Barium: health advisory

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March 31, 19S7
BARIUM
Health Advisory
Office of Drinking Water
U.S. Environmental Protection Agency
I. INTRODUCTION
The Health Advisory (HA) Program, sponsored by the Office of Drinking
Water (ODW), provides information on the health effects, analytical method-
ology and treatment technology that would be useful in dealing with the
contamination of drinking water. Health Advisories describe nonregulatory
concentrations of drinking water contaminants at which adverse health effects
would not be anticipated to occur over specific exposure durations. Health
Advisories contain a margin of safety to protect sensitive members of the
popijldticn.
Health Advisories serve as informal technical guidance to assist Federal,
State and local officials responsible for protecting public health when
emergency spills or contamination situations occur. They are not to be
construed as legally enforceable Federal standards. The HAs are subject to
chance as new information becomes available.
Health Advisories are developed for One-day, Ten-day, Longer-term
(approximately 7 years, or 10% of an individual's lifetime) and Lifetime
exposures based on data describing noncarcinogenic end points of toxicity.
Health Advisories do not quantitatively incorporate any potential carcinogenic
risk from such exposure. For those substances that are known or probable
hur.an carcinogens, according to the Agency classification scheme (Group A or
31, Lifetime HAs are not recommended. The chemical concentration values for
Group A or 3 carcinogens are correlated with carcinogenic risk estimates by
employing a cancer potency (unit risk) value together with assumptions for
lifetime exposure and the consumption of drinking water. The cancer unit
risk is usually derived from the linear multistage model with 95% upper
confidence limits. This provides a low-dose estimate of cancer risk to
humans that is considered unlikely to pose a carcinogenic risk in excess
of the stated values. Excess cancer risk estimates may also be calculated
using the One-hit, Weibull, Logit or Probit models. There is no current
understanding of the biological mechanisms involved in cancer to suggest that
any one of these models is able to predict risk more accurately than another.
3ecause each model is based on differing assumptions, the estimates that are
derived can differ by several orders of magnitude.

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This Health Advisory is based on information presented in the Office
of Drinking Water's Health Effects Criteria Document (CD) for barium (U.S.
EPA, 1985). The HA and CD formats are similar for easy reference. Individuals
desiring further information on the toxicological data base or rationale for
risk characterization should consult the CD. The CD is available for review
at each EPA Regional Office of Drinking Water counterpart (e.g., Water Supply
3ranch or Drinking Water 3ranch), or for a fee from the National Technical
Information Service, U.S. Department of Commerce, 5285 Port Royal Rd.,
Springfield, VA 22161, PB #86-118031/45. The toll-free number is (800)
336-4700; in the Washington, D.C. area: (703) 487-4650.
GENERAL INFORMATION AND PROPERTIES
CAS No.
Barium --
Barium Chloride -- 10361-37-2
Barium Sulfate -- 7727-43-7
Sy nony :ns
Barium Sulfate; Barite (Windholz, 1976)
Uses
c Depending upon the specific compound, barium salts are used for a
number of purposes including drilling mud (Kirkpatrick, 1978), pigment
(Miner, 1969), and as x-ray contrast nedium (Miner, 1969). Other
uses are summarized by Pidgeon (1964).
Properties (Pidgeon, 1964; Preisman, 1964; Miner, 1969; Chilton, 1 973;
Kirkpatrick, 1978; Reeves, 1979)
° The properties of barium compounds vary with the specific compound;
some examples are as follows:
Barium
Barium
Chloride
Barium
Sulfate
Chemical Formula
Atomic/Molecular Weight
Physical State
3oili.ng Point
Melting Point
Density (20°C)
Vapor Pressure
Water Solubility (pph)
Log Octanol/Water
Partition Coefficient
Taste Threshold
Odor Threshold
Ba
137.33
Silver-white solid
1637-1638°C
729-730°C
3.6 g/cm^
1810 x 10-5 mm Hg
reacts
BaCl2
208.24
White solid
1560°C
960°C
3.856 g/cm^
31 (0°C)
BaSO^
233.40
Colorless solid
1580°C
4.50 g/cm^
0.000285 (30°C)

