(edited September 1990)
GuidelineThe maximum acceptable concentration (MAC) for barium in drinking water is 1.0 mg/L (1000
Identity, Use and Sources in the
Barium is present as a trace element in both igneous
and sedimentary rocks. Although it is not found free in
barium occurs in a number of compounds, most
commonly barite (BaSO
) and, to a lesser extent,witherite (BaCO
).Barium compounds have a wide variety of
industrial applications. They are used in the plastics,
rubber, electronics and textiles industries. Barium
compounds are used in ceramic glazes and enamels, in
glass making and paper making, as a lubricant additive
and in pharmaceuticals and cosmetics.
Barite is usedextensively in the oil and gas industry as a wetting agent
for drilling mud.
Domestic consumption of barite inCanada in 1984 was 78 565 tonnes, 90% of which was
used in oil and gas well drilling.
Witherite is used in theproduction of optical glasses, in brick making, in
case-hardening of steel and as a rodenticide. Organo-
metallic compounds containing barium have been used
in diesel fuel to reduce black smoke emissions from
The acetate, nitrate and halide salts of barium aresoluble in water, but the carbonate, chromate, fluoride,
oxalate, phosphate and sulphate salts are quite insoluble.
The aqueous solubility of barium compounds increases
as the pH decreases.
Organometallic bariumcompounds are ionic and are hydrolysed in water.
Theconcentration of barium ions in natural aquatic systems
will be limited by naturally occurring anions, such as
sulphates and carbonates, and by the possible adsorption
of barium ions onto metal oxides and hydroxides.
Barium levels were determined in 122 munici-
palities in 10 provinces in samples of raw, treated and
distributed drinking water serving approximately 36%
of the Canadian population.
The provincial medianconcentrations of barium in distributed water ranged
from not detectable (
0.005 mg/L) in British Columbia,Newfoundland, Nova Scotia and Quebec to 0.084 mg/L
in Alberta. The Canada-wide median concentration was
0.018 mg/L. The maximum level of barium in a sample
of distributed water was 0.602 mg/L, measured at a site
in Ontario. Barium levels in raw water were not
significantly different from those in treated water.
Barium is generally present in air in particulate
form, and its presence is attributed mainly to industrial
emissions, specifically the combustion of coal and diesel
oil and waste incineration. No data on concentrations of
barium in ambient air in Canada have been found. In the
United States, concentrations have been found to range
from 0.0015 to 0.95
8Most foods contain less than 0.002 mg/g of
The major dietary sources of barium in the
United States are milk, potatoes and flour.
Some cerealproducts and nuts tend to contain high amounts of
barium; for example, pecans contain 0.0067 mg/g,
peanuts 0.0021 mg/g, bran flakes 0.0039 mg/g and
Brazil nuts up to 4 mg/g.
Certain species of plantsaccumulate barium when grown in barium-rich soil.
The International Commission on RadiologicalProtection (ICRP) reported that the long-term mean
dietary barium intake for four individuals, including
both food and fluids, was 0.9 mg/d, with a range of 0.44
to 1.8 mg/d.
In a survey by Schroeder et al. of the dietsof five adults over 30 to 347 days, the mean daily intake
of barium from food was 1.2 mg, with a range of 0.65 to
13 Owing to the lack of data on barium levels inCanadian foodstuffs, it is difficult to estimate daily
intake of barium in the diet. However, on the basis of the
data reported by the ICRP
and Schroeder et al.,13
mean intake of barium by Canadians from this source is
estimated to be approximately 1 mg/d.
Assuming average daily water consumption to be
1.5 L and based on the median concentration of barium
found in a national survey of Canadian drinking water
the barium intake from drinking waterfor most Canadians would be approximately 0.03 mg/d.
For individuals consuming drinking water containing
the highest barium concentration measured in the
national survey (0.6 mg/L),
the maximum daily intakeof barium in drinking water would be 0.9 mg. At the
levels of barium measured in U.S. air,
intake of bariumthrough inhalation would be negligible compared with
the amount ingested.
