INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY
ENVIRONMENTAL HEALTH CRITERIA 107
BARIUM
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experts and does not necessarily represent the decisions or the stated
policy of the United Nations Environment Programme, the International
Labour Organisation, or the World Health Organization.
Published under the joint sponsorship of
the United Nations Environment Programme,
the International Labour Organisation,
and the World Health Organization
World Health Orgnization
Geneva, 1990
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chemicals.
WHO Library Cataloguing in Publication Data
Barium.
(Environmental health criteria ; 107)
1.Barium
I.Series
ISBN 92 4 157107 1 (NLM Classification: QV 618)
ISSN 0250-863X
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CONTENTS
1. SUMMARY AND CONCLUSIONS
1.1. Summary
1.1.1. Identity, natural occurrence, and analytical methods
1.1.2. Production, uses, and sources of exposure
1.1.3. Kinetics and biological monitoring
1.1.4. Effects on experimental animals
1.1.5. Effects on human beings
1.1.6. Effects on organisms in the environment
1.2. Conclusions and recommendations
2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, ANALYTICAL METHODS
2.1. Identity
2.2. Physical and chemical properties of barium
2.3. Physical and chemical properties of barium compounds
2.4. Analytical sampling
2.4.1. Water
2.4.2. Soils and sediments
2.4.3. Air
2.4.4. Biological materials
2.5. Analytical procedures
2.5.1. Commonly used analytical methods
2.5.1.1 AAS - direct aspiration method
2.5.1.2 AAS - furnace technique
2.5.1.3 AAS - ICP
2.5.2. Analytical methods used for special applications
2.5.2.1 Mass spectrometry
2.5.2.2 X-ray fluorescence spectrometry
2.5.2.3 Neutron activation analysis
3. SOURCES IN THE ENVIRONMENT
3.1. Natural occurrence
3.2. Man-made sources
3.2.1. Production levels, processes, and uses
4. ENVIRONMENTAL TRANSPORT AND DISTRIBUTION
4.1. Transport and distribution between media
4.1.1. Air
4.1.2. Water
4.1.3. Soil
4.1.4. Vegetation and wildlife
4.1.5. Entry into the food chain
4.2. Biotransformation
5. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE
5.1. Environmental levels
5.1.1. Air
5.1.2. Water
5.1.2.1 Surface waters
5.1.2.2 Drinking-water
5.1.2.3 Ocean waters
5.1.3. Soil and sediment
5.1.4. Food
5.1.5. Feed
5.1.6. Other products
5.1.7. Nuclear fallout
5.2. General population exposure
5.2.1. Environmental sources, food, drinking-water, and air
5.2.2. Other sources
5.2.3. Subpopulations at special risk
5.3. Occupational exposure during manufacture, formulation, or use
6. KINETICS AND METABOLISM
6.1. Absorption
6.1.1. Inhalation route
6.1.1.1 Laboratory animals
6.1.1.2 Humans
6.1.2. Oral route
6.1.2.1 Laboratory animals
6.1.2.2 Humans
6.1.3. Parenteral administration
6.2. Distribution
6.2.1. Levels in tissues of experimental animals
6.2.2. Levels in human tissue
6.3. Elimination and excretion
6.3.1. Laboratory animals
6.3.2. Humans
6.4. Metabolism
6.4.1. Laboratory animals
7. EFFECTS ON ORGANISMS IN THE ENVIRONMENT
7.1. Microorganisms
7.1.1. Viruses
7.1.2. Bacteria
7.1.3. Inhibition of growth
7.1.4. Specific effects
7.2. Aquatic organisms
7.2.1. Aquatic plants
7.2.2. Aquatic animals
7.2.3. Effects of marine drilling muds
7.3. Bioconcentration
8. EFFECTS ON EXPERIMENTAL ANIMALS AND IN VITRO SYSTEMS
8.1. Acute exposure
8.1.1. Oral route
8.1.2. Inhalation route
8.1.3. Parenteral administration
8.1.4. Topical route
8.2. Short-term exposures
8.2.1. Inhalation route
8.2.2. Oral route
8.3. Long-term exposure
8.3.1. Inhalation route
8.3.2. Oral route
8.4. Reproduction, embryotoxicity, and teratogenicity
8.4.1. Reproduction
8.4.2. Embryotoxicity and teratogenicity
8.5. Mutagenicity and related end-points
8.6. Tumorigenicity and carcinogenicity
8.7. Special studies
8.7.1. Effects on the heart
8.7.2. Vascular effects
8.7.3. Electrophysiological effects
8.7.4. Effects on synaptic transmission and catecholamine release
8.7.5. Effects on the immune system
8.7.6. Ocular system
9. EFFECTS ON MAN
9.1. General population exposure
9.1.1. Acute toxicity - poisoning incidents
9.1.2. Short-term controlled human studies
9.1.3. Epidemiological studies
9.1.3.1 Cardiovascular disease
9.1.3.2 Other effects
9.2. Occupational exposure
9.2.1. Effects of short- and long-term exposure
9.3. Carcinogenicity of barium chromate
10. EVALUATION OF HUMAN HEALTH RISKS AND EFFECTS ON THE ENVIRONMENT
10.1. Evaluation of human health risks
10.1.1. Exposure levels
10.1.1.1 General population
10.1.1.2 Occupational - air exposures
10.1.1.3 Acute exposures
10.1.2. Toxic effects; dose-effect and dose-response relationships
10.1.3. Risk evaluation
10.2. Evaluation of effects on the environment
11. RECOMMENDATIONS FOR FURTHER STUDIES
12. PREVIOUS EVALUATIONS BY INTERNATIONAL BODIES
REFERENCES
RESUME ET CONCLUSIONS
EVALUATION DES RISQUES POUR LA SANTE HUMAINE ET EFFETS SUR L'ENVIRONNEMENT
RECOMMANDATIONS EN VUE D'ETUDES COMPLEMENTAIRES
RESUMEN Y CONCLUSIONES
EVALUACION DE LOS RIESGOS PARA LA SALUD HUMANA Y DE LOS EFECTOS SOBRE EL
MEDIO AMBIENTE
RECOMENDACIONES PARA ULTERIORES ESTUDIOS
WHO TASK GROUP ON ENVIRONMENTAL HEALTH CRITERIA FOR BARIUM
Members
Dr V. Bencko, Department of Hygiene, Institute of Tropical
Health, Postgraduate School of Medicine and Pharmacy,
Prague, Czechoslovakia
Dr X.C. Ding, Department of Toxicology, Institute of Occu-
pational Health, Shanghai, People's Republic of Chinaa
Dr T. Eikmann, Institute for Hygiene and Occupational
Medicine, Medical Faculty, Technical University of
Rhineland-Westphalia, Aachen, Federal Republic of
Germany
Dr J.P. Flesch, Division of Standards Development and
Technology Transfer, National Institute for Occu-
pational Safety and Health, Robert A. Taft Labora-
tories, Cincinnati, Ohio, USA
Ms K. Hughes, Environmental Health Directorate, Department
of National Health and Welfare, Tunney's Pasture,
Ottawa, Ontario, Canada
Dr F. Izumi, Department of Pharmacology, University of
Occupational and Environmental Health, School of Medi-
cine, Fukuoka, Japan
Dr M.L. Tosato, Istituto Superiore di Sanità, Rome, Italy
(Chairperson)
Secretariat
Dr B.H. Chen, International Programme on Chemical Safety,
World Health Organization, Geneva, Switzerland
(Secretary)
Dr P.G. Jenkins, International Programme on Chemical
Safety, World Health Organization, Geneva, Switzerland
Dr T. Ng, Office of Occupational Health, World Health
Organization, Geneva, Switzerland
Dr L. Papa, Environmental Criteria and Assessment Office,
US Environmental Protection Agency, Cincinnati, Ohio,
USA (Rapporteur)
a Invited but unable to attend.
NOTE TO READERS OF THE CRITERIA MONOGRAPHS
Every effort has been made to present information in
the criteria monographs as accurately as possible without
unduly delaying their publication. In the interest of all
users of the environmental health criteria monographs,
readers are kindly requested to communicate any errors
that may have occurred to the Manager of the International
Programme on Chemical Safety, World Health Organization,
Geneva, Switzerland, in order that they may be included in
corrigenda, which will appear in subsequent volumes.
* * *
A detailed data profile and a legal file can be
obtained from the International Register of Potentially
Toxic Chemicals, Palais des Nations, 1211 Geneva 10,
Switzerland (Telephone No. 7988400 or 7985850).
ENVIRONMENTAL HEALTH CRITERIA FOR BARIUM
A WHO Task Group on Environmental Health Criteria for
Barium met in Geneva from 20 to 24 November 1989. Dr M.
Mercier, Manager, IPCS, opened the meeting and welcomed
the participants on behalf of the heads of the three IPCS
cooperating organizations (UNEP/ILO/WHO). The Task Group
reviewed and revised the draft criteria monograph and made
an evaluation of the risks for human health and the en-
vironment from exposure to barium.
The first draft of this monograph was prepared by
Dr L. PAPA of the US Environmental Protection Agency.
The second draft was also prepared by Dr L. Papa, incor-
porating comments received following the circulation of
the first draft to the IPCS Contact Points for Environ-
mental Health Criteria documents. Dr B.H. Chen and Dr
P.G. Jenkins, both members of the IPCS Central Unit, were
responsible for the overall scientific content and
editing, respectively.
The efforts of all who helped in the preparation and
finalization of the document are gratefully acknowledged.
ABBREVIATIONS
AAS Atomic absorption spectrophotometry
BUN Blood urea nitrogen
CNS Central nervous system
ECG Electrocardiogram
IARC International Agency for Research on Cancer
ip Intraperitoneal
iv Intravenous
LLD Lowest lethal dose
PNS Peripheral nervous system
sc Subcutaneous
1. SUMMARY AND CONCLUSIONS
1.1. Summary
1.1.1. Identity, natural occurrence, and analytical methods
Barium is one of the alkaline earth metals, having a
relative atomic mass of 137.34 and an atomic number of 56.
It has seven naturally occurring stable isotopes, of which
138Ba is the most abundant. Barium is a yellowish-white
soft metal that is strongly electropositive. It combines
with ammonia, water, oxygen, hydrogen, halogens, and sul-
fur, energy being released by these reactions. It also re-
acts strongly with metals to form metal alloys. In nature
barium occurs only in a combined state, the principal
mineral forms being barite (barium sulfate) and witherite
(barium carbonate). Barium is also present in small quan-
tities in igneous rocks and in feldspar and micas. It may
be found as a natural component of fossil fuel and is
present in air, water, and soil.
Certain barium compounds, such as acetate, nitrate,
and chloride are relatively water soluble, whereas the
fluoride, carbonate, oxalate, chromate, phosphate, and
sulfate salts have very low solubility. With the exception
of barium sulfate, the water solubility of the barium
salts increases with decreasing pH.
Sampling of barium in aqueous and gaseous media is
conducted in the same way as it is for any other material.
Sediments, sludge, and soil samples are oven-dried or
sintered. The samples are then extracted in 1% HCl for
analysis of trace elements, including barium. Biological
samples are frozen or lyophilized and are prepared for
barium analysis using dry-washing procedures.
Atomic absorption and flame and plasma emission
spectrometry are the most commonly employed analytical
methods. Neutron activation, isotope dilution mass spec-
trometry, and X-ray fluorescence are also used.
