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OCR for page 152
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
OCR for page 153
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
OCR for page 157
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;
OCR for page 162
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.
OCR for page 192
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
OCR for page 193
Toxicity of Selected Inorganic Contaminants in Drinking Water 193
changes for 1980. American Conference of Governmental Industrial Hygienists, Cincin-
nati, Ohio. 93 pp.
Anonymous. 1976. Dialysis dementia: Aluminium again? Lancet 1:349.
Arena, J. M. 1963. Poisoning: Chemistry-Symptoms-Treatments. Charles C Thomas,
Baltimore, Md. 440 pp.
Becker, T., E. Markgraf, H. Oswald, B. Sachyra, and K. Winnefeld. 1967. Behavior of
metallic foreign bodies in animals. Pp. 1722-1727 in Th. Matthes, ed. Wissenschaftliche
Chirurgen-Tagung der Deutschen Demokratischen Republik mit Internationaler
Beteiligung, 6th, Berlin, 1966, volume 2, Barth, Leipzig. [Chem. Absts. 70:076383t,
1969.]
Beliles, R.P. 1979. The lesser metals: Strontium. Pp. 556-557 in F.W. Oehme, ed. Toxicity
of Heavy Metals in the Environment. Part 2. Marcel Dekker, New York.
Benes, V. 1978. Toxicological aspects of the water we drink. Pp. 35-45 in G.L. Plaa and
W.A.M. Duncan, eds. Proceedings of the First International Congress on Toxicology.
Toxicology as a Predictive Science. Academic Press, New York.
Berlyne, G.M., J. Ben-Ari, D. Pest, J. Weinberger, M. Stern, G.R. Gilmore, and R. Levine.
1970. Hyperaluminemia from aluminum resins in renal failure. Lancet 2:494-496.
Berlyne, G.M., J. Ben-Ari, E. Knopf, R. Yagil, G. Weinberger, and G.M. Danovitch. 1972.
Aluminium toxicity in rats. Lancet 1:564-568.
Bianchine, J.R., J.R. Lubbers, S. Chavhan, and J. Miller. 1980. The safety study of chlorine
dioxide and its metabolites in man. Summa~y Report. Grant No. 805643. Submitted to
U.S. Environmental Protection Agency, Cincinnati, Ohio.
Bienvenu, P., C. Nofre, and A. Cier. 1963. [In French] Toxicite generale comparee des ions
metalliques. Relation avec la classification periodique. C.R. Acad. Sci. 256:1043-1044.
Bland, J. 1979. Trace elements in human health and disease: IV. Influence of trace elements
on development and as environmental toxicants. Osteopath. Med. 4(10):105-108,
110-111, 113.
Bornschein, R., D. Pearson, and L. Reiter. 1980. Behavioral effects of moderate lead ex-
posure in children and animal models: Part 1, Clinical studies. Crit. Rev. Toxicol.
8:43-99.
Boyle, R.W. 1968. Geochemistry of silver and its deposits with notes on geochemical pros-
pecting for the element. Geol. Surv. Can., Bull. No. 160.264 pp. [Chem. Absts. 71:5300y,
1969.1
Brenniman, G.R., T. Namekata, W.H. Kojola, B.W. Carnow, and P.S. Levy. 1979. Car-
diovascular disease death rates in communities w*h elevated levels of barium in drinking
water. Environ. Res. 20:318-324.
Brenniman, G.R., W.H. Kojola, P.S. Levy, B.W. Carnow, and T. Namekata. 1981. High
barium levels in public drinking water and its association with elevated blood pressure.
Arch. Environ. Health 36(1):28-32.
Browning, E., ed. 1969. Toxicity of Industrial Metals. Second edition. Appleton-Century-
Crofts, New York.
Buchet, J. P., H. Roels, and R. Lauwerys. 1978. Influence of sex honnones on free
erythrocyte protoporphyrin response to lead in rats. Toxicology 9:361-369.
Cabe, P.A., N.G. Carmichael, and H.A. Tilson. 1979. Effects of selenium, alone and in
combination with silver or arsenic, in rats. Neurobehav. Toxicol. 1:275-278. [Chem.
Absts. 92:192218w, 1980.]
Calabrese, E.J., G.S. Moore, R.W. Tuthill, and T. L. Sieger, eds. 1980. Drinking Water
and Cardiovascular Disease. Pathotox Publishers, Inc., Park Forest South, Illinois.
Cam, J.M., V.A. Luck, J.B. Eastwood, and H.E. De Wardener. 1976. The effect of
OCR for page 194
194 DRINKING WATER AND HEALTH
aluminum hydroxide orally on calcium, phosphorus and aluminum metabolism in normal
subjects. Clin. Sci. Mol. Med. 51:407-414.