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Occu rrence
0 Barium is a reactive metal which is not found free in nature but
exists as a number of salts. Barium occurs in nature chiefly as the
mineral barite {BaSO^) and in much smaller amounts as witherite
(BaCC^). The mineral forms are relatively insoluble in water, having
high melting and boiling points and very low vapor pressures (Preisman,
1964'. Barium compounds occur in most geologic materials at levels
of 300-500 ppm. Barium occurs at low levels in most surface and
ground waters with reported levels of less than 340 ug/L. While
barium compounds are used commercially in a number of processes,
contamination of drinking water is usually the result of naturally -
occurring barium and not industrial releases (U.S. EPA, 1987).
0 There are limited survey data on the occurrence of barium in drinking
water. Most supplies contain less than 290 ug/L of barium. Currently,
60 ground water supplies and 1 surface water supply exceed the interim
maximum contaminant level (MCL) of 1,000 ug/L. Barium also occurs in
most foods as a low level contaminant. 3ased upon the limited infor-
mation available on barium exposure, food is the major source of
barium exposure (U.S. EPA, 19S7).
III. PHARMACOKINETICS
Absorption
° In laboratory animals, the absorption of barium varies with a nunber
of factors including the species of animal (U.S. EPA, 1985), the
compound tested (McCauley anc Washington, 1983), the age of the animal
(Taylor et al., 1962) and the composition of the diet (Lengemann, 1959).
0 While no definitive human barium absorption studies were found i'J.5.
EPA, 1985\ barium absorption has been estimated to be approximately
5% in the adult (ICRP, 1973). However, other data (Harrison et al.,
1967) suggest that barium absorption probably is greater than this.
While data in laboratory animals (Lengemann, 1959) suggest that barium
absorption in children may be significantly greater than in adults,
there is currently inadequate information to resolve this issue.
Distribution
° In the mouse, intravenously injected barium (1333aCl2) is distributed
widely throughout the organism, but is localized principally in the
bone (Dencker et al., 1976).
° Based on autopsy data, barium levels in human bone are relatively
constant and do not appear to increase with age, ranging from an
average value of 7.0 ppm in bone at age 0 to 3 months to an average
of 8.5 ppm at age 33 to 74 years (Sowden and Stitch, 1957).

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Metabolis ji
° The skeletal metabolism of barium in humans is qualitatively similar
to that of calcium, although the incorporation of these two elements
is quantitatively very different (Bauer et al., 1956,1957).
Excretion
° In humans, ingested barium is eliminated principally via fecal excretion
(approximately 72%) following oral exposure (Tipton et al., 1565).
IV. HEALTH EFFECTS
Humans
0 Acute barium toxicity is associated with hypokalemia and electrocar-
diographic changes as well as other symptoms (Diengott et al., 1964;
Gould et al., 1973; Talwar and Sharma, 1979).
0 NAS (1977) has concluded that: "The fatal dose of barium chloride for
man has been reported to be about 0.3 - 0.9 g, or 550 - 600 my of
bari um."
0 Schroeder and Kraemer (1974) concluded that there was a significant
negative correlation between barium in drinking water and athero-
sclerotic heart disease.
0 In an epidemiology study, Brenniman et al. (1981) concluded that
there was no statistically significant difference in blood pressure
between those ingesting drinking water containing barium at 7.3 mg/L
as compared to 0.1 mg/L. A concentration of 7.3 mg/L corresponds to
a dose of 0.20 mg/kg/day (assuming a 70-kg adult drinks 2 L per day).
Ihe duration of exposure was not identified.
Animals
Short-term Exposure
° The acute oral LD^q of barium varies markedly with species, compound,
age and other factors (U.S. EPA, 1985). For example, the acute oral
LD^q of barium chloride is 220 mg/kg in weanling rats and 132 mg/kg m
adult rats (Tardiff et al., 1980).
Long-term Exposure
° Tardiff et al. (1980) exposed rate to barium at 0, 10, 50, or 250
ppm in drinking water for 4, 8 and 13 weeks. The barium concentrations
were approximately 0, 2.75, 13.7 and 66.25 mg/kg/day at the beginning
of the study and 0, 1.7, 6.6 and 31.5 mg/kg/day at the end of the
study. Although the barium body burden increased with increasing
barium dosage, no conclusive signs of barium toxicity were observed
in these animals. A weakness of this study is that, unlike Perry
et al. (1983) below, blood pressure was not measured.