1.1.2. Production, uses, and sources of exposure
Barite ore is the raw material from which nearly all
other barium compounds are derived. World production of
barite in 1985 was estimated to be 5.7 million tonnes.
Barium and its compounds are used in diverse industrial
products ranging from ceramics to lubricants. It is used
in the manufacture of alloys, as a loader for paper, soap,
rubber, and linoleum, in the manufacture of valves, and as
an extinguisher for radium, uranium, and plutonium fires.
Anthropogenic sources of barium are primarily indus-
trial. Emissions may result from mining, refining, or
processing of barium minerals and manufacture of barium
products. Barium is also discharged in waste water from
metallurgical and industrial processes. Deposition on soil
may result from man's activities, including the disposal
of fly ash and primary and secondary sludge in landfill.
It was estimated that in 1976, mining and processing of
barite ore in the USA released approximately 3200 tonnes
of particulates into the air, and fugitive dusts from the
use of barite in oil drilling and oil-related industries
accounted for approximately 100 tonnes of particulates. In
1972, the barium chemical industry in the USA released an
estimated 1200 tonnes of particulates into the atmos-
phere.
Environmental transport of barium occurs through the
air, water, and soil. Atmospheric barium consists of par-
ticulates whose transport is regulated by normal atmos-
pheric and meteorological circumstances. Transport of
barium in water is subject to interaction with other ions,
including sulfate, which regulates and limits barium con-
centration. Little information is available regarding the
aqueous transformations and transport of barium.
Exposure to barium can occur through air, water, or
food. The levels of barium in the air are not well docu-
mented. In the USA, the usual concentration is estimated
to be 0.05 µg/m3 or less. No distinct correlation has
been observed between ambient levels of barium in the air
and the extent of industrialization, although higher con-
centrations occur around smelters.
The presence of barium in sea water, river water, and
well-water has been documented, and it is also found in
sediments and natural waters in contact with sedimentary
rocks. Barium is present in almost all surface waters at
concentrations up to 15 000 µg/litre and contributes to
the hardness of the water. The barium concentration in
wells depends on the content of leachable barium in rocks.
Drinking-water contains 10-1000 µg/litre, although water
in certain regions of the USA has been shown to have con-
centrations in excess of 10 000 µg/litre. Municipal water
supplies depend upon the quality of surface and ground
water and, depending on the hardness, contain a wide range
of barium concentration. Studies from USA show levels in
drinking-water ranging from 1-20 µg/litre. Based on this
information and assuming a consumption rate of 2 litres
per day, the daily intake would be 2-40 µg barium.
Several studies have estimated a daily dietary intake
range of 300-1770 µg with large variations. Humans seldom
eat plants in which barium is present in significant
amounts or the part of the plant in which the barium ac-
cumulates. The Brazil nut tree is an exception, reported
concentrations being 1500-3000 µg/g. Tomatoes and soy
bean are also known to concentrate soil barium, the bio-
concentration factor ranging from 2 to 20.
In general, barium does not accumulate in common
plants in sufficient quantities to be toxic to animals.
However, it has been suggested that the large quantities
of barium (as high as 1260 mg/kg) accumulated in legumes,
alfalfa, and soybeans could cause problems in domestic
cattle.
The barium content of dry tobacco leaves averages 105
mg/kg, most of which is likely to remain in the ash during
burning. No values for barium concentrations in tobacco
smoke have been reported.
Another source of barium exposure is nuclear fallout.
However, with the establishment of atmospheric test ban
treaties, the quantity of radioactive barium in the en-
vironment has decreased.
1.1.3. Kinetics and biological monitoring
The average person (70 kg) contains approximately
22 mg of barium, most of which (91%) is localized in the
bone. Trace quantities are found in various tissues such
as the aorta, brain, heart, kidney, spleen, pancreas, and
lung. Total barium in human beings tends to increase with
age. The levels in the body depend on the geographical
location of the individual. Barium has also been found in
all samples of stillborn babies, suggesting that it can
cross the placenta.
It is difficult to assess the uptake of ingested
barium because a number of factors affect absorption. For
instance, the presence of sulfate in food results in the
precipitation of barium sulfate. Studies on experimental
animals and limited human data indicate that soluble
barium is absorbed through the intestine to the extent of
< 10% in adults but more in the young. Uptake occurs rap-
idly in the salivary and adrenal glands, heart, kidney,
mucosal tissue and blood vessels, and finally in the
skeleton. Like calcium, barium accumulates in bone. It is
deposited preferentially in the most active areas of bone
growth, primarily at the periosteal surfaces. Other fac-
tors important in absorption and deposition include age
and dietary restriction. Older rats exhibit decreased
absorption and bone concentrations of barium. Fasting
elicits an increase in barium absorption.
Inhaled barium can be absorbed through the lung or
directly from the nasal membrane into the bloodstream. In
rats, exposure results in deposition in the bones, but
continued exposure results in decreased deposition both in
the bones and the lungs. Insoluble compounds, such as
barium sulfate, accumulate in the lungs and are cleared
slowly by ciliary action.
Barium is eliminated in the urine and in the faeces,
the rates varying with the route of administration. Within
24 h, approximately 20% of a barium dose, injected into
humans, was eliminated in the faeces and approximately 5%
in the urine. Plasma barium is almost entirely cleared
from the bloodstream within 24 h. The elimination of
ingested barium in both human beings and animals occurs
principally in the faeces rather than in the urine. Fol-
lowing inhalation exposure, there is a slow elimination of
barium from bone and, thus, from the whole body. An esti-
mate of the biological half-life for barium in the rat is
90-120 days. For adequate biological monitoring of human
exposure, the elimination of barium in urine as well as in
faeces should be monitored.
1.1.4. Effects on experimental animals
In the rat, oral LD50 values of 118, 250, and 355
were measured for barium chloride, fluoride, and nitrate,
respectively. The acute effects of barium ingestion
include salivation, nausea, diarrhoea, tachycardia, hypo-
kalaemia, twitching, flaccid paralysis of skeletal muscle,
respiratory muscle paralysis, and ventricular fibril-
lation. Respiratory muscle paralysis and ventricular fib-
rillation may lead to death. Various studies have demon-
strated the detrimental effect of barium upon ventricular
automaticity and pacemaker current in the heart. Intra-
venous barium injections to anaesthetized dogs indicated
that these acute effects were due to prompt and substan-
tial hypokalaemia and could be prevented or reversed by
potassium administration.
Barium causes mild skin and severe eye irritation in
rabbits.
When rats ingested tap water containing up to 250 mg
barium/litre for 13 weeks, no signs of toxicity were
observed, although some groups showed a decrease in the
relative weight of the adrenals.
Rats given 10 or 100 mg barium/litre in their
drinking-water for 16 months experienced hypertension, but
a level of 1 mg/litre did not induce any blood pressure
changes. Analysis of myocardial function at 16 months
(100 mg barium/litre) revealed significantly altered car-
diac contractility and excitability, myocardial metabolic
disturbances, and hypersensitivity of the cardiovascular
system to sodium pentobarbital.
Oral or inhalation administration of barium carbonate
in rats resulted in adverse reproductive effects. In
addition, the death rate was higher for the newborn off-
spring of barium-treated dams. There is limited evidence
of teratogenicity of barium, but no conclusive evidence of
carcinogenicity is available.
Barium possesses chemical and physiological properties
that allow it to compete with and replace calcium in pro-
cesses mediated normally by calcium, particularly those
relating to the release of adrenal catecholamines and
neurotransmitters, such as acetylcholine and noradrena-
line.
Limited information is available regarding the immuno-
logical effects of barium in animals.
1.1.5. Effects on human beings
Several cases of poisoning due to the ingestion of
barium compounds have been reported. Barium doses as low
as 0.2-0.5 mg/kg body weight, generally resulting from the
ingestion of barium chloride or carbonate, have been found
to lead to toxic effects in adult humans. Clinical fea-
tures of barium poisoning include acute gastroenteritis,
loss of deep reflexes with onset of muscular paralysis,
and progressive muscular paralysis. The muscular paralysis
appears to be related to severe hypokalaemia. In most
reported cases, rapid and uneventful recovery occurred
after treatment with infused potassium salts (carbonate or
lactate) and/or oral administration of sodium sulfate.
Limited epidemiological studies have been conducted to
investigate the possible relationship between barium con-
centrations in drinking-water and cardiovascular mor-
tality, but the results have been inconsistent and incon-
clusive.
No increase in the incidence of elevated blood press-
ure, stroke, or heart and kidney disease was observed in a
population exposed to high concentrations of barium in
drinking-water when compared to a similar group exposed to
lower levels. In a short-term human volunteer study, no
effects on blood pressure were induced by the consumption
of barium in drinking-water.
An increase in the incidence of hypertension was
reported among workers exposed to barium, compared with
non-exposed workers. Baritosis has been observed in indi-
viduals occupationally exposed to barium compounds. A
study group consisting of barium-exposed workers and
people residing near a landfill site containing barium was
found to have an increased prevalence of musculoskeletal
symptoms, gastrointestinal surgery, skin problems, and
respiratory symptoms.
No conclusive association was found between the level
of barium in drinking-water and the incidence of congeni-
tal malformations. There is no evidence that barium is
carcinogenic.
1.1.6. Effects on organisms in the environment
Barium directly affects the physico-chemical proper-
ties as well as the infectivity of several viruses and
their ability to multiply. It also affects the development
of germinating bacterial spores and has a variety of
specific effects on different microorganisms, including
the inhibition of cellular processes.
Little information is available on the effects of
barium on aquatic organisms. There were no effects on sur-
vival in fish following exposure for 30 days. However, in
a 21-day study, impairment of reproduction and reduction
in growth were observed in daphnids at a dose of 5.8 mg
barium/litre. No evidence has been found to indicate that
barite is toxic to marine animals. However, exposure to
barite in large amounts could adversely affect coloniz-
ation by benthic animals.
Marine plants, as well as invertebrates, may actively
accumulate barium from sea water.
1.2. Conclusions and recommendations
Barium, at concentrations normally found in our en-
vironment, does not pose any significant risk for the gen-
eral population. However, for specific subpopulations and
under conditions of high barium exposure, the potential
for adverse health effects should be taken into account.
Few data are available for evaluating the risk to the
environment posed by barium. However, based on the avail-
able information on the toxic effects of barium in
daphnids, it appears that barium may represent a risk to
populations of some aquatic organisms.
There is a need for epidemiological studies, for
research on bioavailability and cardiovascular and immuno-
logical toxicity, and for additional information on
chronic aquatic toxicity. In order to establish better
protection measures, more data on exposures in the work-
place and the use of biomarkers are necessary.
2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, ANALYTICAL METHODS
2.1. Identity
Barium is a member of the alkaline earth metals in
Group IIA of the periodic table, along with beryllium,
magnesium, calcium, strontium, and radium. The symbol for
the element is Ba. Barium has an atomic number of 56 and a
relative atomic mass of 137.34. The CAS registry and RTECS
registry numbers for barium are 7440-39-3 and CQ8370000,
respectively. Metallic barium is obtained by reducing
barium oxide with aluminum or silicon in a vacuum at high
temperature.