Casarett. L.J., and J. Doull, eds. 1977. Toxicology-The Basic Science of Poisons. Mac-
millan Publishing Co.. Inc.' New York.
Chen. P.S., Jr.. A.R. Terepka, and H.C. Hodge. 1961. The pharmacology and toxicology of
the bone seekers. Annul Rev. Pharmacol. 1:369-396.
Christensen, H.E.. ed. 1971. Toxic Substances Annual List. 1971. U.S. National Institute
for Occupational Safety and Health. Rockville. Md. 512 pp.
Clark, J.B. 1953. The mutagenic action of various chemicals on Micrococcus pvogenes var.
aureus. Proc. Okla. Acad. Sci. 34:114-118. [Chem. Absts. 49:8373f, 1955.]
Clarkson. E.M., V.A. Luck, W.V. Hynson. R.R. Bailey, J.B. Eastwood, J.S. Woodhead,
V.R. Clements, J.L.H. O'Riordan, and H.E. De Wardener. 1972. The effects of
aluminium hydroxide on calcium phosphorus and aluminium balances, the serum
parathyroid hormone concentration and the aluminium content of bone in patients with
chronic renal failure. Clin. Sci. 43:519-531.
Committee II on Permissible Dose for Internal Radiation. 1960. International Commission
on Radiological Protection. Health Phys. 3:1-380.
Couri, D., and M.S. Abdel-Rahman. 1979. Effect of chlorine dioxide and metabolites on
glutathione dependent system in rat, mouse and chicken blood. J. Environ. Pathol. Tox-
icol. 3:451-460.
Crapper, D.R. 1973. Experimental neurofibrillary degeneration and altered electrical activ-
ity. Electroencephalogr. Clin. Neurophysiol. 35:575-588.
Crapper, D.R.. and A.J. Dalton. 1973a. Alterations in short-term retention, conditioned
avoidance response acquisition and motivation following aluminum induced
neurofibrillary degeneration. Physiol. Behav. 10:925-933.
Crapper, D.R., and A.J. Dalton. 1973b. Aluminum induced neurofibrillary degeneration,
brain electrical activity and alterations and acquisition and retention. Physiol. Behav.
10:935-945.
Crapper. D.R., and U. DeBoni. 1980. Aluminum. Pp. 326-335 in P.S. Spencer and H.H.
Schaumburg, eds. Experimental and Clinical Neurotoxicology. Williams & Wilkins,
Baltimore, Md.
Crapper, D.R., S. S. Krishnan, and A.J. Dalton. 1973. Aluminum distribution in
Alzheimer's disease and mental neurofibrillary degeneration. Science 180:511-513.
Crapper, D. R. , S.S. Krishnan, and S. Quittkat. 1976. Aluminium, neurofibrillary
degeneration and Alzheimer's disease. Brain 99:67-80.
Cuddihy, R.G., and J.A. Ozog. 1973. Nasal absorption of CsCI2, SrCI2, BaCI2, and CeCI3 in
Syrian hamsters. Health Phys. 25:219-224.
Dawson, G.W. 1974. The Chemical Toxicity of Elements. Report Prepared for the U.S.
Atomic Energy Commission under Contract AT(45-1):1830. Battelle. Pacific Northwest
Laboratories, Richland, Wash. 25 pp. [BNWL-1815, UC-70.]
DeBoni, U., A. Otvos, J.W. Scott, and D.R. Crapper. 1976. Neurofibrillary degeneration in-
duced by systemic aluminum. Acta Neuropathol. 35:285-294.
Decker. L. E., R. U. Byerrum, C. F. Decker, C. A. Hoppert, and R. F. Langham. 1958.
Chronic toxicity studies. 1. Cadmium administered in drinking water to rats. AMA Arch.
Ind. Health 18:228-231.
Deknudt, Gh., and G.B. Gerber. 1979. Chromosomal aberrations in bone-marrow cells of
mice given a normal or a calcium-deficient diet supplemented with various heavy metals.
Mutat. Res. 68:163-168.
Demerec, M., G. Bertani, and J. Flint. 1951. A survey of chemicals for mutagenic action on
E. coli. Am. Nat. 85:119-136.
OCR for page 195
Toxicity of Selected Inorganic Contaminants in Drinking Water 195
Denny. J.J., W.D. Rob son, and D.A. Irwin. 1939. The prevention of silicosis by metalic
aluminum. II. Can. Med. Assoc. J. 40:213-228.
Dipaolo, J.A., and B.C. Casto. 1979. Quantitative studies of i'' vitro' morphological transfor-
mation of Syrian hamster cells by inorganic metal salts. Cancer Res. 39:1008-1013.