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0 Perry et al. (1983) exposed weanling rats to barium at 1, 10 or 100
ppm in drinking water for up to 16 months (average daily barium doses
of 0.051, 0.51 and 5.1 mg/kg, respectively). With the exception of
an increase in blood pressure, there were no signs of toxicity at
any barium dose level. Systolic blood pressure measurements revealed
no increase in pressure in animals exposed to 1 ppm for 16 months,
an increase of 4 mm Hg (p ~.01) in animals exposed to 10 ppm barium
for 16 months, and an increase in systolic pressure of 16 mm Hg (p
<0.001) in animals exposed to 100 ppm barium for 16 months. The
animals in this study were maintained in a special contaminant-free
environment and fed a diet designed to reduce exposure to trace
metals. It is possible that the restricted intake of certain beneficial
metals (e.g., Ca and K) may have predisposed the test animals to the
hypertensive effects of barium (U.S. EPA, 1985).
0 Schroeder and Mitchener (1975a,b) exposed rats and mice to 5 mg/L
barium in drinking water for a lifetime (approximately 0.25 mg/kg/day
for rats and 0.825 mg/kg/day for mice). No compound related adverse
effects were observed. A weakness of this study is that, unlike
Perry et al. (1983) above, blood pressure was not measured.
Reproductive Effects
0 No adequate mammalian study on the potential reproductive effects
of barium was identified (U.S. EPA, 1985).
Developmental Effects
° No adequate mammalian study on the potential developmental effects of
barium was identified (U.S. EPA, 1985).
Mutagenicity
° No adequate studies on the mutagenicity of barium were identified
(U.S. EPA, 1985).
Carcinogenicity
0 No adequate studies on the carcinogenicity of barium were identified
(U.S. EPA, 1985).
V. QUANTIFICATION OF TOXICOLOGICAL EFFECTS
Health Advisories (HAs) are generally determined for One-day, Ten-day,
Longer-term (approximately 7 years) and Lifetime exposures if adequate data
are available that identify a sensitive noncarcinogenic end point of toxicity.
TVie HAs for noncarcinogenic toxicants are derived using the following formula:
HA = (NOAEL or LOAEL) x (BW) = 	 /L (	 „ }
(UF) x ( L/day)

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where:
NOAEL or LOAEL = No- or Lowest-Observed-Adverse-Effect-Level
in mg/kg bw/day.
BW = assumed body weight of a child (10 kg) or
an adult (70 kg .
UF = uncertainty factor (10, 100 or 1,000), in
accordance with NAS/ODW guidelines.
	 L/day = assumed daily water consumption of a child
(1 L/day) or an adult (2 L/day).
One-day Health Advisory
The available data are insufficient to develop a One-day HA for barium.
It is recommended that the modified DWEL of 0.51 mg/L (adjusted for a 10-kg
child) be used as the One-day HA for the 10-kg child.
Ten-day Health Advisory
The available data are insufficient to develop a Ten-day HA for barium.
It is recommended that the modified DWEL of 0.51 mg/L (adjusted for a 10-kg
child) be used as the Ten-day HA for the 10-kg child.
Longer-term Health Advisory
The available data are insufficient to develop Longer-term HAs for barium.
It is recommended that the DWEL of 1.8 mg/L be used as the Longer-term HA
for the 70-kg adult and the modified DWEL of 0.51 mg/L (adjusted for a 10-kg
child) be used as the Longer-term HA for the 10-kg child.
Lifetime Health Advisory
The Lifetime HA represents that portion of an individual's total exposure
that is attributed to drinking water and is considered protective of noncar-
cinogenic adverse health effects over a lifetime exposure. The Lifetime HA
is derived in a three step process. Step 1 determines the Reference Dose
(RfD), formerly called the Acceptable Daily Intake (ADI). The RfD is an esti-
mate of a daily exposure to the human population that is likely to be without
appreciable risk of deleterious effects over a lifetime, and is derived from
the NOAEL (or LOAEL), identified from a chronic (or subchronic) study, divided
by an uncertainty factor(s). From the RfD, a Drinking Water Equivalent Level
(DWEL) can be determined (Step 2). A DWEL is a medium-specific (i.e., drinking
water) lifetime exposure level, assuming 100% exposure from that medium, at
which adverse, noncarcinogenic health effects would not be expected to occur.
The DWEL is derived from the multiplication of the RfD by the assumed body
weight of an adult and divided by the assumed daily water consumption of an
adult. The Lifetime HA is determined in Step 3 by factoring in other sources
of exposure, the relative source contribution (RSC). The RSC from drinking
water is based on actual exposure data or, if data are not available, a
value of 20% is assumed for synthetic organic chemicals and a value of 10%