Twenty-five barium isotopes have been identified
(CRC, 1988). There are seven naturally occurring stable
isotopes with mass numbers of 130, 132, 134, 135, 136,
137, and 138, 138Ba being the most abundant (Lederer et
al., 1967). The others are unstable isotopes with half-
lives ranging from 12.8 days for 140Ba to 12 seconds for
143Ba (CRC, 1988). Two of these isotopes, 131Ba and
139Ba, are used in research as radioactive tracers. A
list of common barium compounds with their formulae and
CAS registry numbers is presented in Table 1.
2.2. Physical and chemical properties of barium
Important physical and chemical properties of barium
relevant to exposure assessment and effects are shown in
Table 2. It is a silver-white, soft metal, relatively
volatile and readily distilled (Goodenough & Stenger,
1973). Powdered barium is pyrophoric and very dangerous
to handle in the presence of air or other oxidizing gases
(Quagliano, 1959). As might be expected from its high
electrode potential (-2.912 V), barium is extremely reac-
tive and the free energy of formation of its compounds is
very high. Therefore it does not exist in nature in the
elemental state but occurs as the divalent cation, Ba2+,
in combination with other elements. Barium reacts readily
with halogens, oxygen, and sulfur to form halides, oxide,
and sulfide. It also reacts with nitrogen and hydrogen at
higher temperatures to form the nitride and hydride, and
it reacts vigorously with water displacing hydrogen to
form the hydroxide. Treatment of barium hydroxide with
hydrogen peroxide at low temperatures forms barium per-
oxide, which can also be formed by direct combination of
oxygen with barium oxide or the metal. Barium exhibits
little tendency to form complexes; the amines formed with
NH3 are unstable and the beta -diketons and alcoholates
are not well characterized.
Table 1. Common barium compoundsa
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Substance Formula CAS No. RTECS No.
-----------------------------------------------------------------------------------
Aluminium barium titanium oxide Not given 52869-91-7 BD 0345400
Barium acetate Ba(C2H3O2)2.H2O 543-80-6 AF 4550000
Barium azide Ba(N3)2 18810-58-7 CQ 8500000
Barium bromate Ba(BrO3)2.H2O 13967-90-3 EF 8715000
Barium cadmium laurate (C12H24O2)4.Ba.Cd Not given OE 9805000
Barium cadmium stearate (C18H36O2)4.Ba,Cd 1191-79-3 WI 2830000
Barium calcium titanium oxide Not given 52869-93-9 CQ 8580000
Barium carbonate BaCO3 513-77-9 CQ 8600000
Barium chlorate Ba(ClO3)2.H2O 13477-00-4 FN 9770000
Barium chloride BaCl2 10361-37-2 CQ 8950000
Barium chloride, dihydrate BaCl2.2H2O 10326-27-9 CQ 8751000
Barium chromate (VI) BaCrO4 10294-40-3 CQ 8760000
Barium cyanide Ba(CN)2 542-62-1 CQ 8785000
Barium fluoborate Ba(BF4)2 13862-62-9 CQ 8925000
Barium fluoride BaF2 7787-32-8 CQ 9100000
Barium hypochlorite Ba(ClO2)2 13477-10-6 NH 3480000
Barium iron oxide BaFe12O19 12047-11-9 CQ 9520800
Barium nitrate Ba(NO3)2 10022-31-8 CQ 9625000
Barium oxide BaO 1304-28-5 CQ 9800000
Barium perchlorate Ba(ClO4)2.4H2O 13465-95-7 SC 7550000
Barium permanganate Ba(MnO4)2 7787-36-2 SD 6405000
Barium peroxide BaO2 1304-29-6 CR 0175000
Barium silicofluoride BaSiF6 17125-80-3 CR 0525000
Barium sulfate BaSO4 7727-43-7 CR 0600000
Barium sulfide BaS 50864-67-0 CR 0270000
Barium sulfide, mixture with sulfur Not given 8077-30-3 CR 0660000
Barium sulfonates Not given Not given CR 0700000
Barium zirconium (IV) oxide BaZr4O4 12009-21-1 CR 0875000
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a Source: RTECS (1985).
Table 2. Physical and chemical properties of bariuma
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Atomic number 56
Relative atomic mass 137.34
Physical state solid metal
Colour yellowish-white
Melting point 725 °C
Boiling point 1640 °C
Solubility in water reacts with release of H2
Solubility in alcohol soluble (decomposes)
Solubility in benzene insoluble
Relative density (at 20 °C) 3.51
Extremely reactive with water, ammonia, halogens, oxygen
most acids
Electrode potential (Eo(aq)Ba2+/Ba)
(at 25 °C, 1 atm.) -2.912 volts
Electronegativity 1.02
Flame coloration test green
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a Source: Weast (1983), Windholz (1983).
Barium attacks most metals with the formation of
alloys; iron is the most resistant to alloy formation.
Barium forms alloys and intermetallic compounds with lead,
potassium, platinum, magnesium, silicon, zinc, aluminium,
and mercury (Hansen, 1958). Metallic barium reduces the
oxides, halides, and sulfides of most of the less reactive
metals, thereby producing the corresponding metal.
2.3. Physical and chemical properties of barium compounds
Barium compounds exhibit close relationships with the
compounds of calcium and strontium, which are also alka-
line earth metals. The physical and chemical properties
of various barium compounds are listed in Table 3. Barium
acetate, nitrate, and chloride are quite soluble, whereas
the arsenate, carbonate, oxalate, chromate, fluoride, sul-
fate, and phosphate salts are very poorly soluble. All
barium salts, except for barium sulfate, become increas-
ingly soluble as the pH decreases. These salts dissolve
partially in carbonic acid and completely in hydrochloric
or nitric acids. Strong sulfuric acid is required to dis-
solve barium sulfate.
Table 3. Physical and chemical properties of various barium compoundsa
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Relative Relative Solubility Melting Boiling
Compound molecular density in waterb pointc point
mass (°C) (°C)
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Barium acetate 255.45 2.468 58.80 - -
Barium arsenate 689.83 5.10 0.55 1605 -
Barium carbonate 197.37 4.43 0.02 1790 (90) -
Barium chloride 208.25 3.856 375 (26) 962 1560
Barium chromate 253.32 4.498 0.0034 (16) - -
Barium fluoride 175.34 4.89 1.2 (25) 1375 2137
Barium hydroxide x 8H20 315.47 2.18 56 (15) 78 78 (-8H20)
Barium nitrate 261.38 3.24 87 592 d
Barium oxalate 225.35 2.658 0.093 (18) 400d -
Barium oxide 153.36 5.72 34.8 1918 ca.2000
Barium phosphate, dibasic 233.5 4.165 0.1-0.2 410 (710)d -
Barium triphosphate 601.93 4.10 insoluble - -
Barium sulfate 233.4 4.5 0.002 1580 -
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a CRC (1988).
b in g/litre at 20 °C; where the solubility was not measured at 20 °C, the temperature
used is shown in parentheses.
c at 760 mmHg; where the pressure was otherwise, it is given in parentheses.
d decomposes.
In aqueous solution, the barium ion can combine with
organic chelating agents. Owing to its similarity to cal-
cium in its chemical properties and because it lies below
calcium in the periodic table, barium is thought to inter-
act with biochemical pathways involving calcium ion-bind-
ing by competing for binding sites of chelation (Sillen &
Martell, 1964). Barium may also bind with organic ligands
to form biological complexes.
2.4. Analytical sampling
Barium does not require sampling or handling pro-
cedures different from those used in general analytical
practice. The greatest sources of sampling error in
environmental studies are the variations in the material
being sampled. Sampling procedures must not only take
into account the physical and chemical properties of the
specific barium compound but must also accurately reflect
variations in the media (water, air, and soil).
2.4.1. Water
The US EPA (1979a) recommended the following procedure
for sampling and preserving metals in aqueous solution. A
minimum of 200 ml is collected in an analytically clean
container, preferably made of polyethylene, with a poly-
propylene cap (no liner). For the determination of dis-
solved constituents (i.e. barium), the sample must be fil-
tered through a membrane filter (0.45 µm) preferably on-
site. The suspended constituents retained by the membrane
filter are saved if total barium analysis is required. The
filtered sample may be initially preserved by icing. How-
ever, as soon as possible, the sample must be acidified to
a pH <2 with nitric acid (normally 3 ml 1:1 nitric acid
per litre is sufficient). A maximum holding time of 6
months is recommended, although the length of time will
also depend on the type of sample used.
2.4.2. Soils and sediments
Samples of soils, sediments, and sludge are oven-dried
and stored in polyethylene containers. The samples are ex-
tracted in 1% hydrochloric acid for analysis of trace el-
ements including barium (Fortescue et al., 1976). Samples
of benthic intertidal sediments from sandy beaches can be
stored in clean polyethylene bottles and frozen (-15 °C)
(Chow et al., 1978). Benthic sediments are collected with
a non-contaminating box-core device, with only the top
1 cm of the core being saved.
2.4.3. Air
Barium is sampled in the same way as other compounds
in air. A known volume of air is drawn through a cellulose
filter to collect the compound in the particulate fraction
(NIOSH, 1977). Samples collected on the filters are
leached into hot water, filtered, and dried.
2.4.4. Biological materials
Biological tissues such as hair, blood, and placenta
are kept frozen or lyophilized before analysing for barium
(Creason et al., 1976). Dry-washing procedures are used
to prepare the samples for barium analysis. Research at
the National Bureau of Standards, Washington, DC, indi-
cated that bovine liver samples, lyophilized and ground,
showed no change in composition after prolonged storage at
room temperature (Becker, 1976). Similar procedures were
used for orchard plant leaves. Samples carefully dried and
lyophilized can be adequately stored at room temperature
for several years with no significant changes in trace
metal composition (Becker, 1976).
2.5. Analytical procedures
In general, analytical procedures measure total barium
ion present rather than specific barium compounds.
Analysis for soluble barium in aqueous solutions re-
quires consideration of contaminating substances that may
interfere with the assay. Certain contaminants can affect
absorption as well as emission spectra. Maruta et al.
(1972) observed that the presence of aluminum depressed
the barium signal and that the addition of alkali com-
pounds (except caesium) suppressed barium ionization.
Magill & Svehla (1974) also noted that several anions and
cations interfered with the analysis of barium.
Separation of barium from interfering components is
achieved by ion-exchange chromatography. Akiyama & Tomita
(1973) employed a chromium phosphate ion exchanger. Other
workers have used Dowex 50 ion-exchange resin, with vari-
ous degrees of cross linking (Dybczynski, 1972; Wolgemuth
& Broecker, 1970; Bacon & Edmond, 1972; Pierce & Brown,
1977). Elution is carried out with hydrochloric acid.
Pierce & Brown (1977) used a chelating agent, ethylenedi-
amine tetraacetic acid (EDTA), to elute barium from the
Dowex 50 column in a semi-automated procedure. Quantifi-
cation of low concentrations of barium using chemical
methods (wet, gravimetric) is at present seldom attempted.
Owing to the high ionization properties of barium and
spectral interference from calcium emissions, the use of
instrumental methods for analysing barium is often diffi-
cult.
2.5.1. Commonly used analytical methods
Atomic absorption spectrophotometry (AAS) is a readily
available and widely used analytical technique for deter-
mining several metals in solution from a variety of
samples. The US EPA (1974, 1979a) recommends two AAS
methods for barium, the direct aspiration method and the
furnace technique.