Dunea, G., S.D. Mahurkar. B. Mamdani. and E.C. Smith. 1978. Role of aluminum in
dialysis dementia. Ann. Intern. Med. 88:502-504.
Durfor, C.N.. and E. Becker. eds. 1962. Public Water Supplies of the 100 Largest Cities in
the United States, 1962. U.S. Department of the Interior, Geological Survey Water-
Supply Paper 1812. Washington, D.C. 364 pp.
Elliott, H.L., F. Dryburgh, G.S. Fell, S. Sabet. and A.I. MacDougall. 1978. Aluminium
toxicity during regular haemodialysis. Br. Med. J. 1:1101-1103.
Flendrig, J.A., H. Kruis, and H.A. Das. 1976. Aluminium intoxication: The cause of
dialysis dementia? Pp. 355-363 in B.H.B. Robinson, ed. Dialysis, Transplantation.
Nephrology. Proceedings of the Thirteenth Congress of the European Dialysis and
Transplant Association, held in Hamburg. Germany. 1976. Pitman Medical Publishing
Co.. Tunbridge Wells, England.
Follis, R.H., Jr. 1955. Bone changes resulting from parenteral strontium administration.
Fed. Proc. Am. Soc. Exp. Pathol. 14:403, Abstr. No. 1301.
Forbes. R.M., and H.H. Mitchell. 1957. Accumulation of dieta~ boron and strontium in
young and adult albino rats. Arch. Ind. Health. 16:489-492.
Friberg, L., M. Piscator, G.F. Nordberg, and T. Kjellstrom, eds. 1974. Cadmium in the En-
vironment. Second edition. CRC Press. Inc.. Cleveland, Ohio. 248 pp.
Furchner, J.E., C.R. Richmond, and G.A. Drake. 1968. Comparative metabolism of ra-
dionuclides in mammals. IV. Retention of silver-llOm in the mouse, rat, monkey, and
dog. Health Phys. 15:505-514.
Furst. A. 1971. Trace elements related to specific chronic diseases: Cancer. Geol. Soc. Am.,
Mem. No. 123:109-130.
Furst, A., and R.T. Haro. 1969. Survey of metal carcinogenesis. Prog. Exp. Tumor Res.
12: 102-133.
Furst, A., and M.C. Schlauder. 1977. Inactivity of two noble metals as carcinogens. J. En-
viron. Pathol. Toxicol. 1 :51-57.
Gilman, A.G., L.S. Goodman, and A. Gilman, eds. 1980. The Pharmacological Basis of
Therapeutics. Sixth edition. MacMillan, New York. 1,843 pp.
Goetz, C.G., and H.L. Klawans. 1979. Neurologic aspects of other metals. Pp. 319-345 in
P.J. Vinken and G.W. Bruyn. eds. Handbook of Clinical Neurology. Vol. 36. North-
Holland, New York.
Goodman, L.S., and A. Gilman, eds. 1975. Silver. Pp. 930-931 in The Pharmacological
Basis of Therapeutics. Fifth edition. MacMillan, New York.
Gorsky, J.E., A.A. Dietz, H. Spencer, and D. Osis. 1979. Metabolic balance of aluminum
studied in six men. Clin. Chem. 25:1739-1743.
Gosselin, R. E., H. C. Hodge, R. P. Smith, and M. N. Gleason. eds. 1976. Section III.
Therapeutics Index: Cadmium. Pp. 69-74 in Clinical Toxicology of Commercial Products:
Acute Poisoning. Fourth edition. Williams & Wilkins, Baltimore, Md.
Goyer, R.A., ed. 1974. Low Level Lead Toxicity. Environ. Health Perspect. Issue No. 7. 252
PP
Goyer, R.A., and P. Mushak. 1977. Lead toxicity. laboratory aspects. Pp. 41-77 in R.A.
Goyer and M.A. Mehlman, eds. Advances in Modern Toxicology: Toxicology of Trace
Elements. Vol. 2. John Wiley & Sons, New York.
Greathouse, D.G., G.F. Craun, and D. Worth. 1976. Epidemiologic study of the relation-
ship between lead in drinking water and blood lead levels. Pp. 9-24 in D.D. Hemphill. ed.
OCR for page 196
196 DRINKING WATER AND HEALTH
Trace Substances in Environmental Health: A Symposium. Vol. 10. University of
Missouri, Columbia, Mo.
Hammond, P. B. 1977. Exposure of humans to lead. Ann. Rev. Pharmacol. Toxicol.
17: 197-214.