Based on the above considerations, the mean daily
intake of barium from food, water and air in Canada is
estimated to be slightly more than 1 mg/d. Of this, food
represents the primary source of barium for the non-
occupationally exposed Canadian population. However,
in cases where barium levels in drinking water are high
(0.6 mg/L), drinking water may contribute significantly
to barium intake (approximately 50%).
Analytical Methods and Treatment
Barium concentrations in water may be determined
by atomic absorption spectroscopy (AAS), either by
direct aspiration into an air–acetylene flame or by
atomization in a furnace. The detection limit for the
furnace technique is much lower than that for the direct
aspiration procedure (2
g/L vs. 100µ
water may also be determined by inductively coupled
plasma atomic emission spectrometry; detection limits
for this method of analysis are reported to be equivalent
or superior to those for flame AAS for most elements.
Based upon data collected in a Canadian nationalsurvey, relatively little, if any, soluble or insoluble
barium is removed by conventional water treatment
Processes effective in removing barium fromdrinking water include ion exchange (93 to 98%), lime
softening (>90%) and the reverse osmosis membrane
technique (>90%); efficiency of removal varies,
depending upon levels in the raw water.
Barium is not considered to be an essential element
for human nutrition.
The degree of absorption of barium from the lungsand gastrointestinal tract depends on the solubility of the
compound, the animal species, the contents of the
gastrointestinal tract, diet and age. Soluble barium salts
are absorbed most readily. Recent data from studies in
rats and man indicate that insoluble barium compounds
may also be absorbed to a significant extent.
Gastrointestinal absorption of barium in rats was foundto decrease with age (85% in rats 14 to 18 days old vs. <10% in rats 60 to 70 weeks old) and was greater in
fasted rats than in fed rats.
Barium is rapidly distributed in blood plasma,principally to the bone.
The whole body content ofbarium in man is approximately 22 mg, of which 93% is
found in the bone and connective tissues, with smaller
amounts being present in the fat, skin and lungs.
Inrats administered drinking water containing 0 to
250 mg/L barium as barium chloride for four, eight or
13 weeks, the concentration of barium in the bone was
proportional to dose but not to duration of exposure.
has also been reported that barium crosses the placental
barrier in humans, based on the determination of barium
content of infant and stillborn foetal tissues.
Miller et al.20
reported that the ratio of barium to
calcium in the teeth of 34 children exposed in one
community to drinking water containing high
concentrations of barium (10 mg/L) was five times
higher than that for 35 children from another community
exposed to lower levels (0.2 mg/L). The two
communities were similar with respect to population,
ethnic composition and socioeconomic status.
The principal route of excretion of barium in
humans and animals is faecal;
20% is excreted in thefaeces and 7% is excreted in the urine within 24 hours.
Soluble barium salts are highly acutely toxic. Athigh concentrations, barium causes strong
vasoconstriction by its direct stimulation of arterial
muscle, peristalsis due to the violent stimulation of
smooth muscle, and convulsions and paralysis following
stimulation of the central nervous system.
Dependingon the dose and solubility of the barium salt, death may
occur in a few hours or a few days. The acute lethal oral
dose of barium chloride for humans has been estimated
to be between 3 and 4 g; the acute toxic dose is 0.2 to
23 Repeated exposures to barium chloride in tablesalt are believed to have caused recurrent outbreaks of
“Pa-Ping” disease (a transient paralysis resembling
familial periodic paralysis) in the Szechwan province of
The prevalence of dental caries was reported to be
significantly lower in 39 children from one community
ingesting drinking water with a barium concentration of
8 to 10 ppm than in 36 children from another
community ingesting drinking water with much lower
barium concentrations (<0.3 ppm).
There was nostatistically significant relationship between the
prevalence of dental caries and age, sex, presence of
detectable mottling, use of water softener or income.