2.5.1.1 AAS - Direct aspiration method
The optimal concentration range for determining barium
by the AAS direct aspiration method, using a wavelength of
553.6 nm, is 1-20 mg/litre, with a sensitivity of 0.4
mg/litre and a detection limit of 0.03 mg/litre (US EPA,
1979a). An AAS direct aspiration method for the determi-
nation of water-soluble barium components in air has been
described by NIOSH (1977). The air sample is drawn through
a cellulose membrane filter on which the analyte is col-
lected. The working range of the method was estimated to
be 0.15-1.3 mg/m3, with a sensitivity of 0.0004 mg/m3.
2.5.1.2 AAS - Furnace technique
For concentrations of barium <0.2 mg/litre, the fur-
nace technique is recommended. The optimal concentration
range for barium determination by the furnace technique is
10-200 µg/litre, the detection limit being 2 µg/litre. A
detection limit of 0.5 ng/ml using a 20 µl sample was
also reported for this method (Slavin, 1984). The Associ-
ation of Official Analytical Chemists (AOAC, 1984) used
emission spectrography for measuring barium concentrations
in plant tissue. The coefficient of variation for barium
analysis was between 7 and 15%, depending on the type of
plant tissue analysed. The analysis of barium in drinking-
water was performed by Pierce & Brown (1977) using this
method; they reported a detection limit and sensitivity
for barium of 3.0 and 10.0 µg/litre, respectively.
2.5.1.3 AAS - ICP
In recent years, emission spectrometry employing an
inductively coupled plasma (ICP) source has been used
routinely (Garbarino & Taylor, 1979). Detection limits of
<0.1 ng/ml have been reported (Fassel & Kniseley, 1974),
with less of the chemical or ionization interference typi-
cally seen with other emission spectroscopic systems.
Optical emission methods, however, are expensive when used
for a single element analysis, but this problem is largely
offset when several elements are analysed simultaneously.
2.5.2. Analytical methods used for special applications
2.5.2.1 Mass spectrometry
Because of expense and low sample throughput, mass
spectrometry is not a commonly used procedure for the
analysis of barium or other elements. However, aqueous
barium samples, purified by ion exchange, are particularly
amenable to this procedure (Bacon & Edmond, 1972). Peaks
for 135Ba and 138Ba can be scanned and replicate analy-
ses can be performed with a coefficient of variation of
0.17%. Isotope dilution mass spectrometry is an extremely
valuable reference method. Several investigators have
indicated that the isotope dilution mass spectrometric
method circumvents the need for large samples and tedious
purification procedures. Internal standardization provides
a high degree of precision, element selectivity, and sen-
sitivity (Chow & Patterson, 1966; Wolgemuth & Broecker,
1970; Bernat et al., 1972).
2.5.2.2 X-ray fluorescence spectrometry
This technique has been used to measure barium concen-
trations in human tissue (Forssen & Erametsa, 1974) and in
river sediments (Tsai et al., 1978). The coefficient of
variation of this method was 5.6% when river sediments
were analysed (Tsai et al., 1978).
2.5.2.3 Neutron activation analysis
Neutron activation can be used for multi-element
analysis. This technique has been used to determine barium
in sludge (Nadkarni & Morrison, 1974), in marine sediments
(Chow et al., 1978), and biological tissues (Heffron et
al., 1977). The correlation coefficient of the data when
compared with isotope dilution methods is 0.923, and the
limit of detection is 1 µg (Reeves, 1986).
3. SOURCES IN THE ENVIRONMENT
3.1. Natural occurrence
Barium is a relatively abundant element found combined
with other elements in soils, rocks, and minerals. It
ranks seventh in abundance among the minor elements and
sixteenth among the non-gaseous elements in the earth's
crust (Schroeder, 1970), and constitutes about 0.04% of
the earth's crust (Reeves, 1979). Barium also occurs as
gangue in lead and zinc ore deposits. The terrestrial
abundance of barium has been estimated at 250 g/tonne, and
its occurrence in sea water is 0.006 g/tonne (Considine,
1976).
The two most prevalent naturally occurring compounds
of barium are barite (barium sulfate) and witherite
(barium carbonate). Barite crystallizes in the orthorhom-
bic system. It occurs in beds or masses in limestone,
dolomite, shales, and other sedimentary formations; as
residual nodules resulting from the weathering of barite-
bearing dolomite or limestone; and as gangue in beds
together with fluorspar, metallic sulfides, and other
minerals.
Witherite crystallizes in the orthorhombic system. It
is found in veins and is often associated with galena
(lead sulfide), as at Alston Moor, Cumberland, England. It
is also found associated with barite at Freiberg, Saxony,
German Democratic Republic, and at Lexington, Kentucky,
USA.
Barium occurs in coal at concentrations up to 3000
mg/kg (Bowen, 1966). It also occurs in fuel oils, the
barium content varying with the petroleum source.
Barium is ubiquitous in soils, being found at concen-
trations ranging from 100-3000 µg/g (Schroeder, 1970;
Robinson et al., 1950). Brooks (1978) estimated an average
soil concentration of 500 mg/kg. Due to its abundance in
soils, barium may be present in the air in areas with high
natural dust levels.
Barium can be transported into ground-water aquifers
through the leaching and eroding of barium from sedimen-
tary rocks. The level of barium present in the ground
water is related to the hardness of the water, since
barium is always present with calcium (Kopp & Kroner,
1968). Cartwright et al. (1978) reported that the high
barium levels in ground water in Illinois, USA, were
derived from the sandstone formation of the Cambrian-
Ordovician aquifer. The highest concentrations occurred
in fine-grained and older sediments. Barium was found in
94% of the surface waters examined, the concentrations
range being 2-340 µg/litre (Kopp & Kroner, 1967).
Barium in surface waters is ultimately transported
into the oceans where it combines with the sulfate ion
present in salt water to form barium sulfate. Barium in
the ocean is in a steady state; the amount entering from
rivers is balanced by the amount falling to the bottom as
particles to form a permanent part of the sediment on the
ocean floor (Wolgemuth & Brocker, 1970). Barium concen-
trations in sea water of 6 µg/litre and in fresh water of
7-15 000 µg/litre (an average of 50 µg/litre) have been
reported (Reeves, 1986).
3.2. Man-made sources
3.2.1. Production levels, processes, and uses
Barite ore is the raw material from which nearly all
other barium compounds are derived. World production of
barite in 1985 was estimated to be approximately 5.7
million tonnes. The major world producers of barite are
China, the United States, USSR, India, Mexico, Morocco,
Ireland, Federal Republic of Germany, and Thailand. Other
producers are Canada, France, Spain, Czechoslovakia, and
England (Vagt, 1985).
China, as the world's leading producer, accounted for
about 1.0 million tonnes or 17% of world output in 1984.
The USA, the second largest producer, accounted for 0.70
million tonnes in 1984 and also imported 1.6 million
tonnes. Canada produced approximately 64 000 tonnes and
consumed around 78 000 tonnes in 1984 (Vagt, 1985).
Emissions of barium into the air from mining, re-
fining, and processing barium ore can occur during loading
and unloading, stock-piling, materials handling, and
grinding and refining of the ore. According to emission
factors determined by Davis (1972), mining and processing
of barite ore released an estimated 3200 tonnes of par-
ticulates into the air in 1976 in the USA (US Bureau of
Mines, 1976). Emission into water may occur during the
purification of barite ore and subsequent discharge of the
industrial water to the environment.
Fossil fuel combustion may also release barium into
the air. Pierson et al. (1981) found that >90% of the
barium additive in diesel fuels is emitted in vehicle
exhaust, where it is totally in the form of barium sul-
fate.
Coal-fired power plants emit barium into the atmos-
phere via ash. Some barium escapes into the atmosphere as
fly ash (Cuffe & Gerstle, 1967), while the rest is gener-
ally disposed of in landfill. Barium in coal ash ranges
from 100-5000 mg/kg (Miner, 1969). Hildebrand et al.
(1976) reported the presence of barium at a concentration
of 0.02 mg/litre in the effluent from a coal conversion
plant.
In the USA, the barium chemical industries released an
estimated 1200 tonnes of particulates into the atmosphere
in 1972 (Davis, 1972; Rezink & Toy, 1978). Waste water
from barium chemical production processes is another
potential source of barium emission.
Although most fugitive dust emissions and process
effluents are reduced by control technologies, an area of
concern is the emission of soluble barium to the atmos-
phere from dryers and calciners. Baghouses can reduce the
uncontrolled emission factor (up to 10 g/kg final product)
to 0.25 g/kg (Rezink & Toy, 1978). The release of soluble
barium into the atmosphere around these plants was esti-
mated at 56 tonnes for 1972 (Rezink & Toy, 1978), but it
has decreased as barium chemical production has declined.
The plastics industry is a relatively important source of
barium emission to the atmosphere. It utilizes barium as
a stabilizer to prevent discoloration during processing.
Another source of barium emission is the manufacture
of glass. Emissions of barium-containing particulates with
an average size of 1 µm have been reported by various
authors (Stockham, 1971; Davis, 1972). Davis (1972)
estimated an emission of 1 kg/1000 kg of barium used in
the glass industry. In a study of glass furnace emissions,
Stockham (1971) found negligible emissions of barium in
the formation of flint glass but a 1-10% emission level of
the particulates in the effluent of amber glass manufac-
turing.
The detonation of nuclear devices in the atmosphere is
a source of atmospheric radioactive barium. The radioac-
tive isotopes 140Ba and 143Ba are products of the decay
chains from thermal-neutron fission of 235U. Among the
isotopes of barium, 140Ba has the longest half-life (12.8
days) and contributes 10% of the total fission products at
10 days after nuclear fission. At 60 days, however, its
contribution falls to 2% of total activity (French, 1963).
The concentration of barium particles in the atmosphere
due to this source, in terms of actual weight, is im-
measurably small. Due to the short half-life and low con-
centrations of barium radionuclides, this source is not
considered a significant source of barium in the environ-
ment.
Barium is used extensively by man and is an essential
component of a vast number of manufacturing processes,
some of which are identified in Table 4. It is used in the
manufacture of alloys, as a loader for paper, soap, rub-
ber, and linoleum, in the manufacture of valves, and in
the production of lights and green flares. Barium is also
used in cement where concrete is exposed to salt water, in
the radio industry to capture the last traces of gases in
vacuum tubes, in the ceramic and glass industries, as an
insecticide and rodenticide, and as an extinguisher for
radium, uranium, and plutonium fires (Browning, 1969).
Table 4. Main uses of some barium compoundsa
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Barium compound Uses
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Acetate Catalyst for organic reactions; textile mordant; oil and grease
lubricator; paint and varnish driers
Aluminate In ceramics; in water treatment
Azide In high explosives
Bromate Analytical reagent; oxidizing agent; corrosion inhibitor in low
carbon steel; in the preparation of rare earth bromates
Bromide In the manufacture of other bromides; in photographic compounds;
in the preparation of phosphors
Carbonate In the treatment of brines in chlorinealkali cells to remove
sulfates; as a rodenticide; in ceramic flux, optical glass, case-
hardening baths, ferrites, radiation-resistant glass for colour
television tubes; in manufacturing paper
Chlorate In pyrotechnics (green fire); as textile mordant; in the manufac-
ture of other chlorates and of explosives and matches
Chloride In the manufacture of pigments, colour lakes, glass; as a mordant
for acid dyes; in pesticides, lube oil additives, boiler compounds,
and aluminum refining; as a flux in the manufacture of magnesium
metal; in leather tanner and finisher, in photographic paper and
textiles
Chromate In safety matches; as a pigment in paints; in ceramics; in fuses;
in pyrotechnics; in metal primers; in ignition control devices
Citrate As a stabilizer for latex paints
Cyanide In metallurgy and electroplating
Cyanoplatinite In X-ray screens
Diphenylamine sulfonate As an indicator in oxidation-reduction titrations
Ethylsulfate In organic preparations
Fluoride In ceramics; in the manufacture of other fluorides; in crystals
for spectroscopy; in electronics; in dry-film lubricants; in
embalming; in glass manufacture; manufacture of carbon brushes for
DC motors and generators
Fluorosilicate In ceramics; in insecticidal compositions; in the preparation of
silicon tetrafluoride
Table 4. (cont.)