Hammond, P.B., and R.P. Beliles. 1980. Metals: Lead. Pp. 415-421 in J. Doull, C.
Klaassen, and M.O. Amdur, eds. Casarett and Doull's Toxicology: The Basic Science of
Poisons. Second edition. MacMillan, New York.
Hart, M.M., and R.H. Adamson. 1971. Antitumor activity and toxicity of salts of inorganic
Group IIIa metals: Aluminum, gallium, indium, and thallium. Proc. Natl. Acad. Sci.
USA 68: 1623- 1626.
Hart, M.M, C.F. Smith, S.T. Yancey, and R.H. Adamson. 1971. Toxicity and antitumor
activity of gallium nitrate and periodically related metal salts. J. Natl. Cancer Inst.
47:1121-1127.
Heddle, J.A., and W.R. Bruce. 1977. Comparison of tests for mutagenicity of carcinogenic-
ity using assays for sperm abnormalities, formation of micronuclei, and mutations in
Salmonella. Pp. 1549-1557 in H.H. Hiatt, J.D. Watson, and J.A. Winsten, eds. Origins of
Human Cancer: Book C. Human Risk Assessment. Cold Spring Harbor Conferences on
Cell Proliferation, Vol. 4. Cold Spring Harbor Laboratory. Cold Spring Harbor, N.Y.
Heffernan, W.P., C. Guion. and R.J. Bull. 1979a. Oxidative damage to the erythrocyte in-
duced by sodium chlorite. in vivo. J. Environ. Pathol. Toxicol. 2:1487-1499.
Heffernan, W.P., C. Guion, and R.J. Bull. 1979b. Oxidative damage to the erythrocyte in-
duced by sodium chlorite; in vitro. J. Environ. Pathol. Toxicol. 2:1501-1510.
Hill, W.R., and D.M. Pillsbury. 1939. Argyria: The Pharmacology of Silver. Williams &
Wilkins, Baltimore, Md. 172 pp.
International Agency for Research on Cancer. 1972. Lead salts. Pp. 40-50 in IARC
Monographs on the Evaluation of Carcinogenic Risk of Chemicals to Man, Vol. 1. World
Health Organization/International Agency for Research on Cancer, Lyon, France.
International Commission on Radiological Protection. 1972. Alkaline earth metabolism in
adult man. ICRP Publication 20. Pergamon Press, New York.
Johnson, A.R. 1973. The influence of strontium on characteristic factors of bone. Calcif.
Tissue Res. 11:215-221.
Jones, A.M., and J.A. Bailey. 1974. Effect of silver from cloud seeding on rabbits. Water Air
Soil Pollut. 3(3):353-363.
Just, J., and A. Szniolis. 1936. Germicidal properties of silver in water. J. Am. Water Works
Assoc. 28:492-S06.
Kaehny, W.D., A.P. Hegg. and A.C. Alfrey. 1977a. Gastrointestinal absorption of
aluminum from aluminum-containing antacids. N. Engl. J. Med. 296:1389-1390.
Kaehny, W.D., A.C. Alfrey, R.E. Holman, and W. J. Shorr. 1977b. Aluminum transfer
during hemodialysis. Kidney Int. 12:361-365.
Kehoe, R.A., J. Cholak, and R.V. Story. 1940. A spectrochemical study of the normal
ranges of concentration of certain trace metals in biological materials. J. Nutr.
19:579-592.
Klatzo, I., H. Wisniewski, and E. Streicher. 1965. Experimental production of
neurofibrillary degeneration. 1. Light microscopic observations. J. Neuropathol. Exp.
Neurol. 24:187-199.
Kleeman, C.R., and O.S. Better. 1973. Disordered divalent ion metabolism in kidney
disease: Comments on pathogenesis and treatment. Kidney Int. 4:73-79.
Kopp, J.F. 1969. The occurrence of trace elements in water. Pp. S9-73 in D.D. Hemphill,
ed. Trace Substances in Environmental Health-III. Proceedings of the University of
OCR for page 197
Toxicity of Selected Inorganic Contaminants in Drinking Water 197
Missouri's Third Annual Conference on Trace Substances in Environmental Health, June
24-26. University of Missouri, Columbia, Mo.
Kopp, J.F., and R.C. Kroner. 1970. Trace Metals in Waters of the United States. A Five
Year Summary of Trace Metals in Rivers and Lakes of the United States (Oct. 1,
1962-Sept. 30, 1967). U.S. Department of the Interior, Federal Water Pollution Control
Administration, Division of Pollution Surveillance, Cincinnati, Ohio. [207 pp.]
Kortus, J. 1967. The carbohydrate metabolism accompanying intoxication by aluminium
salts in the rat. Experientia 23:912-913.