The concentrations of other trace elements (i.e.,
magnesium, calcium, strontium and fluoride) in the
water supplies of the two communities were not
markedly different; however, the study population was
small, and dental examinations were not conducted
In several ecological epidemiological studies,
associations between the barium content of drinking
water and mortality from cardiovascular disease have
been observed. For example, based on analysis of
mortality rates in relation to variations in the amounts of
numerous trace elements in drinking water in different
geographical areas, Schroeder and Kramer
Elwood et al.
reported significant negative correlationsBarium (01/90)
between barium concentrations in drinking water and
mortality from atherosclerotic heart disease and total
cardiovascular disease, respectively. Conversely,
Brenniman et al.
reported significantly higher sex- andage-adjusted death rates for “all cardiovascular diseases”
and “heart disease” in an unspecified number of Illinois
communities with high concentrations of barium in
drinking water (
2 to 10 mg/L) than in communitieswith low concentrations (0.0 to 0.2 mg/L) for the period
1971 to 1975. Although the communities were matched
for similar demographic and socioeconomic status
characteristics, population mobility varied between the
communities with high and low barium levels (i.e., two
of the communities with high barium concentrations in
drinking water had a considerable increase in population
size over the study period).
The lack of data on exposure of individuals in
populations in the ecological studies described above
and the resulting inability to adjust rigorously for
confounding factors and population mobility limit their
usefulness in assessing cause–effect relationships.
Moreover, the results of the ecological study in Illinois
conducted by Brenniman et al.
were not confirmed ina further cross-sectional study by Brenniman and Levy
of cardiovascular disease prevalence in 1175 adult
residents of West Dundee, Illinois (with a mean barium
concentration in drinking water of 7.3 mg/L and a range
of 2.0 to 10.0 mg/L) and in 1203 adult residents of
McHenry (with a mean barium concentration in drinking
water of 0.1 mg/L).
Blood pressures of all participantsin the study were measured, and data on occurrence of
cardiovascular, cerebrovascular and renal disease and
possible confounding factors were determined by
questionnaires administered by trained survey workers.
(It was not specified whether or not the study was
conducted blindly.) The socioeconomic status and
demographic characteristics of the populations in the
two towns were similar. There were no significant
differences in the prevalence of hypertension, stroke and
heart and kidney disease between the two populations,
even when the use of water softeners, medication,
duration of exposure, smoking and obesity were taken
into account. The authors concluded that blood pressure
in adults does not appear to be adversely affected even
following prolonged ingestion of drinking water
containing more than 7 mg/L barium.
In a recently completed but unpublished clinical
study, 11 “healthy” men were exposed to barium (as
barium chloride) in drinking water: 0 mg/L for two
weeks, 5 mg/L for the next four weeks and 10 mg/L for
the last four weeks.
Attempts were made to controlseveral of the risk factors for cardiovascular disease,
including diet, exercise, smoking and alcohol
consumption throughout the study period (although
study subjects were not continuously monitored in this
regard). Based on twice daily monitoring of blood
pressure, periodic monitoring of blood (for total
cholesterol, triglycerides, HDL cholesterol,
apolipoproteins A1, A2 and B and serum potassium,
glucose, calcium and albumin) and urine (for
vanillymandelic acid and total metanephrines),
electrocardiographic monitoring at the end of each
exposure period and liver function tests, there was no
consistent indication of any adverse effects. There was,
however, a trend towards increased serum calcium
between 0 and 5 mg/L that persisted at 10 mg/L, which,
for total calcium, normalized for differences in albumin
level, was statistically significant. The authors suggested
that this increase would not be expected to be clinically
important. The lack of adverse effects observed in this
study may be attributable to the small number of
subjects included or the short period of exposure.