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Barium compound Uses
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Hydroxide, monohydrate In the manufacture of oil and grease additives; in barium soaps
and chemicals; in the refinishing of beet sugar and animal and
vegetable oils; as an alkalizing agent in water softening; as a
sulfate removal agent in the treatment of water and brine; in
boiler scale removal; as a depilatory agent; as a catalyst in the
manufacture of phenol-formaldehyde resins; as insecticide and
fungicide; as a sulfate-controlling agent in ceramics; as a
purifying agent for caustic soda; as a steel carbonizing agent; in
glass; synthetic rubber vulcanization; as a corrosion inhibitor;
in drilling fluids, lubricants
Hydroxide, octahydrate In organic preparations; in barium salts; in analytical chemistry
and pentahydrate (and uses described for the monohydrate)
Hypophosphite In medicine and nickel plating
Iodide In the preparation of other iodides
Manganate (VI) As a paint pigment
Metaphosphate In glasses, porcelain, and enamels
Molybdate In electronic and optical equipment, as a pigment in paints and
protective coatings
Nitrate In pyrotechnics (green light); in incendiaries; chemicals (barium
peroxide); ceramic glazes; as a rodenticide; in vacuum-tube
industry
Nitrite In diazotization reactions; for the prevention of corrosion of
steel bars; in explosives
Oxalate As an analytical reagent; in pyrotechnics
Oxide As a dehydrating agent; in the manufacture of lubricating oil
detergents
Perchlorate In explosives; in rocket fuels (experimentally); in the determi-
nation of ribonuclease; as an absorbent of water in C and H analy-
sis
Permanganate As a strong disinfectant; in the manufacture of permanganates; as
a dry cell depolarizer
Peroxide In bleach; decolorizing glass; thermal welding of aluminum; in the
manufacture of hydrogen peroxide and oxygen in cathodes; in dyeing
and printing textiles; as an oxidizing agent in organic synthesis
Phosphate, secondary In fireproofing compositions; in the preparation of phosphors
Potassium chromate As a component of anticorrosive paints for use on iron, steel, and
light metal alloys
Table 4. (cont.)
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Barium compound Uses
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Selenide In photocells; in semiconductors
Silicate In refining sugar from molasses
Sodium niobate In lasers, electro-optical modulators, and optical parametric
oscillators
Stearate As a waterproofing agent; as a lubricant in metalworking, plastics,
and rubber; in wax compounding; in the preparation of greases; as
a heat and light stabilizer in plastics
Sulfate As weighting mud in oil-drilling; in paper coatings; in paints; as
filler and delustrant for textiles, rubber, linoleum, oilcloth,
plastics, and lithograph inks; as base for lake colours; as X-ray
contrast medium; as opaque medium for gastrointestinal radiography;
in battery plate expanders, radiation shields, photographic paper,
artificial ivory, cellophane; in heavy concrete for radiation
shields
Sulfide In luminous paint; as a depilatory; as a fireproofing agent; in
barium salts; in vulcanizing rubber; in the manufacture of litho-
pone; in generating pure hydrogen sulfide for analytical purposes;
as the main starting material for the production of most barium
compounds
Sulfite In analysis; in the manufacture of paper
Tartrate In pyrotechnics
Thiocyanate To make aluminum or potassium thiocyanates; in dyeing; in photo-
graphy; as a dispersing agent for cellulose
Thiosulfate In explosives, luminous paints, matches, varnishes; as an iodometry
standard; in photographic diffusion-transfer processes.
Titanate (IV) In ferroelectric ceramic; pure or combined with iron, used in
electronic storage devices, dielectric amplifiers, digital calcu-
lators, memory devices, and magnetic amplifiers
Tungstate As a pigment; in X-ray photography for the manufacture of inten-
sifying and phosphorescent screens
Zirconate In the manufacture of silicone rubber compounds stable up to
246 °C; in electronics
Zirconium silicate In the production of electrical resistor ceramics and glaze
opacifiers; as a stabilizer for coloured ground coat enamels
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a Source: Hawley (1977), Windholz (1983), Shreve (1967).
Barite is a valuable industrial mineral because of its
high specific gravity, low abrasiveness, chemical stab-
ility, and lack of magnetic effects. Its main use is as a
weighting agent for oil- and gas-well drilling muds
required to counteract high pressures confined by the
substrata. The oil- and gas-well drilling industries used
90% of the 2.24 million tonnes of barite consumed in the
USA in 1976 (US Bureau of Mines, 1976). In the same year,
unloading and handling this material released an estimated
112 tonnes of particulates into the atmosphere (Davis,
1972; US Bureau of Mines, 1976).
Complexes of barium with other compounds are used as
additives, which act as dispersants, stabilizers, and
inhibitors in several kinds of oils. A barium-based
organometallic compound is used to reduce stack smoke
emissions from diesel engines. Miner (1969) estimated the
amount of barium emitted in diesel exhaust to be a maximum
of 12 mg/m3 (<25% soluble barium at full load). This
estimate was based on the presence of an additive concen-
tration in diesel fuel of 0.075% barium by weight.
Barium compounds are used in the electronics and com-
puter industries, as contrast media in roentgenography, in
sugar processing, and as an ingredient in various products
such as cosmetics, cloth, leather, linoleum, oil cloth,
plastics, pharmaceuticals, printer's ink, photographic
paper, depilatories, pyrotechnics, detergents, high-tem-
perature greases, and water softeners (US Bureau of Mines,
1976).
The manufacture of paint also uses barium compounds,
including the sulfate, carbonate, and lithopone (a white
pigment consisting of a mixture of zinc sulfide, barium
sulfate, and zinc oxide). These compounds are relatively
unreactive, and their most important pigment properties
are high specific gravity, relatively low oil absorption,
and easy wettability by oils and grinding agents. The
amount of barium that these products add to the environ-
ment has not been determined, but most atmospheric
emissions are related to material handling (US Bureau of
Mines, 1976).
One of the routinely used technologies for treating
radium-containing water is to precipitate the radium as
barium-radium sulfate or adsorb it on materials containing
natural or activated barium sulfate (Havlik et al.,
1980).
4. ENVIRONMENTAL TRANSPORT AND DISTRIBUTION
4.1. Transport and distribution between media
4.1.1. Air
Examination of dust falls and suspended particulates
indicates that most contain barium. The presence of barium
is mainly attributable to industrial emissions, especially
the combustion of coal and diesel oil and waste inciner-
ation, and may also result from dusts blown from soils and
mining processes. Barium sulfate and carbonate are the
forms of barium most likely to occur in particulate matter
in the air, although the presence of other insoluble com-
pounds cannot be excluded. The residence time of barium
in the atmosphere may be several days, depending on the
particle size. Most of these particles, however, are much
larger than 10 µm in size, and rapidly settle back to
earth.
Particles can be removed from the atmosphere by rain-
out or wash-out wet deposition. These two forms of depo-
sition efficiently clear the atmosphere of pollutants, but
they are not well understood. Without knowing the amount
of barium in the atmosphere, it is difficult to evaluate
the processes of deposition, transport, and distribution.
4.1.2. Water
Soluble barium and suspended particulates can be
transported great distances in rivers, depending on the
rates of flow and sedimentation. In the absence of any
possible removal mechanisms, the residence time of barium
in aquatic systems could be several hundred years.
Cartwright et al. (1978) studied the chemical control of
barium solubility and showed that for most water samples,
barium ion concentration is controlled by the amount of
sulfate ion in the water.
Unless it is removed by precipitation, exchange with
soil, or other processes, barium in surface waters ulti-
mately reaches the ocean. Once freshwater sources dis-
charge into sea water, barium and the sulfate ions present
in salt water form barium sulfate. Due to the relatively
higher concentration of sulfate present in the oceans,
only an estimated 0.006% of the total barium brought by
freshwater sources remains in solution (Chow et al.,
1978). This estimate is supported by evidence that outer
shelf sediments have lower barium concentrations than
those closer to the mainland.
Upon entering the ocean, barium is transported down-
ward by the physical processes of mixing. It is depleted
in the upper layers of the ocean by incorporation into
biological matter, which settles toward the ocean floor
(Goldberg & Arrhenius, 1958). The higher concentration of
barium in deep water relative to surface water probably
reflects the deposition of barium onto suspended particles
forming at the ocean surface and the subsequent release of
barium to the deep water as the particles are destroyed in
transit to the ocean floor. In the ocean, barium is in
steady state; the amount entering the ocean through rivers
is balanced by the amount falling to the bottom as par-
ticles forming a permanent part of the sediment (Wolgemuth
& Brocker, 1970).
4.1.3. Soil
Barium is present in the soil through the natural pro-
cess of soil formation, which includes the breakdown of
parent rocks by weathering. Barium levels are high in
soils formed from limestone, feldspar, and biotite micas
of the schists and shales (Clark & Washington, 1924). When
soluble barium-containing minerals weather and come into
contact with solutions containing sulfates, barium sulfate
is deposited in available geological faults. If there is
insufficient sulfate to combine with barium, the soil
material formed is partially saturated with barium. Barium
replaces other cations in the soil particles by ion
exchange.
Barium salts are preferentially absorbed by argil-
laceous elements. Colloidal clays have been found to
decompose insoluble barium sulfate by binding barium.
Bradfield (1932) found that, in the reaction between
purified sodium clay and barium sulfate, the sulfate ion
became much more soluble, thus releasing the barium into
the clay.
Barium in soils would not be expected to be very
mobile because of the formation of water-insoluble salts
and its inability to form soluble complexes with humic and
fulvic materials. Under acid conditions, however, some of
the water-insoluble barium compounds may become soluble
and move into ground water (US EPA, 1984).
4.1.4. Vegetation and wildlife
Despite relatively high concentrations in soils, only
a limited amount of barium accumulates in plants. Barium
is actively taken up by legumes, grain stalks, forage
plants, red ash leaves, and the black walnut, hickory, and
brazil nut trees. The Douglas fir tree and plants of the
genus Astragallu also accumulate barium. No studies of
barium particle uptake from the air have been reported,
although vegetation is capable of removing significant
amounts of contaminants from the atmosphere. Plant leaves
act only as deposition sites for particulate matter. There
is no evidence that barium is an essential element in
plants (Reeves, 1979).
No information is available on barium levels in wild-
life.
4.1.5. Entry into the food chain
Certain plants used by humans as food sources actively
accumulate barium. It is also found in dairy products and
eggs (Gormican, 1970).
4.2. Biotransformation
There is no evidence that barium undergoes biotrans-
formation other than as a divalent cation.
5. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE
5.1. Environmental levels
Environmental levels are generally reported as total
barium ion rather than as specific barium compounds.