Kotsonis, F.N., and C.D. Klaassen. 1978. The relationship of metallothionein to the toxicity
of cadmium after prolonged oral administration to rats. Toxicol. Appl. Pharmacol.
46:39-54.
Krasovskii, L., Y. Vasukovich, and O.G. Chariev. 1979. Experimental study of biological ef-
fects of lead and aluminum following oral administration. Environ. Health Perspect.
30:47-51.
Krigman, M.R., T.W. Bouldin, and P. Mushak. 1980. Lead. Pp. 490-507 in P.S. Spencer
and H.H. Schaumburg, eds. Experimental and Clinical Neurotoxicology. Williams &
Wilkins, Baltimore, Md.
Kroes, R., E.M. Den Tonkelaar, A. Minderhoud, G.J.A. Speijers, D.M.A. Vonk-Visser,
J.M. Berkvens, and G.J. Van Esch. 1977. Short-term toxicity of strontium chloride in
rats. Toxicology 7:11-21.
Leonard, A., and R.R. Lauwerys. 1980. Carcinogenicity, teratogenicity, and mutagenicity of
arsenic. Mutat. Res. 75:49-62.
Loeb, L.A., M.A. Sirover, L.A. Weymouth, D.K. Dube, G. Seal, S.S. Aganval, and E.
Katz. 1977. Infidelity of DNA synthesis as related to mutagenesis and carcinogenesis. J.
Toxicol. Environ. Health 2:1297-1304.
Loser, E. 1980. A 2 year oral carcinogenicity study with cadmium on rats. Cancer Lett.
9:191 -198.
Lundin, A.P., C. Caruso, M. Sass, and G.M. Berlyne. 1978. Ultrafilterable aluminum in
serum of normal man. Clin. Res. 26:636A.
Mahaffey, K.R. 1977. Relation between quantities of lead ingested and health effects of lead
in humans. Pediatrics 59:448-456.
Mallick, N.P., and G.M. Berlyne. 1968. Arterial calcification after vitamin-D therapy in
hyperphosphataemic renal failure. Lancet 2:1316-1320.
Martin, E.W., ea.-in-chief. 1965. Remington's Pharmaceutical Sciences. Thirteenth edi-
tion. Mac Publishing Co., Easton, Pa.
Mayor, G.H., J.A. Keiser, D. Markdani, and P.K. Ku. 1977a. Aluminum absorption and
distribution: Effect of parathyroid hormone. Science 197:1187-1189.
Mayor, G. H., D.D. Makdani, and J.A. Keiser. 1977b. The effect of parathyroid honnone
(PIH) on the gastrointestinal (GI) absorption and distribution of aluminum. Pp. 41 44 in
S.S. Brown, ed. Clinical Chemistry and Chemical Toxicology of Metals: Proceedings of
the First International Symposium organized by the Commission on Toxicology, IUPAC
Section on Clinical Chemistry, held at Monte Carlo, March 2-5. Elsevier/North-Holland,
New York.
Mayor, G.H., J.A. Keiser, T.V. Sanchez, S.M. Sprague, and J.B. Hook. 1978. Factors af-
fecting tissue aluminum concentration. J. Dialysis 2:471-481.
McCabe, L.J. 1970. Metal levels found in distribution samples. In Control of Corrosion by
Soft Waters, presented by Education Committee of American Water Works Association
and U.S. Public Health Service, Washington, D.C. 6 pp.
OCR for page 198
198 DRINKING WATER AND HEALTH
McCance, R.A., and E.M. Widdowson. 1939. The fate of strontium after intravenous ad-
ministration to normal persons. Biochem. J. 33:1822-1825.
McCormack, K.M., L.D. Ottosen, V.L. Sanger, S. Sprague, G.H. Mayor, and J.B. Hook.
1979. Effect of prenatal administration of aluminum and parathyroid hormone on fetal
development in the rat. Proc. Soc. Exp. Biol. Med. 161:74-77.
McCoy, E.C., and H.S. Rosenkranz. 1978. Silver sulfadiazine: Lack of mutagenic activity.
Chemotherapy 24:87-91.
McDermott, J.R.. A.I. Smith, M.K. Ward, I.S. Parkinson, and D.N.S. Kerr. 1978. Brain-
aluminium concentration in dialysis encephalopathy. Lancet 1 :901-904.
McKee, J.E., and H.W. Wolf. 1963. Reprinted 1971. Water Quality Criteria. Second edi-
tion. Publ. No. 3-A. The Resources Agency of California State Water Resources Control
Board, Sacramento, Calif. 548 pp.
