointestinal tract or from parenteral administration during dialysis with a solution that contains aluminum. Following absorption or parenteral administration, aluminum dis- tributes to nearly all of the organs including the brain (Crapper and DeBoni, 1980; Norseth, 1979; Sorenson et al., 19741. Lundin et al. (1978) have found that approximately 50% of the aluminum in the plasma of normal humans is bound to protein with a molecular weight greater than 8,000. The major route of excretion of aluminum in humans appears to be the bile. Only a small amount is excreted via the urine (Gorsky et al.' 1979~. Parenteral administration of aluminum to laboratory animals increases urinary excretion (Norseth, 19791. HEALTH ASPECTS Since aluminum constitutes a substantial portion of the earth's crust and atmosphere and is a common contaminant in food and drinking water, environmental exposure is virtually universal (Bland. 1979; Goetz and Klawans, 1979; Sorenson et al., 1974~. Its extensive uses in cosmetics. such as aluminum hexahydrate (aluminum chloride) in deodorants, and in medicines also provide opportunities for exposure of humans. In its predominant medical application it serves as an antacid to control gastric hyperacidity. Aluminum hydroxide is generally used for this purpose. In

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Toxicity of Selected Inorganic Contaminants in Drinking Water 159 addition, aluminum is frequently combined with a magnesium-containing compound to prevent constipation (Sorenson et al., 1974~. Aluminum hydroxide antacids are administered orally in large doses (5-10 g/day) in renal-failure patients to limit the accumulation of phos- phate (hyperphosphatemia) and the consequent development of meta- static calcifications. The treatment induces phosphate loss by stopping the adsorbability of phosphate in the gastrointestinal tract (Mallick and Berlyne, 1968~. In general, aluminum has been considered to be nontoxic (Sorenson et al., 1974~. However, toxic syndromes have been observed in animals in- jected with the element (Sorenson et al., 1974~. There is also a good deal of interest in the role of aluminum in various syndromes of the central ner- vous system in humans. Recent studies indicate that it may be selectively toxic to certain neurons in the central nervous system (Crapper and DeBoni, 1980; Goetz and Klawans, 1980; Norseth, 19791. Observations in Humans Recently reported adverse effects of aluminum in humans have resulted from inhalation or ingestion of aluminum in concentrations many times greater than the amounts present in normal circumstances. Following large oral doses of aluminum, toxic syndromes involve gastrointestinal tract irritation and, eventually, interference with phosphate absorption, which results in rickets (Casarett and Doull, 19771. Industrial exposure to high concentrations of aluminum-containing airborne dusts has resulted in a number of cases of occupational pneumoconiosis (Norseth, 1979; Sorenson et al., 19741. Most of these exposures were chronic, and other substances were involved in nearly all instances. For example, an asthma- like disease has been reported in workers engaged in the production of aluminum from its oxide. This condition may result from the hydrogen fluoride that evolves from the use of fluorine-bearing materials in the pro- duction of metallic aluminum (Sorenson et al., 1974~. Silicosis, alumi- nosis, aluminum lung, and bauxite pneumoconiosis are the result of pul- monary fibrotic reactions to silica and aluminum-containing compounds' which have been observed in the lung tissue in humans (Sorenson et al.' 1974~. Paradoxically, aluminum powder has been used in the prevention and therapy of silicosis. The rationale is that small amounts of metallic aluminum inhibit the solubility of siliceous materials in the lungs or diminish their fibrogenic properties (Casarett and Doull, 1977; Denny et al., 1939~. There is no unequivocable evidence that the procedure is clini- cally effective (Sorenson et al., 1974~. In one of the earliest cases reported by McLaughlin et al. (1962), an

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160 DRINKING WATER kND HEALTH aluminum-ball-mill worker died with encephalopathy and pulmonary fibrosis. After having been exposed to aluminum-containing compounds more than 13 years, the concentration of aluminum in his brain was 20 times greater than that in the brains of controls. In more recent studies, aluminum deposition in the brain has been implicated as an etiologic factor in two necrologic disorders: Alzheimer's disease and chronic renal failure accompanied by senile dementia (Alfrey et al., 1976; Crapper et al., 1973~. Nonetheless, the importance of aluminum as a pathogenic factor in human disease has not yet been established (Crapper and DeBoni, 1980~. Alzheimer's disease usually occurs in humans after the age of 40. It is a slowly progressive, fatal encephalopathy associated with behavioral altera- tions, memoir disturbances, special disorientation, agnosia, dysphasia, and seizures (Crapper and Dalton, 1973a,b; Crapper and DeBoni, 1980~. The role of aluminum as an etiologic agent in Alzheimer's disease rests on circumstantial evidence such as the resemblance between aluminum- induced neurofilamentous aggregates and human neurofibrillar tangles that characterize Alzheimer's disease and senile dementia (Goetz and Klawans, 1980; Klatzo et al., 1965; Terry, 1963~. However, there are im- portant differences between the morphological changes induced in ani- mals by aluminum and those observed in humans with Alzheimer's dis- ease (Crapper and DeBoni, 1980~. Additional circumstantial evidence has been provided by studies of Crapper et al. (1976), who reported elevated aluminum levels in some regions of the brains of patients who had died from Alzheimer's disease. For example, in 28% of the 585 brain regions sampled, aluminum levels exceeded 4 ,ug/g the minimum concentration of metal associated with neurofibrillar degeneration in cats observed in the same laboratory (Crapper et al., 1973~. Trapp et al. (1978) also reported increased aluminum levels in patients who had died from Alz- heimer's disease. However, McDermott et al. (1978) did not find any sig- nificant differences in aluminum levels in brain samples taken from patients suffering from Alzheimer's disease and healthy, age-matched controls. Before aluminum is assigned a role in Alzheimer's disease, further investi- gations must be undertaken (Crapper and DeBoni, 198l)~. Another encephalopathic syndrome in which aluminum has been sug- gested as an etiologic agent has been described as "dialysis enceph- alopathy" or "dialysis dementia," which is a relentlessly progressive form of dementia observed in chronic dialysis patients (AIfrey et al., 1976; Anonymous, 1976; Elliott et al., 1978; Goetz and Klawans, 1979~. This disorder is characterized by an insidious onset of altered behavior, speech disturbances, dyspraxia, tremor, myoclonus, convulsions, personality changes, and psychoses. This syndrome, which results in death within ap- proximately 6 to 7 months (Alfrey et al., 1976; Bland, 1979; Crapper and