5.1.1. Air
The levels of barium in the air are not well docu-
mented, and in some cases the results are contradictory.
Tabor & Warren (1958) detected barium concentrations from
<0.005 to 1.5 µg/m3 in the air in 18 cities and 4 sub-
urban areas in the USA (Table 5). Of 754 samples analysed,
most of the observations made were at concentrations up to
0.05 µg/m3. No distinct pattern between ambient levels
of barium in the air and the extent of industrialization
was observed. In general, however, a higher concentration
was observed in areas where metal smelting occurred (Tabor
& Warren, 1958; Schroeder, 1970). In a more recent survey
in the USA, barium concentration ranged from 0.0015 to
0.95 µg/m3 (US EPA, 1984).
In three communities in New York City, barium was
measured in dustfall and household dust (Creason et al.,
1975). With standard methods (US EPA, 1974), the dustfall
was found to contain an average of 137 µg barium/g dust,
while the house dust contained 20 µg barium/g.
5.1.2. Water
The presence of barium in sea water, river water, and
well water has been well documented. It occurs in almost
all surface waters that have been examined (NAS, 1977).
The concentration present is extremely variable and de-
pends on factors (e.g., local geology) that affect
aquifers and any water treatment that has occurred. The
concentration of barium in water is related to the hard-
ness of the water, which is defined as the sum of the
polyvalent cations present, including the ions of calcium,
magnesium, iron, manganese, copper, barium, and zinc (NAS,
1977). Barium concentrations of 7 to 15 000 µg/litre have
been measured in fresh water and 6 µg/litre in sea water
(Schroeder et al., 1972).
Table 5. Barium in the ambient air of various cities in the USAa
-----------------------------------------------------------------------------------------
Percentage of samples at various concentrations (ug/m3)
City --------------------------------------------------------
< 0.005 > 0.005-0.05 > 0.05-0.5 > 0.5-1.5
-----------------------------------------------------------------------------------------
Houston (urban, suburban) 24 60 10 6
Boston (urban), Chicago, Denver, 32 52 16 0
E. St. Louis, Louisville,
Minneapolis, New Orleans,
Portland, Salt Lake City, Tampa
Boston (suburban), Chattanooga, 36 64 0 0
E. Chicago, Washington, DC
Fort Worth, Jersey City, New York, 66 34 0 0
Philadelphia,
Lakehurst (NJ), Paulsboro (NJ) 100 0 0 0
(suburban)
-----------------------------------------------------------------------------------------
a Source: Tabor & Warren (1958)
5.1.2.1 Surface waters
In the USA, levels of barium in water vary greatly
depending on local geochemical influences. Levels reported
in various studies are shown in Table 6.
Table 6. Barium content in USA surface waters
------------------------------------------------------------------------
Barium Concentration (µg/litre)
Source Range Mean Reference
------------------------------------------------------------------------
Fresh water 7-15 000 50 Schroeder (1970)
River water 9-150 57 (54 median) Durum (1960)
Surface water 2-340 43 Kopp (1969);
Kopp & Kroner (1970)
Surface water 10-12 000 50 Bradford (1971)
------------------------------------------------------------------------
5.1.2.2 Drinking-water
Municipal water supplies depend upon the quality of
surface waters and ground waters, and these, in turn,
depend upon local geochemical influences. Studies of the
water quality in cities in the USA have revealed levels of
barium ranging from a trace to 10 000 µg/litre (Durfor &
Becker, 1964; Barnett et al., 1969; McCabe et al., 1970;
McCabe, 1974; Calabrese, 1977; AWWA, 1985). Drinking-water
levels of at least 1000 µg barium/litre have been
reported when the barium is present mainly in the form of
insoluble salts (Kojola et al., 1978). Levels of barium in
Canadian water supplies have been reported to range from
5 to 600 µg/litre (Subramanian & Meranger, 1984), and
municipal water levels in Sweden ranging from 1 to
20 µg/litre have been measured (Reeves, 1986).
5.1.2.3 Ocean waters
The concentration of barium in sea water varies
greatly with factors such as latitude, depth, and the
ocean in question. Several studies have shown that the
barium content in the open ocean increases with the depth
of water (Chow & Goldberg, 1960; Bolter et al., 1964;
Turekian, 1965; Chow & Patterson, 1966; Anderson & Hume,
1968). A Geosecs III study of the southwest Pacific by
Bacon & Edmond (1972) found a barium profile of
4.9 µg/litre in surface waters to 19.5 µg/litre in deep
waters. Later studies by Chow (1976) and Chow et al.
(1978) corroborated these values. The barium concen-
tration in the northeast Pacific ranges from 8.5 to
32 µg/litre (Wolgemuth & Brocker, 1970). Bernat et al.
(1972) found that barium concentration profiles for the
eastern Pacific Ocean and the Mediterranean Sea ranged
from 5.2 to 25.2 µg/litre and from 10.6 to 12.7 µg/litre,
respectively.
Anderson & Hume (1968) reported concentrations in the
Atlantic Ocean ranging from 0.8 to 37.0 µg/litre in the
equatorial region and from 0.04 to 22.8 µg/litre in the
North Atlantic, with mean values of 6.5 and 7.6 µg/litre,
respectively. In Atlantic Ocean waters off Bermuda, barium
concentrations of 15.9-19.1 µg/litre have been measured
(Chow & Patterson, 1966).
5.1.3. Soil and sediment
The presence of barium in soils has received attention
since it was first documented in the muds of the River
Nile (Knop, 1874) and the soils of the USA (Crawford,
1908). In the earth's crust the barium concentration is
400 to 500 mg/kg (Wells, 1937; Schroeder, 1970; Davis,
1972). Later works have verified the levels found in the
early studies. The background level of barium in soils is
considered to range from 100 to 3000 mg/kg, the average
abundance being 500 mg/kg (Brooks, 1978).
The concentrations of barium in sediments of the Iowa
river are 450 to 3000 mg/kg (Tsai et al., 1978), sugges-
ting that barium in the water is removed by precipitation
and silting and may possibly affect the ecology of benthic
organisms.
5.1.4. Food
A review of the early literature summarizes the quan-
tity of barium present in many plants (Robinson et al.,
1950). Barium has been found in grain stalks, forage
plants, red ash leaves, and in the black walnut, hickory,
and Brazil nut trees. With the exception of the Brazil nut
tree, those parts of the plants that accumulate barium are
seldom eaten by man. Various studies document the concen-
trations of barium in Brazil nuts ranging from 1500-3000
mg/kg (Robinson et al., 1950; Smith, 1971a). Barium is
also present in wheat, although most is concentrated in
the stalks and leaves rather than in the grain (Smith,
1971b). Tomatoes and soybeans also concentrate soil
barium, the bioconcentration factor ranging from 2 to 20
(Robinson et al., 1950). Gormican (1970) determined the
barium content of a large number of food items, including
dairy products, cereals, fruits and vegetables, and meats
(Table 7). In the beverages group, tea and cocoa had the
highest barium content (2.7 and 1.2 mg/100 g, respect-
ively) on a dry-weight basis. Among breads, cereal prod-
ucts, and cracker products, bran flakes (0.39 mg/100 g)
and enriched instant cream of wheat (0.2 mg/100 g) had the
highest levels. Eggs were found to have 0.76 mg/100 g, and
swiss cheese 0.22 mg/100 g. Fruits and fruit juice had low
barium levels, the highest values being in raw, unpeeled
apples (0.075 mg/100 g). These levels are similar to those
found in grapes (<0.05 mg/100 g) and cooked prunes (0.064
mg/100 g). All meats showed concentrations of 0.04 mg per
100 g or less. Vegetables had relatively low barium
levels, with the exception of beets (0.26 mg/100 g) and
sweet potatoes (0.22 mg/100 g). Among nuts, pecans had the
highest barium content (0.67 mg/100 g).
5.1.5. Feed
Barium generally does not accumulate in common plants
in sufficient quantities to be toxic to animals. However,
Robinson et al. (1950) suggested that the large quantities
of barium (as high as 1260 mg/kg) accumulating in legumes,
alfalfa, and soybeans grown in soils containing high
exchangeable barium content may cause problems in domestic
cattle.
Table 7. Barium contents of some common foodsa
------------------------------------------------------------------
Food Barium content
(mg/100 g)
------------------------------------------------------------------
Beverages and dietary concentrates
Chocolate syrup 0.17
Coffee
Instant, dry 0.36
Ground, dry 0.32
Beverage, brewed <0.008
Cocoa, dry 1.2
Meritene, plain flavour, dry 0.11
Sustagen, imitation vanilla flavour 0.056
Tea, orange pekoe
Bag, dry 2.7
Beverage, steeped <0.004
Breads, cereal products, crackers, and pastas
Bread
Rye 0.062
White 0.051
Whole wheat 0.11
Bran flakes, 40% 0.39
Cheerios (cereal) 0.13
Corn flakes (cereal) 0.04
Crackers
Graham 0.11
Saltines 0.04
Egg noodles, uncooked 0.16
Macaroni, uncooked 0.11
Oatmeal, rolled oats (quick), uncooked 0.11
Puffed Rice <0.04
Quick Cream of Wheat (cereal)
Enriched, uncooked 0.2
Regular, uncooked 0.15
Rice Krispies <0.04
Rice, white uncooked <0.04
Shredded Wheat 0.22
Wheaties (cereal) 0.14
Spaghetti, uncooked 0.11
Cheese
American 0.12
Cottage, creamed <0.04
Swiss 0.22
Eggs
Whole 0.76
White <0.01
Yolk 0.058
Milk
Nonfat solids <0.08
Fluid
Whole <0.01
Skim <0.01
Buttermilk <0.01
Ice cream, vanilla <0.01
Sherbet, orange <0.01
Fruits and fruit juices
Apple
Raw, unpeeled 0.075
Juice, canned <0.002
Sauce, canned, drained <0.01
Apricots, canned, drained <0.01
Banana, ripe <0.01
Blueberries, waterpack, drained 0.014
Table 7. (cont.)
------------------------------------------------------------------
Food Barium content
(mg/100 g)
------------------------------------------------------------------
Cantaloupe <0.01
Cherries, Royal Anne, canned, drained 0.029
Grapes
Fresh, with peel <0.05
Juice, canned 0.023
Grapefruit
Juice, canned <0.008
Sections
Fresh, skinless <0.01
Canned, drained <0.01
Orange
Juice, frozen, reconstituted <0.008
Sections, skinless <0.008
Pineapple
Crushed, canned, drained 0.014
Juice, canned 0.008
Peach, cling, canned, drained <0.01
Pear, canned, drained 0.047
Prunes
Cooked 0.064
Juice 0.014
Watermelon 0.022
Meat, poultry, fish, and shellfish
Beef, fresh, uncooked
Flank, round, rump, sirloin, or tenderloin <0.02
Ground <0.02
Liver <0.04
Lamb, fresh, uncooked
Chop <0.02
Leg <0.02
Luncheon meat, big bologna <0.02
Pork, fresh, uncooked
Bacon <0.04
Ham <0.02
Liver <0.04
Loin <0.02
Veal, fresh, uncooked
Round or steak <0.02
Poultry, uncooked
Chicken, roaster
Dark meat <0.02
White meat <0.02
Turkey, roaster
Dark meat <0.02
White meat <0.02
Fish and shellfish
Crab, haddock, salmon, sockeye, sole, or tuna <0.02
Shrimp <0.02
Table 7. (cont.)