McLaughlin, A.I.G., G. Kazantzis, E. King, D. Teare, R.J. Porter. and R. Owen. 1962.
Pulmonary fibrosis and encephalopathy associated with the inhalation of aluminium dust.
Br. J. lnd. Med. 19:253-263.
Michaelson, I.A., and M.W. Sauerhoff. 1974. An improved model of lead-induced brain
dysfunction in the suckling rat. Toxicol. Appl. Pharmacol. 28:88-96.
Moore, G.S., E.J. Calabrese, S.R. DiNardi, and T.W. Tuthill. 1978. Potential health effects
of chlorine dioxide as a disinfectant in potable water supplies. Med. Hypotheses
4:481-496.
Moore, M.R., P.A. Meredith, B.C. Campbell. A. Goldberg, and S.J. Pocock. 1977. Con-
tribution of lead in drinking water to blood-lead. Lancet 2:661-662.
Morse, D.L., VV.N. Watson, J. Houseworth, L.E. Witherell, and P.J. Landrigan. 1979. Ex-
posure of children to lead in drinking water. Am. J. Public Health 69:711-712.
Moseley, J.I., G.A. Ojemann, and A.A. Ward, Jr. 1972. Unit activity in experimental
epileptic foci during focal cortical hypothermia. Exp. Neurol. 37:164-178.
National Academy of Sciences. 1973. Water Quality Criteria 1972. A report prepared by the
Committee on Water Quality Criteria, Environmental Studies Board, Commission on
Natural Resources, National Research Council, National Academy of Sciences. EPA-
R3-73-003. U.S. Government Printing Office, Washington, D.C. 594 pp.
National Academy of Sciences. 1977. Drinking Water and Health. A report prepared by the
Safe Drinking Water Committee, Advisory Center on Toxicology, Assembly of Life
Sciences, National Research Council. National Academy of Sciences, Washington, D.C.
939 pp.
National Academy of Sciences. 1980a. Lead in the Human Environment. A report prepared
by the Committee on Lead in the Human Environment, Environmental Studies Board,
Commission on Natural Resources, National Research Council. National Academy of
Sciences, Washington, D.C. 525 pp.
National Academy of Sciences. 1980b. Drinking Water and Health, Volume 3. A report
prepared by the Safe Drinking Water Committee, Board on Toxicology and Environmen-
tal Health Hazards, National Research Council. National Academy of Sciences,
Washington, D.C. 415 pp.
Newton, D., and A. Holmes. 1966. A case of accidental inhalation of zinc-65 and silver-
110m. Radiat. Res. 29:403-412.
Nishioka, H. 1975. Mutagenic activities of metal compounds in bacteria. Mutat. Res.
31: 185-189.
Nordberg, G.F., ed. 1976. Effects and Dose-Response Relationships of Toxic Metals.
Elsevier, New York. 559 pp.
Norseth, T. 1979. Aluminum. Pp. 275-281 in L. Friberg, G.F. Nordberg, and V.B. Vouk,
OCR for page 199
Toxicity of Selected Inorganic Contaminants in Drinking Water 199
eds. Handbook on the Toxicology of Metals. Elsevier/North-Holland Biomedical Press,
Ned York.
Northdurft, H. 1955. Die experimentelle Erzeugung von Sarkomen bei Ratten und Mausen
durch Implantation von Rundscheiben aus Gold, Silber, Platin oder Elfenbein. Natur-
wiss. 42: 75-76.
Omdahl, J.L., and H.F. DeLuca. 1971. Strontium induced rickets: Metabolic basis. Science
174:949-951.
Omdahl J.L., and H.F. DeLuca. 1972. Rachitogenic activity of dietary strontium. I. lnhibi-
tion of intestinal calcium absorption and 1,2S-dihydroxycholecalciferol synthesis. J. Biol.
Chem. 247:5520-5526.
Ondreicka, R., E. Ginter, and J. Kortus. 1966. Chronic toxicity of aluminium in rats and
mice and its effects on phosphorus metabolism. Br. J. Ind. Med. 23:305-312.
Pariser, R.J. 1978. Generalized argyria. Clinicopathologic features and histochemical
studies. Arch. Dermatol. 114:373-377.
Phalen, R.F., and P.E. Morrou. 1973. Experimental inhalation of metallic silver. Health
Phys. 24:509-518.
Pierides, A.M. 1978. Dialysis dementia' osteomalacic fractures and myopath`: A syndrome
due to chronic aluminum intoxication. Int. J. Artif. Organs 1:206-208.
Platts, M.M., G.C. Goode, and J.S. Hislop. 1977. Composition of the domestic uater supply
and the incidence of fractures and encephalopathy in patients on home dialysis. Br. Med.