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Toxicity of Selected Inorganic Contaminants in Drinking Water 161 DeBoni, 1980), has been reported to be the leading cause of death in long- term dialysis patients (Crapper and DeBoni, 1980; Goetz and Klawans, 1979~. The majority of the patients in whom this syndrome developed had been on intermittent hemodialysis for 3 to 7 years before the onset of symptoms. All had routinely received aluminum-containing antacids for the purpose of binding gastrointestinal phosphates for at least 2 years. The possible hazard of aluminum intoxication in dialysis patients was first described by Berlyne et al. (1970~. Subsequent studies by Alfrey et al. ~ 1976) showed that patients dying of the syndrome had significantly higher tissue concentrations of aluminum in their bones, skeletal muscles, and gray matter of the brain. These authors reported that the aluminum concentrations in the gray matter of the brain were approximately 4 times higher in these patients than in any other group. The source of aluminum was not limited to the antacids given to these patients, but was contained in the water used to prepare the dialysate solution as well (Alfrey et al., 1976; Crapper and DeBoni, 1980; Elliott et al., 1978~. Because only a few of the dialysis patients taking large doses of aluminum-containing antacids develop the syndrome. it has been sug- gested that the syndrome may be related to aluminum contamination of the water used for dialysis. One outbreak occurring in Chicago between September 1972 and January 1976 affected 20 patients who had been maintained on long-term hemodialysis (Dunea et al., 1978~. It was later established that the city's adoption of a water purification method using pure aluminum sulfate resulted in higher concentrations of aluminum in the water. The relation- ships of the onset of the dementia to documentations of aluminum in the water and changes in water treatment are shown in Figure VI-1. The first cases of dementia appeared in September 1972, 3 months after the change in water treatment. They coincided with a peak water concentration of aluminum in the water (360 ,ug/liter). Thirteen patients became demented between September 1973 and August 1974, the later cases ap- pearing during the winters of 1974- 1975 and 1975- 1976, shortly after addi- tional peaks in aluminum concentrations in the water. Before the method of water treatment was changed, aluminum concentrations varied from 0 to 150 ~Ag/liter. After the change, concentrations of aluminum were higher, peaking between 300 and 400 ,ug/liter. The other constituents of the water were not significantly altered. Studies by Elliot et al. (1978~. Flendrig et al. (1976), and Ward et al. (1978) also suggest that high concentrations of aluminum in dialysate are important etiologic factors in outbreaks of the dialysis dementia syndrome. Dialysis patients often exhibit multiple osteomalacic fractures and myopathic changes, mostly in the proximal muscles (Flendrig et al., 1976;

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400 300 - At ~ 200 a: G 1 00 o L 6 1971 12 6 1 972 1 ~ 12 6 1973 162 DRINKING WATER AND HEALTH ~ Alarm Purif icat~o;;~ A ~ ~ I iA~ 1 12 6 12 6 12 G 12 1974 1975 1976 YEAR _ 2 11 6 O FIGURE VI-1 Relationship between changes in water treatment and dialysis dementia: ~ = period of aluminum sulfate purification; = cater aluminum levels; * * = installation of deionizers at the too hospitals; dementia. Pierides, 1978; Platts et al., 1977~. The clinical features of this syndrome in- clude progressive skeletal pain. proximal muscle weakness, and spon- taneous fractures affecting primarily the ribs, pelvic rami, femoral necks, metatarsals, and other parts of the peripheral skeleton (Pierides, 1978~. The skeletal demineralization may result from the binding of gastrointestinal phosphate by aluminum, leading to a decrease in phosphate absorption, decreased urinary phosphate levels, and an increase in urinary calcium (Spencer and Lender, 19791. In a second interaction, aluminum in the gut also binds with fluoride, thereby decreasing fluoride absorption (Spencer et al., 1979~. This may further contribute to the skeletal demineralization, since fluoride might play a role in the maintenance of normal bone structure. = new cases of dialysis The major etiologic factor associated with this syndrome is untreated aluminum-rich tap water that is used to prepare the dialysis fluid. Aluminum is known to accumulate in the serum and tissues of chronic renal failure patients either after it is absorbed from the gastrointestinal tract (Alfrey et al., 1976) or after parenteral administration of a dialysis fluid containing a high concentration of aluminum (Elliott et al., 1978; Kaehny et al., 1977b). Interestingly, although many chronic renal failure patients consume large amounts of aluminum-containing antacids, this