Tardiff et al.
exposed groups of 30 female and30 male Charles River rats to 0, 10, 50 or 250 mg/L
barium as barium chloride (equivalent to mean doses of
0, 1.7 and 2.1, 8.1 and 9.7, and 38.1 and 45.7 mg/kg bw
per day for males and females, respectively) in drinking
water for 13 weeks with interim kills (five of each sex)
at four and eight weeks. No adverse histological or
haematological effects were observed; there were also
no effects on serum enzymes or ions, body weight gain
or food consumption. Water consumption was slightly
depressed in the highest dose group (38.1/45.7 mg/kg
bw per day); there was also a slight decrease in adrenal
weights in some dose groups, but it did not appear to be
There were no effects on blood pressure in Sprague-
Dawley rats exposed to 100 ppm barium in drinking
water as barium chloride (equivalent to 15 mg/kg bw per
day, based on the authors’ calculations that 10 ppm was
equal to 1.5 mg/kg bw per day) for up to 20 weeks.
the same series of studies, there were no changes in
blood pressure in hypertension-susceptible Dahl and
uninephrectomized rats exposed for 16 weeks to up to
1000 ppm barium in distilled water or 0.9% saline. At
the highest dose level (1000 ppm), however, there were
ultrastructural changes in the glomeruli of the kidney
discernible by electron microscopy. In addition, no
significant electrocardiographic changes during
L-norepinephrine challenge were observed in Sprague-
Dawley rats ingesting drinking water containing
250 ppm barium for five months.
In a limited study in which the survival, incidenceof tumours upon gross examination at autopsy and
serum levels of cholesterol, glucose and uric acids were
determined in Long-Evans rats exposed for their lifetime
to 5 ppm barium as barium acetate in drinking water,
there was a slight enhancement in growth of females and
a significant increase in proteinuria in males.
should be noted that mortality due to an epidemic of
males and 22% in females; there were 52 animals of
each sex per group at the initiation of the study.) In a
similar study in which 5 ppm barium as barium acetate
was administered in drinking water to Charles River CD
mice over their life span, there was a significant
reduction in the survival of males but no effects on body
weight gain, oedema, incidence of tumours or blanching
of incisor teeth based on gross examination at autopsy.
McCauley et al.31
reported no histopathological
effects upon examination of 34 tissues in male and
female Sprague-Dawley rats exposed to 1, 10, 100 or
250 ppm barium as barium chloride in drinking water
for up to 68 weeks.
Perry et al.
studied the effect of the ingestion ofbarium in drinking water on blood pressure in rats.
Groups of female Long-Evans rats were exposed to 1,
10 or 100 ppm barium as barium chloride in drinking
water for one, four or 16 months, equivalent to average
daily barium doses of 0.051, 0.51 and 5.1 mg/kg bw per
There were no changes in mean systolic pressure
in animals exposed to 1 ppm barium (0.051 mg/kg bw
per day) for one to 16 months. At 10 ppm barium
(0.51 mg/kg bw per day), there were mean increases in
blood pressure of 4 to 7 mmHg by eight months, which
persisted thereafter. In rats receiving 100 ppm barium
(5.1 mg/kg bw per day), there were significant and
persistent increases in mean systolic pressure
(12 mmHg) after only one month, which gradually
increased to a mean of 16 mmHg after 16 months of
exposure. Rates of cardiac contraction, electrical
excitability and high energy phosphate and
phosphorylation potential were decreased. It has been
suggested that the calcium content of the diet in this
study may have been less than the minimum daily
requirement; however, manifestations of calcium
deficiency on growth patterns were not observed.
Increases in systolic pressure of 4 to 7 mmHg are
deemed sufficiently small so as to not constitute an
adverse effect; therefore, 5.1 mg/kg bw per day is
considered to be the lowest-observed-adverse-effect
level (LOAEL), and 0.51 mg/kg bw per day is
considered to be the no-observed-adverse-effect level
(NOAEL). This judgement is consistent with the
opinion of the U.S. Environmental Protection Agency.
Perry et al.34
estimated that a 0.1 to 1% increase in the
clinical appearance of coronary heart disease in the U.S.
population over a six-year period could result from an
increase of 15 mmHg in mean systolic blood pressure.