J. 2:657-660.
Pocock, S.J. 1980. Factors influencing household u ater lead: A British national sur~ey.
Arch. Environ. Health 35:45-51.
Reeves, A.L. 1979. Barium. Pp. 321-328 in L. Friberg, G.F. Nordberg, and V.B. Vouk, eds.
Handbook on the Toxicology of Metals. Elsevier/North Holland Biomedical Press.
Amsterdam, The Netherlands.
Saffiotti, U., and P. Shubik. 1963. Pp. 489-507 in F. Urbach. ed. The First International
Conference on the Biology of Cutaneous Cancer. Monograph No. 10. National Cancer In-
stitute, Washington, D.C.
Sax, I.N. 1963. Silver-Silver thioarsenite. Pp. 1174-1178 in Dangerous Properties of In-
dustrial Materials. Second edition. Reinhold Publishing Corp.~ Neu York.
Schroeder, H.A., and M. Mitchener. 1975. Life-term studies in rats: Effects of aluminum,
barium, beryllium, and tungsten. J. Nutr. 105:421-427.
Schroeder, H.A., I.H. Tipton, and A.P. Nason. 1972. Trace metals in man: Strontium and
barium. J. Chronic Dis. 25:491 -517.
Scott, K.G., and J.G. Hamilton. 1950. The metabolism of silver in the rat uith radio-silver
used as an indicator. Univ. Calif. Berkeley Publ. Pharmacol. 2:241-261.
Shubik, P., and J.L. Hartwell, eds. 1969. Pp. 3-4 in Survey of Compounds Which Have
Been Tested for Carcinogenic Activity. U.S. Public Health Service Publication No. 149,
Supplement 2. National Cancer Institute, Bethesda, Md.
Six, K.M., and R.A. Goyer. 1972. The influence of iron deficiency on tissue content and tox-
icity of ingested lead in the rat. J. Lab. Clin. Med. 79:128-136.
Snyder, W.S., M.J. Cook, E.S. Nasset, L.R. Karhausen, G.P. Howells, and I.H. Tipton,
eds. 1975. Report of the Task Group on Reference Man. A Report prepared by a Task
Group of Committee 2 of the International Commission on Radiological Protection. ICRP
No. 23. Pergamon Press, Ne~ York. 480 pp.
Sollman, T., ed. 1957a. Barium. Pp. 665-667 in A Manual of Pharmacology and Its Ap-
plication to Therapeutics and Toxicology. W. B. Saunders, Philadelphia. Pa.
Sollmann, T., ed. 1957b. Strontium. Pp. 1101-1102 in A Manual of Pharmacology and Its
Applications to Therapeutics and Toxicology. Eighth edition. W. B. Saunders, Ne~ York.
OCR for page 200
200 DRINKING WATER AND HEALTH
Sorenson, J.R.J., I.R. Campbell. L.B. Tepper, and R.D. Lingg. 1974. Aluminum in the en-
vironment and human health. Environ. Health Perspect. 8:3-95.
Spector, W.S., ed. 1956. Handbook of Toxicology: Acute Toxicities of Solids. Liquids and
Gases to Laboratory Animals. Vol. 1. W.B. Saunders, Philadelphia, Pa. 408 pp.
Spencer, H., and M. Lender. 1979. Adverse effects of aluminum-containing antacids on
mineral metabolism. Gastroenterology 76:603-606.
Spencer, H., L. Kramer, C.A. Gatza, and M. Lender. 1979. Calcium loss. calcium absorp-
tion and calcium requirement in osteoporosis. Pp. 65-90 in U.S. Barzel, ed. Osteoporosis
II. Grune and Stratton, New York.
Stacy, B.D. E.J. King, C.V. Harrison, G. Nagelschmidt, and S. Nelson. 1959. Tisse changes
in rats' lungs caused by hydroxides, oxides and phosphates of aluminum and iron. J.
Pathol. Bacteriol. 77:417-426.
Stokinger, H.E., and R.L. Woodward. 1958. Toxicologic methods for establishing drinking
water standards. J. Am. Water Works Assoc. 50(4):515-529.
Strauch, B., W. Buch, W. Grey, and D. Laub. 1969. Successful treatment of
methemoglobinemia secondary to silver nitrate therapy. N. Engl. J. Med. 281:257-258.
Tardiff, R.G., M. Robinson and N.S. Ulmer. 1980. Subchronic oral toxicity of BaCl2 in
rats. J. Environ. Pathol. Toxicol. 4:267-275.
Terry, R.D. 1963. The fine structure of neurofibrillary tangles in Alzheimer's disease. J.
Neuropathol. Exp. Neurol. 22:629-634.