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March 31, 19S7
is assumed for inorganic chemicals. If the contaminant is classified as a
Group A or B carcinogen, according to the Agency's classification scheme of
carcinogenic potential (U.S. EPA, 1986), then caution should be exercised in
assessing the risks associated with lifetime exposure to this chemical.
Considering the kind, nature and partially contradictory results of the
various barium studies, ODW does not believe that it is appropriate to use
any simplistic formula to determine a Lifetime HA for barium in drinking
water. Rather:
° No single study, considered alone, is appropriate to calculate a Lifetime
HA for barium.
0 A Darium HA must be based on the weight of all the pertinent data,
considered together.
In the Perry et al. (1 983) rat drinking water study, 10 ppm barium
(0.51 mg/kg/day) produced a small (4 to 7 mm Hg) out statistically significant
increase in blood pressure by 8 to 15 months; 100 ppm barium (5.1 mg/kg/day)
produced clear hypertension and cardiotoxic effects.
A major shortcoming of the Perry, et al. (1983) study is that the animals
were maintained in a special environment and received both a special diet and
special water, all intended to reduce exposure to trace metals. Because of
the beneficial effects of some metals (i.e., cadmium) and the interactions
of barium with other metals, it is possible that the restricted intake of
other metals may have contributed to the apparent toxicity of barium. In
addition, the results of the Perry, et al. (198 3) rat study clearly contradict
the results of the Brenniman, et al. (1981) human study which suggests that
barium m drinking water has no appreciable effect upon blocc pressure m
humans, at least at a level of 7.3 ppm (0.20 mg/kg/day) in drinking water.
While the 4 to 7 mm Hg increase in blood pressure observed at 10 ppm
barium (0.51 mg/kg/day) in the Perry, et al. (1983) study may be a compound
related effect, ODW has serious doubts as to whether this 4 to 7 am Hg increase
in rat blood pressure should be considered an adverse effect in the light of
the negative effects observed in the Brenniman, et al. (1981) human study.
Considering the contradiction between the rat and human data, it was ODW's
judgment that it was not prudent either to ignore the results of Perry et al.
(1983) or to treat the results with the same seriousness they would warrant,
had they been observed in humans.
In ODW's judgment, the most appropriate way to balance the contradiction
between the Perry, et al. (1983) rat study and the Brenniman, et al. (1931)
human study is to use the results of the Perry, et al. (1983) study, with a
reduced uncertainty factor of 10x and to treat the 0.51 mg/kg/day value as
if it were a NOAEL.
Thus, based on the previous discussion, the Lifetime Health Advisory
is derived as follows:

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Step 1: Determination of tne Reference Dose (RfD)
RfD = (0,S1 mg/kg/day ) = q.051 mg/kg/day
(10)
where:
0.51 mg/kg/day = NOAEL (see discussion above).
10 = uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a NOAEL from an animal study.
However, as previously discussed, ODW believes that
an uncertainty factor of 10 is appropriate in this
specific case (see discussion above).
Step 2: Determination of the Drinking Water Equivalent Level (DWEL)
DWEL = <0-051 mg/kg/day) (70 kg) = 1>3 nq/L (1,800 ug/L)
(2 L/day)
where:
0.051 .ng/kg/day = RfD.
70 kg = assumed body weight of an adult.
2 L/day = assumed daily water consumption of an adult.
Step 3: Determination of the Lifetime Healtn Advisory
Lifetime HA = (1.8 mg/L) (33%) = 1.5 mg/L (1,500 ug/L)
where:
1.8 mg/L = DWEL.
83% = assumed relative source contribution from water (Federal
Register, November 13, 1985).
Evaluation of Carcinogenic Potential
0 Due to the absence of toxicological evidence to classify barium as
a potential carcinogen, a quantification of carcinogenic risks for
barium is not appropriate.
° No information was located in the available literature regarding the
carcinogenic potential of barium in humans nor were any animal studies
found wnich were adequate to evaluate the carcinogenic potential of
barium.
° Applying the criteria described in EPA's guidelines for assessment of
carcinogenic risk (U.S. EPA, 1986) barium is classified in Group D:
Not classified. This category is for agents with inadequate animal
and human evidence.

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0 The International Agency for Research on Cancer has not evaluated the
carcinogenic potential of barium.
VI. OTHER CRITERIA, GUIDANCE AND STANDARDS
0 The National Interim Primary Drinking Water Regulations of 1975
established a Maximum Contaminant Level (MCL) drinking water standard
for barium of 1 mg/L (U.S. EPA, 1976).
0 The National Academy of Sciences (NAS, 1982) derived a 1-day Suggested
No-Adverse-Response Level (SNARL) for barium of 6.0 mg/L.
0 The National Academy of Sciences (NAS, 1982) derived a chronic Sug-
gested No-Adverse-Response Level (SNARL) value for barium of 4.7 mg/L.
° The American Conference of Governmental Industrial Hygienists estab-
lished an occupational threshold limit value (TLV) of 0.5 mg/m^ for
barium nitrate in air (ACGIH, 1980).
0 The USSR standard for waterborne barium is 4 mg/L (NAS, 1977).
0 The OS HA 8-hour time-weighted average exposure limit for soluble
barium compounds is 0.5 mg/m3 in workplace air (OSHA, 1985).
VII. ANALYTICAL METHODS
0 Determination of barium is by atomic absorption (AA) using either
direct aspiration into a flame (U.S. EPA, 1979a) or a furnace technique
(U.S. EPA, 1979b).
0 The direct aspiration AA procedure is a physical method based on the
absorption of radiation at 553.6 nm by barium. The sample is
aspirated into an air-acetylene flame and atomized. A light beam is
directed through the flame into a monochromator, and onto a detector
that measures the amount of light absorbed. Absorbance is proportional
to the concentration of barium in the sample. The detection limit is
100 ug/L using this procedure.
° The furnace AA procedure is similar to direct aspiration AA except a
furnace, rather than a flame, is used to atomize the sample. The
detection limit is 2 ug/L using this procedure.
VIII. TREATMENT TECHNOLOGIES
° Experience indicates that ion exchange, lime softening and reverse
osmosis are effective to remove barium from drinking water. Conven-
tional coagulation/filtration processes are not effective to remove
barium from drinking water (U.S. EPA, 1977).
0 Weinberg (1973) and Logsdon et al. (1974) reported that ion exchange
softening systems are highly efficient (93 to 98 percent) for reducing