Wilkins and Calabrese
suggested that, whereas anincrease in systolic blood pressure of 5 mmHg would
have virtually no short-term clinical implications for
persons 35 years old and younger, a shift of 5 mmHg
may become a difference of nearly 10 mmHg by age 65.
In the United States, an increase of 10 mmHg in systolic
blood pressure at this age would increase the average
risk of a heart attack by 14%.
There has been no evidence of the carcinogenicity
of barium in extremely limited lifetime bioassays of rats
and mice exposed to 5 mg/L in drinking water, based on
gross examination only of tumours at autopsy.
Barium chloride did not increase the frequency of
mutation in repair-deficient strains of Bacillus subtilis.
Results were also negative for the induction of errors inviral DNA transcription in vitro.
It has been reported that the oestrous cycle wasshortened and that the morphological structure of the
ovaries was disturbed in female rats exposed to
± 0.7 mg/m3
carbonate dust for four months.
Mortality increasedand body weight gain decreased in the offspring of the
dams in the high dose group; the lability of the
peripheral nervous system decreased, and blood
disorders (erythropenia, leukocytosis, eosinophilia,
neutrophilia) related to the irritant effect of barium on
the bone marrow in two-month-old offspring were also
In a similar inhalation study in male ratsexposed to 22.6
barium carbonate dust,
deleterious effects on spermatogenesis were reported.However, data presented in the published account were
insufficient to permit evaluation of the protocols of these
Classification and Assessment
Because there are few data available regarding the
carcinogenicity of barium, it has been classified in
Group VA (inadequate data for evaluation). For
compounds classified in Group VA, the maximum
acceptable concentration (MAC) is derived on the basis
of division of the NOAEL or LOAEL in an animal
species by an uncertainty factor.
In studies in which Long-Evans rats ingested
drinking water containing 100 mg/L (5.1 mg/kg bw per
day) for up to 16 months, there were significant
increases in mean systolic blood pressure (12 mmHg
after one month, 16 mmHg after 16 months), depressed
rates of cardiac contraction, depressed electrical
excitability and decreased high energy phosphate and
Increases of 4 to 7 mmHgin mean systolic blood pressure were observed in rats
exposed to a barium concentration of 10 mg/L
(0.51 mg/kg bw per day) in drinking water after eight
months. In a study with Sprague-Dawley rats, however,
there were no effects on blood pressure following
exposure to barium at 100 ppm in drinking water
(approximately 15 mg/kg bw per day) for 20 weeks.
It has been suggested by some authors that small
increases in mean systolic blood pressure in the human
population similar to those observed in rats by Perry et al.
(5 to 15 mmHg) could result in significant
increases in clinical cases of coronary heart disease.
However, in the most sensitive epidemiological study
conducted to date, there were no significant differences
in blood pressure or the prevalence of cardiovascular
disease between a population drinking water containing
7.3 mg/L barium and one ingesting water containing
0.1 mg/L barium.
On the basis of the results of the epidemiologicalstudy by Brenniman and Levy,
in which adverseeffects on blood pressure and increases in the prevalence
of cardiovascular disease were not observed in a
population ingesting water containing a mean concen-
tration of 7.3 mg/L barium, the MAC is derived as
= 0.73 mg/L
7.3 mg/L is the NOAEL in the most sensitive epidemiological study
conducted to date
•10 is the uncertainty factor (to account for intraspecies variation).
This value is not substantially different from that
derived on the basis of the results of toxicological
studies in animals, based on the NOAEL of 0.51 mg/kg
bw per day for effects on blood pressure in rats
an uncertainty factor of 10 (
10 for intraspeciesvariation;
1 for interspecies variation, as the results of awell-conducted epidemiological study indicate that
humans are less sensitive than rats to barium in drinking
Because the MAC derived above does not differgreatly from the MAC of 1.0 mg/L included in the 1978
Guidelines, a MAC for barium of 1.0 mg/L has been
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