Tipton, I.H., P.L. Stewart, and P.G. Martin. 1966. Trace elements in diets and excrete.
Health Phys. 12:1683-1689.
Trapp, G.A., G.D. Miner, R.L. Zimmerman. A.R. Mastri, and L.L. Heston. 1978.
Aluminum levels in brain in Alzheimer's disease. Biol. Psychiatry 13:709-718.
Underwood, E.J., ed. 1971. Other elements. 1. Aluminum. Pp. 425-427 in Trace Elements
in Human and Animal Nutrition. Third edition. Academic Press, Neu York.
U.S. Environmental Protection Agency. 1977. National Interim Primary Drinking Water
Regulations. EPA-570/9-76-003. U.S. Environmental Protection Agency, Office of Water
Supply. Washington, D.C. 159 pp.
U.S. Environmental Protection Agency. 1979a. Lead: Ambient Water Quality Criteria.
[PB-292-437.] Criteria and Standards Division, Office of Water Planning and Standards.
U.S. Environmental Protection Agency, Washington, D.C. 151 pp.
U.S. Environmental Protection Agency. 1979b. Cadmium: Ambient Water Quality Criteria.
[PB-292-423.] Criteria and Standards Division, Office of Water Planning and Standards.
U.S. Environmental Protection Agency, Washington, D.C. 108 pp.
U.S. Environmental Protection Agency. 1979c. Silver: Ambient Water Quality Criteria.
[PB-292-441.] Criteria and Standards Division, Office of Water Planning and Standards.
U.S. Environmental Protection Agency, Washington, D.C. 161 pp.
Venugopal, B., and T.D. Luckey, eds. 1978. Toxicity of group II metals: Strontium (Sr). Pp.
58-63 in Metal Toxicity in Mammals. 2. Chemical Toxicity of Metals and Metalloids.
Plenum Press, New York.
Vilkina, G.A., M.D. Pomerantzeva, and L.K. Ramaya. 1978. Lack of mutagenic effect of
cadium and zinc salts in somatic and germ mouse cells. Genetika 14:2212-2214.
Waldron, H.A., and D. Stofen, eds. 1974. Sub-Clinical Lead Poisoning. Academic Press,
New York. 224 pp.
Ward, A.A. 1972. Topical convulsant metals. Pp. 13-35 in D.P. Purpura, J.K. Penny, D.B.
Tower, D.M. Woodbury, and R.D. Walter, eds. Experimental Models of Epilepsy-A
Manual for the Laboratory Worker. Raven Press, New York.
Ward, M.K. , T.G. Feest, H.A. Ellis, I. S. Parkinson, D.N. S. KeIT, J. Herrington, and G.L.
OCR for page 201
Toxicity of Selected Inorganic Contaminants in Drinking Water 201
Goode. 1978. Osteomalacic dialysis osteodystrophy: Evidence for a uater-borne
aetiological agent, probably aluminum. Lancet I :841 -845.
Watanabe, T., T. Shimada, and A. Endo. 1979. Mutagenic effects of cadmium on mam-
malian oocyte chromosomes. Mutat. Res. 67:349-356.
Wong, C.S., and P. Berrang. 1976. Contamination of tap water by lead pipe and solder.
Bull. Environ. Contam. Toxicol. 15:530-534.
Wood, M. 1965. Silver nitrate and burns-caution!!! Ariz. Med. 22:817.
World Health Organization. 1970. European Standards for Drinking Water, 2nd ed.
Geneva, Switzerland.
World Health Organization. 1971. international Standards for Drinking Water, 3rd ed.
Geneva, Switzerland.
World Health Organization. 1973. Health Aspects Relating to the Use of Polyelectrolytes in
Water Treatment for Community Water Supply. Tech. Paper No. 5. WHO international
Reference Center for Community Water Supply, The Hague, The Netherlands. 32 pp.
Wyckoff, R.C., and F.R. Hunter. 1956. A spectrographic analysis of human blood. Arch.
Biochem. Biophys. 63:454-460.
Wysor, M.S. 1975. Orally-administered silver sulfadiazine. Chemotherapy and toxicology in
CF-1 mice. Plasn20dinn7 berghei (malaria) and Psezld~J,20~2c~s aer21~gil~c~sa. Chemotherapy
(Baser) 21:298-306. [Chem. Absts. 83:71889w, 1975.1
Ziegler, E.E., B.B. Edwards, R.L. Jensen, K.R. Mahaffey, and S.J. Fomon. 1978. Absorp-
tion and retention of lead by infants. Pediatr. Res. 12:29-34.
Representative terms from entire chapter:
chlorine dioxide