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barium in water, even after water hardness breakthrough. Field
data from two Midwestern full-scale ion exchange softening plants
showed that barium removal was comparable to hardness removal on well
water containing 11-19 mg/L of barium and 225-230 mg/L of hardness as
CaCo3 (BIF, 1970). When these softening units were performing ef-
ficiently and removing all of the hardness from the water, they also
removed all of the barium.
Experience indicates that lime softening is very effective in removing
barium from drinking water. Lime softening achieved greater than
90 percent removal in the 10-11 pH range on well water containing
7-8.5 mg/L of naturally occurring barium. Removals decreased below
and above this range. Pilot plant studies conducted at the EPA
Municipal Research Laboratory and full-scale treatment information on
similar types of ground water verified the laboratory data. Pilot
plant test runs on water containing 10-12 mg/L of barium at pH 9.2,
10.5 and 11.6 resulted in removals of 84, 93 and 82 percent, respec-
tively. Grab samples from two full-scale lime softening plants
showed removals of 83 and 95 percent. These plants operated at pH
10.5 and 10.3; the raw water barium concentrations were measured
at 7.5 and 17.4 mg/L, respectively (BIF, 1970).
A number of studies indicate that reverse osmosis membranes can remove
more than 90 percent of the barium from drinking water. In an experi-
mental long term study, 99 percent barium removal was obtained using
cellulose acetate membrane at 400-800 psi operating pressures (BIF,
1970). Other studies by Sorg et al. (1980) achieved similar results,
where 95-99 percent removals were obtained by passing water containing
7 mg/L barium through cellulose acetate membranes at 165-180 psi
operating pressures.

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Threshold limit values for chemical substances and physical agents in
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Ohio: American Conference of Governmental Industrial Hygienists. p. 35
Bauer, G.C.H., A. Carlsson and B. Lindquist. 1957. Metabolism of 140Ba in
man. Acta. Orth. Scand. 26:241-254.
Bauer, G.C.K., A. Carlsson and B. Lindquist. 1956. A comparative study of
the metabolism of ^'-'Ba and 45Ca in rats. Biochem. J. 63: 535-542.
BIF. 1970. Chemicals Used on Treatment of Water and Waste Water Engineering
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3renniman, G.R., W.H. Kojola, P.S. Levy, 3.W. Carnow and T. Namekata. 1981.
High barium levels in public drinking water and its association with
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Dencker, L., A. .Vilsson, C. Ronnback ana G. Walmder. 1 976. Uptake and
retention of 13^3a and 14'^3a-14^La in mouse tissue. Acta Radiol.
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Diengott, D., 0. Rozsa, N. Lev/ and S. Muamrnar. 1964. Hypokalemia in
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Gould, D.3., M.R. Sorreil and A.D. Lupeneilo. 1 373. Barium sulfide poison-
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Harrison, G.E., T.E.F. Carr and A. Sutton. 1967. Distribution of radioactiv
calcium, strontium, barium and radium following intravenous injection
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Kirkpatrick, T. 1978. Barium compounds. In: Kirk-Othmer encyclopedia of
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Lengemann, F.W. 1959. The site of action of lactose in the enhancement of
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Logsdon, G.S., Sorg, T.J. et al. 1974. Removal of Heavy Metals by Conven-
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Metals in Water Supplies: Occurrence, Significance and Control.
University of Illinois.

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McCauiey, P.?., and I.S. Washington. 1983. Barium bioavailability as the
chloride, sulfate or carbonate salt in the rat. Drug Chem. Toxicol.
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Miner, S. 1969. Air pollution aspects of barium and its compounds. Techni-
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Perry, H.M., S.J. Kopp, M.w. Erlanger and E.F. Perr/• 1983. Cardiovascular
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Schroeder, H.A., and L.A. Kraemer. 1974. Cardiovascular mortality, municipal
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primary drinking water regulations for inorganics: Part 5. AWWA.
72(7):411-22.

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Sowden, E.M., and S.R. Stitch. 1957. Trace elements in human tissue. 2.
Estimation of the concentrations of stable strontium and barium in
human bone. Biochem. J. 67:104-109.
Talwar, K.K., and B.K. Sharma. 1979. Myocardial damage due to barium chloride
poisoning. Indian Heart J. 31(4):244-245.
Tardiff, R.G., M. Robinson and N.S. Ulmer. 1980. Subchronic oral toxicity
of BaCl2 in rats. J. Environ. Path. Tox. 4:267-275.
Taylor, D.M., P.H. Bligh and M.H. Duggan. 1962. The absorption of calcium,
strontium, barium and radium from the gastrointestinal tract of the rat.
Biochem. J. 83:25-29.
Tipton, I.H., P.L. Stewart and P.G. Martin. 1966. Trace elements in diets
and excreta. Health Phys. 12:1683-1689.
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