------------------------------------------------------------------
Food Barium content
(mg/100 g)
------------------------------------------------------------------
Nuts
Peanuts
Butter <0.04
Salted, blanched 0.21
Pecans 0.67
Walnuts 0.072
Sugars and flours
Sugar
Brown <0.04
Powdered <0.04
White <0.04
Flour, bleached, enriched 0.072
Vegetables
Asparagus spears, frozen, uncooked <0.02
Beans
Baked with pork <0.02
Green, frozen, uncooked 0.16
Lima, baby, frozen, uncooked 0.031
Wax, canned, salt-free, drained 0.11
Beets, canned, salt-free, drained 0.26
Broccoli, frozen, uncooked <0.02
Brussels sprouts, frozen, uncooked <0.02
Cabbage, uncooked <0.02
Carrots, uncooked 0.052
Cauliflower, frozen, uncooked <0.02
Celery, fresh <0.02
Corn, whole kernel, canned, salt-free, drained <0.02
Cucumber <0.02
Lettuce <0.02
Mushrooms, stems and pieces, canned <0.02
Onions, fresh, mature 0.053
Peas, canned, salt-free, drained <0.02
Potato
Fresh, uncooked <0.02
Instant, uncooked 0.056
Pumpkin, canned 0.053
Spinach, frozen, uncooked 0.04
Squash, frozen, cooked 0.083
Sweet potatoes, canned 0.22
Tomato
Fresh <0.02
Juice, canned, salt-free <0.008
------------------------------------------------------------------
a Source: Gormican (1970)
5.1.6. Other products
McHargue (1913) reported that the barium content of
dry tobacco leaves was in the range 88-293 mg/kg. Later
measurements yielded 24-170 mg/kg, with an average value
of 105 mg/kg (Voss & Nicol, 1960). Most of this barium is
likely to remain in the ash during burning. The concen-
trations of barium in tobacco smoke have not been
reported.
Bowen (1956) reported the following levels of barium
in plants: 15 mg/kg dry weight in plankton; 31 mg/kg dry
weight in brown algae; 18 mg/kg dry weight in ferns; and
14 mg/kg dry weight in angiosperms.
5.1.7. Nuclear fallout
The principal potential source of radioactive isotopes
of barium is nuclear weapons testing. Atmospheric testing
suspends radioactive dusts in the upper troposphere where,
depending on atmospheric conditions, dusts are carried
around the world several times.
The lightest dust particles reach the stratosphere.
Several years are required for the bulk of this radioac-
tive material to be deposited on the ground. Since 1952,
when tests began on nuclear weapons with high explosive
yields, fall-out from the stratosphere has been more or
less continuous. Most of this nuclear fall-out occurs in
the temperate and polar regions of the earth. The total
radiation from nuclear testing has added 10-15% to the
naturally occurring radiation throughout the world.
Because 140Ba and 143Ba are radioactive by-products
of the thermal nuclear fission of 235U, their concen-
tration in the environment increases after the detonation
of a nuclear device in the atmosphere. After a single
atmospheric nuclear detonation in China, Gudiksen et al.
(1965) detected 140Ba at an altitude of 10 670 m at
levels of 177-530 x 106 atoms/m3 over north-western USA.
This far exceeds the levels normally present in the atmos-
phere.
Radioactive particles are normally cleared from the
atmosphere by rain and snow. Cooper et al. (1970) moni-
tored 140Ba concentrations in rain and snow in 772
samples collected between 1958 and 1969 and found that
debris containing 140Ba was deposited after the atmos-
pheric testing of nuclear weapons in China. Evans et al.
(1973) reported the atmospheric level of barium, 4 days
after a test in China, to be 4.5 pCi/m3, which is ap-
proximately 30 times higher than the normal background
level (0.14 pCi/m3).
5.2. General population exposure
5.2.1. Environmental sources, food, drinking-water, and air
The most important route of exposure to barium appears
to be ingestion of barium through drinking-water and food.
Particles containing barium may be inhaled into the lung,
but little is known regarding the absorption of barium by
this route.
In studies of dietary intake in two hospitals, 300
schools, and individual subjects in the USA, Underwood
(1977) determined that the average intake of barium ranged
from 300 to 1700 µg/day. An earlier study had found that
the barium intake from diets served to adults in American
hospitals in the summer was not more than 303 µg/day and
in winter not more than 592 µg/day (Gormican, 1970).
Tipton et al. (1966, 1969) studied five adult subjects
whose self-selected diets were examined for varying
lengths of time. Barium concentrations were measured in
all foods consumed for 30 days by two subjects, 70 days by
one other, and 347 days by the remaining two subjects. In-
takes of barium showed large variations and ranged from
650 to 1770 µg/day.
In the United Kingdom, the total intake of barium from
the diet was estimated by Hamilton & Minski (1972) to be
approximately 603 µg/day and by the ICRP (1959) to be
900 µg/day. Schroeder et al. (1972) estimated that the
mean daily intake of barium in food is 1.24 mg, in water
0.086 mg, and in air 0.001 mg, giving a total of 1.33
mg/day. The ICRP (1974) reported the dietary intake of
barium to be 0.75 mg/day, including both food and fluids.
The contribution from drinking-water was estimated to be
about 0.08 mg/day, which leaves 0.67 mg/day from other
dietary sources. When Murphy et al. (1971) analysed school
lunches from 300 schools in 19 states in the USA, the
barium content ranged from 0.09 to 0.43 mg/lunch, with a
mean of 0.17 mg. Milk, potatoes, and flour have been
suggested to be the major sources of barium in diets in
the USA (Calabrese et al., 1985).
The barium content in drinking-water seems to depend
on regional geochemical conditions. In a study of the
water supplies of the 100 largest cities in the USA, a
median value of 43 µg/litre was reported; 94% of all de-
terminations were <100 µg/litre (Durfor & Becker, 1964).
This represents an average intake of <200 µg/day.
More recent studies by Letkiewicz et al. (1984) indi-
cated that approximately 214 million people in the USA
using public water supplies are exposed to barium levels
ranging from 1 to 20 µg/litre. In certain regions of the
USA, however, barium may reach 10 000 µg/litre. In these
areas, the average intake could be as high as 20 000 µg/day
(Calabrese, 1977).
Drinking-water appears to be an important source of
human exposure to barium. The digestive system is
extremely permeable to soluble barium, allowing rapid
absorption into (and removal from) the bloodstream
(Castagnou et al., 1957). This is important when consider-
ing uptake of barium from drinking-water, since a large
percentage of barium in water is in the soluble form.
Due to the paucity of information on the ambient
levels of barium in the air, it is difficult to estimate
the intake from this source. As described earlier
(section 5.1.3), the levels of barium in air rarely exceed
0.05 µg/m3 (Tabor & Warren, 1958). This value can be
used to estimate daily barium intake via the lungs.
Assuming that the average lung ventilation (LV) rate for
newborn babies, male adults undergoing light activity, and
male adults undergoing heavy activity is 0.5, 20, and 43
litres/min, respectively (ICRP, 1975), the intake via
inhalation would range from 0.04 to 3.1 µg/day. Other age
groups and females are included in this range. Earlier,
the ICRP (1974) reported that intake of barium through
inhalation ranges from 0.09 to 26 µg/day.
Because the chemical properties of the barium entering
the lung are not known, it is difficult to ascertain the
amount retained. Retention in adult animals is approxi-
mately 20% (Cuddihy & Ozog, 1973), which suggests that
insoluble barium accumulates and is slowly removed.
Another source of exposure is radioactive isotopes of
barium from nuclear fall-out after the explosion of nu-
clear weapons. 140Ba and 143Ba are the main radioactive
products of the thermal-nuclear fission of 235U, and
their half-lives are 12.8 days and 12 seconds, respect-
ively (CRC, 1988). Therefore, the potential for exposure
depends on its presence at ground level (air, soil, water
contamination), as well as on the time elapsed since
explosion. In terms of biochemical and pharmacological
effects, the exposure to barium from this source is not
significant. However, because exposure to radioactive
isotopes results in bone deposition, retention may be a
concern.
5.2.2. Other sources
Barium sulfate is the major barium compound used med-
icinally. This very poorly soluble compound is employed
as an opaque contrast medium for roentgenographic studies
of the gastrointestinal tract. There is limited evidence
that the ingestion of the compound may cause deleterious
biological effects. However, one study suggested that
radiation-induced gastrointestinal effects may be reduced
by the ingestion of barium sulfate (Conard & Scott,
1961).
5.2.3. Subpopulations at special risk
Patients receiving drugs such as acetazolamide (glau-
coma treatment; diuretic agent) or thiazide diuretics have
increased urinary potassium excretion (¾60% and 400%,
respectively) and would be at higher risk of potassium
deficiency due to barium toxicity. Patients subject to X-
ray studies of the gastrointestinal tract have shown
occasional increases in serum protein-bound iodine (PBI)
(Wallach, 1978).
5.3. Occupational exposure during manufacture, formulation, or use
The US National Institute for Occupational Safety and
Health (NIOSH) has investigated occupational exposures to
barium in a variety of industrial operations in response
to requests submitted by employers and workers for health
hazard evaluations and technical assistance. Table 8
summarizes the exposures and adverse health effects found
in these investigations.
Occupational exposure to soluble barium compounds has
been reported for workers exposed to welding fumes (Dare
et al., 1984). The wiring used in arc welding processes
was shown to contain 20-40% soluble barium compounds, and
fumes produced during these processes contained 25%
barium. Urine analysis of workers revealed barium concen-
trations ranging from 31 to 234 µg/litre after 3 h of
exposure. Follow-up samples taken approximately 12 h
after exposure contained levels ranging from 20 to
110 µg/litre. The level in the urine of controls ranged
from 1.8 to 4.7 µg/litre. No air samples were collected,
but NIOSH (1978) reported that welders using the same wire
were exposed to 2200 to 6200 µg soluble barium per m3.
Table 8. Occupational exposure to barium in various industries
---------------------------------------------------------------------------------------------------------
Concentration Number of
Industry Compound range, mg/m3 samplesa Health effects Comments Reference
---------------------------------------------------------------------------------------------------------
Magnetic plastic BaFe12O19 < 0.08-2.2 22 none reported NIOSH
Ba (soluble) < 0.01-0.27 (1976)
Steel, arc welding Ba (soluble) 2.2-6.1 5 none reported see Dare NIOSH
et al. (1984) (1978)
Vinyl floor Ba (soluble) < 0.4 9 none reported NIOSH
(1979)
Metal alloys Ba (soluble) 0.02-1.7 12 musculoskeletal, exposures to NIOSH
gastrointestinal, lead, zirconim, (1980)
skin, respiratory UV, visible,
and IR radiation
Mineral ores Ba (soluble) 0.01-1.92 27 hypertension exposure to NIOSH
lead, zinc (1982)
Petroleum refinery, Ba (soluble) 0.03-0.05 (mean) NR none NIOSH
TCCU turn-around 0.015-2.50 (max) (1984)
Auto parts Ba (soluble) 0.002-0.68 68 none reported NIOSH
(1985)
Aluminium foundry Ba (soluble) 0.001-0.037 13 eye, nasal exposures to NIOSH
irritation silica, (1987a,
formaldehyde b,c)
Fire extinguisher BaO 0.08-1.7 4 none reported ZnO fumes NIOSH
(1987a,
b,c)
---------------------------------------------------------------------------------------------------------
a NR = not reported.