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Toxicity of Selected Inorganic Contaminants in Drinking Water 191 panted by a marked reduction in bone ash, elevated magnesium and potassium levels, and a depressed calcium content in bone. Mechanism studies by Omdahl and DeLuca (1971, 1972) indicate that the bone aberrations result from an inhibition of calcium absorption by dietary strontium as a result of a block in the renal synthesis of 1,25-dihydroxycholecalciferol from 25-hydroxycholecalciferol (Omdahl and DeLuca. 1971, 1972~. In 90-day studies, Kroes et al. (1977) fed male and female Wistar rats strontium in strontium chloride at 75, 300, 1,200, and 4,800 mg,'kg diet. They did not find any changes in behavior, growth, food intake, or food efficiency, but observed minor changes in hematology and blood chemistry at the highest dose. In the female rats given the highest dose, the glycogen content of the liver was decreased at 12 weeks. Thyroid weights were increased in males in the 1,200 and 4,800 mg/kg groups. Forbes and Mitchell ( 1957) fed adult male and weanling male and female rats strontium in the diet at levels of 10, 30, 100, and 1,000 mg/kg for 8 weeks. They found no differences in food intake, weight gain, total bone ash, calcium and phosphorus composition of the bone ash, or other signs of toxicity in the strontium-fed rats. Mutagenicity Loeb et al. (1977) using an i''-vitro assay to measure the fidelity of DNA synthesis, observed no effects from strontium added in vitro. Carcinogenicity No data available for evaluation. Teratogenicity No data available for evaluation. CONCLUSIONS AND RECOMMENDATIONS The chemical toxicity of the stable isotopes of strontium is considered to be quite low. Although Dawson (1974) suggested that strontium in potable water should not exceed 10 mg/liter based on LDSo data, he evaluated this calculation as having the "lowest level of reliability." Suggested No-Adverse-Response Level {SNARLJ 24-Hour Exposure There are no data from which to calculate the 24-hour SNARL for strontium. However, based on the 90-day study of Kroes et al. (1977), the 24-hour exposure level would be at least 8.4 mg/liter.

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192 DRINKING WATER AND HEALTH 7-Day Exposure Using the data of Kroes et al. (1977), who found the no-effect level of strontium to be 3~)0 mg/kg after 90 days of exposure in the diet, and assuming that the rats consumed 20 g of food daily and that their average weight was 250 g, one may calculate the daily exposure level as: 300 mg/kg/day X 0.02 kg/day = 24 mucky 0 25 k -~ ~~~-~ ~~-~ O O Using a safety factor of 100 and assuming that a 70-kg human con- sumes 2 liters of water per day, and that 100% of exposure is from water during this period, one may calculate the 7-day SNARL as: 24mg/kg X70 kg 84 /li tion. Chronic Exposure There are no data from which to make this calcula Sulfate (S04) Sulfate was reviewed in the first volume of Drinking Water and Health (National Academy of Sciences, 1977~. The no-adverse-health-effect level recommended at that time was 500 mg/liter, whereas the taste threshold may be as low as 200 mg/liter. No additional data pertaining to the effects of inorganic sulfates have been reported since that report was published. REFERENCES Abdel-Rahman, M.S, and D. Couri. 1980. Toxicity of chlorine dioxide in drinking water. P. A-29, No. 86 in Abstracts of Papers, Society of Toxicology. Nineteenth Annual Meeting, March 9-13. Washington, D.C. Abdel-Rahman, M.S., D. Couri, and J.D. Jones. 1980a. Chlorine dioxide metabolism in rat. J. Environ. Pathol. Toxicol. 3:421-430. Abdel-Rahman, M.S., D. Couri, and R.J. Bull. 1980b. Kinetics of CIO2, and effects of CIO2, ClO2-, and C103- in drinking water and blood glutathione and hemolysis in rat and chicken. J. Environ. Pathol. Toxicol. 3:431-449. Alfrey, A.C., G. R. LeGendre, and W.D. Kaehny. 1976. The dialysis encephalopathy syn- drome. Possible aluminum intoxication. N. Engl. J. Med. 294:184-188. Angle, C.R., M.S. Mclntire, and G. Brunk. 1977. Effect of anemia on blood and tissue lead in rats. J. Toxicol. Environ. Health 3:557-563. American Conference of Governmental industrial Hygienists. 1980. Threshold limit values for chemical substances and physical agents in the workroom environment with intended

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