6. KINETICS AND METABOLISM
6.1. Absorption
Barium enters the body primarily through the inha-
lation and ingestion processes. The degree of absorption
of barium from the lungs and gastrointestinal tract varies
according to the animal species, the solubility of the
compound, gastrointestinal tract content, and age. Studies
with soluble barium salts have shown that these compounds
are readily absorbed (Cuddihy & Griffith, 1972; Cuddihy &
Ozog, 1973; Cuddihy et al., 1974; McCauley & Washington,
1983). Recent studies have indicated that poorly soluble
barium compounds may also be absorbed (McCauley &
Washington, 1983; Clavel et al., 1987).
6.1.1. Inhalation route
6.1.1.1 Laboratory animals
Cuddihy & Ozog (1973) studied the absorption of
labelled barium chloride (133BaCl2) solutions in
1-year-old Syrian hamsters. Absorption into the general
circulation of solutions deposited on nasal membranes was
compared with gastrointestinal tract absorption. During
the first 4 h after administration, barium absorption from
the nasal passages was approximately 61%, compared with
11% gastric absorption. The authors concluded that the
nasopharynx is a major absorption site for inhaled aero-
sols of soluble barium, especially for readily soluble
aerosols having mass median aerodynamic diameters >5 µm.
Gutwein et al. (1974) observed that on day 24 after
the exposure of male Sprague-Dawley rats (275 g) by nasal
intubation to combustion products from diesel fuel con-
taining a barium-based additive in solution (vehicle not
specified), more than 85% of the administered dose was
found in the bone, indicating significant absorption in
the respiratory tract.
The principle mechanism for removing insoluble par-
ticles from the lung is transport by the ciliated epi-
thelium and its associated mucosal lining, followed by
swallowing. Spritzer & Watson (1964) evaluated the ciliary
clearance of poorly soluble barium sulfate and found that
52% of the compound introduced into rat lung was removed
by ciliary action. The other 48% was removed by ``lung-to-
blood transfer mechanisms'' (probably macrophage ac-
tivity), which led to disposal of the sulfate particles.
These mechanisms suggest that solubilization of the barium
sulfate occurs in vivo.
Clearance from the lungs of various forms of barium
after inhalation exposure of rats and beagle dogs was
studied by Einbrodt et al. (1972) and Cuddihy et al.
(1974). Einbrodt et al. (1972) exposed rats to barium sul-
fate (40 mg/m3) for 2 months, and this was followed by a
4-week observation interval. Animals were killed at 2-week
intervals. After 2 weeks of exposure, the barium content
in the lungs was high but decreased rapidly over the next
4 weeks of exposure and then increased again during the
observation period. Barium accumulation in bone tissue in-
creased initially, but with continued exposure decreased.
There was no absorption into lymph tissue.
In beagle dogs exposed to various barium compounds
(chloride, sulfate, heat-treated sulfate, or barium in
fused montmorillonite clay), barium was cleared from the
lungs at a rate of proportional to its solubility (Cuddihy
et al., 1974). The longest retention time in the lungs
was for barium adsorbed to clay; more than 500 days after
exposure, 10% of the initial body burden was still in the
lungs and skeleton (Cuddihy et al., 1974). For barium sul-
fate, there was a long-term slow clearance, with virtually
no change in lung tissue levels of barium from 8 to 16
days after exposure. The clearance rate depended on the
specific surface area of the inhaled particles. In Syrian
hamsters, barium sulfate was found to be cleared from the
lungs with a biological half-life of 8-9 days (Morrow et
al., 1964). This indicated some dispersion of barium sul-
fate in body fluids, possibly in a colloidal form.
6.1.1.2 Humans
There are no quantitative data on the deposition and
absorption of barium compounds through inhalation in
humans.
6.1.2. Oral route
6.1.2.1 Laboratory animals
The absorption of ingested barium depends on factors
such as the presence of food in the intestine, the sulfate
content in the food, the age of the animal, and the
location of the barium in the gastrointestinal tract.
Absorption of barium from the gastrointestinal tract has
been studied in rats (Taylor et al., 1962). Labelled
barium chloride was administered by intragastric intu-
bation to groups of 5-10 brown-hooded female rats (14 days
to 70 weeks old). Absorption was estimated as the radio-
activity 7 h after exposure in the carcass plus urine
minus gastrointestinal tract in relation to the dose. The
absorption decreased with age, from approximately 85% of
the administered dose at 14-18 days of age, to 63% at 22
days, to approximately 7% after 6-8 or 60-70 weeks of age.
Deprivation of food before administration (18 h) markedly
increased the absorption of barium, from approximately 7%
in fed animals to 20% in fasted animals 6-8 or 60-70 weeks
old. Administration of the compound in cow's milk did not
affect absorption.
In studies by Cuddihy & Ozog (1973), groups of 5-10
Syrian hamsters (1 year old) were administered labelled
barium chloride by intragastric intubation. The absorption
estimate was based on carcass radioactivity 4 h after
exposure in relation to carcass radioactivity immediately
after intravenous administration (100%). Results show that
following a 12 h fasting, a combination of gastric (32%)
and intestinal (11%) absorption was found during the first
4 h after administration. McCauley & Washington (1983)
examined the absorption of specific barium salt anions in
male Sprague-Dawley rats, administering radiolabelled
barium chloride, sulfate, or carbonate to fasted (24 h)
and non-fasted rats by gastric intubation. Animals were
sacrificed from 2 to 480 min after administration and
blood concentrations were measured. In general, barium
blood concentrations were higher in fasted animals and
reached a peak 15 min after dosing, whereas non-fasted
animals had lower barium blood concentrations and peaked
60 min after dosing. The peak blood concentrations of the
carbonate and sulfate salts were 45% and 85%, respect-
ively, of that of the chloride.
Orally administered barium chloride (133BaCl2) was
found to be rapidly absorbed from the gastrointestinal
tract of male weanling rats, the peak concentration in the
bloodstream and soft tissues occurring 30 min after
dosing. Total uptake of barium increased with increasing
dosage, but, there appeared to be a saturation point for
oral absorption (Clary & Tardiff, 1974).
6.1.2.2 Humans
There are few data on the absorption of barium from
the human gastrointestinal tract. Tipton et al. (1969)
reported that two males fed controlled diets for 80 weeks
absorbed between 2 and 6% of the barium content in their
diet, based on urinary elimination. Elimination via the
gastrointestinal tract was not given. Recent studies by
Clavel et al. (1987) have shown that insoluble barium
salts commonly used during radiological investigations are
absorbed by the intestine and are excreted in the urine.
6.1.3. Parenteral administration
The in vivo solubility of four barium compounds (the
chloride, sulfate, and carbonate salts and fused clay
forms of previously aerosolized material resuspended in
distilled water) was studied in rats after intramuscular
injection (Thomas et al., 1973). The chloride and carbon-
ate salts were found to be equally soluble in the soft
tissues and were absorbed from the injection site very
rapidly.
6.2. Distribution
6.2.1. Levels in tissues of experimental animals
Studies in rats and mice have shown that barium is
incorporated into the bone matrix in much the same way as
calcium (Bauer et al., 1956; Taylor et al., 1962; Bligh &
Taylor, 1963; Domanski et al., 1969; Dencker et al.,
1976). This means that the major part of the body burden
will be in the skeleton. Soft tissues generally have low
concentrations of barium, an exception being pig-mented
areas of the eye (Sowden & Pirie, 1958). Barium is
incorporated into the bone, especially in young animals
that are still growing. In mature animals, 60-80% of the
barium initially deposited is removed from the femur
during the first 14 days after exposure (Bligh & Taylor,
1963). The uptake of barium into bone decreases with the
age of the animal. No detrimental effects on the
integrity of the bone have been seen.
Dencker et al. (1976) injected labelled barium chlor-
ide (133BaCl2) intravenously in pigmented and albino
mice (63 µg barium/kg body weight). Autoradiography
revealed that uptake was rapid and retention times were
longest in calcified tissues, cartilage, and melanin-con-
taining tissues. In other tissues, the radioactivity
rapidly disappeared. In the mouse fetus, the authors found
that barium is mainly taken up by the skeleton, especially
in the growth zones. Except for the eye, soft tissues had
a low uptake.
Barium deposition appears to occur preferentially in
the most active areas of bone growth (Bligh & Taylor,
1963), although research indicates that the preferential
uptake of barium is localized primarily in the periosteal,
endosteal, and trabular surfaces of the bone (Ellsasser et
al., 1969).
McCauley & Washington (1983) found that 24 h after an
intragastric dose of labelled barium chloride to rats, the
highest concentration was in the heart, followed by the
eye, kidney, liver, and blood. Clary & Tardiff (1974)
found that labelled barium chloride (133BaCl2) admin-
istered orally to weanling male rats entered the blood-
stream and soft tissues, peak concentrations occurring 30
min after administration. Uptake was observed in the sub-
maxillary salivary gland, adrenal gland, kidney, gastric
mucosa, and blood vessels. The deposition of barium in
hard tissues was detected after 2 h. In a more recent
study, Tardiff et al. (1980) administered barium chloride
(10, 50, or 250 mg barium/litre of drinking-water) to
young adult rats of both sexes for 4, 8, or 13 weeks.
Barium deposition in liver, skeletal muscle, heart, and
bone was dose-dependent but not related to the length of
exposure. The highest concentration of barium was observed
in the bones. In the soft tissues, concentrations were <1
mg/kg even after 13 weeks of exposure to 250 mg barium per
litre. In the bone, the average concentration was 226
mg/kg.
In dogs, inhalation of radioactive barium (the chlor-
ide or sulfate salts) resulted in significant (when com-
pared to other tissues) radioactive deposition in the bone
(chloride) and in the lung (sulfate) (Cuddihy & Griffith,
1972). Rats that inhaled 40 mg barium sulfate over a 2-
month period initially accumulated barium in their bones
(jaw and femur). However, the rate of deposition decreased
with continued exposure (Einbrodt et al., 1972). Simi-
larly, 2 weeks after the initiation of exposure, lung
barium content was high, whereas it decreased over the
next 4 weeks but increased again during 4 weeks in the
post-inhalation period. No evidence for the transport of
barium in lymph was noted by these authors.
6.2.2. Levels in human tissue
It has been estimated that the ``Standard Man'' (a
term borrowed from radiation dosimetry) of 70 kg contains
approximately 22 mg of barium (Tipton et al., 1963). A
major part of the element is concentrated in the bone
(nearly 91%), the remainder being in soft tissues such as
the aorta, brain, heart, kidney, spleen, pancreas, and
lung (Schroeder, 1970). In human beings there is no
increase of total barium with age, except in the aorta and
lung (Venugopal & Luckey, 1978). Sowden & Stitch (1957)
reported that uptake of barium into bone did not increase
with age (Table 9). Bligh & Taylor (1963) and Ellsasser et
al. (1969) found that barium deposition in the bone oc-
curred preferentially in the active sites of bone growth.
Table 9. Concentration of barium in human bone (µg/g) according to agea
-------------------------------------------------------------------------
0-3 months 1-13 years 19-33 years 33-74 years
-------------------------------------------------------------------------
No. of subjects 7 9 9 10
Concentration range 1.9-13.0 2.1-21.0 4.3-7.9 3.7-17.3
Mean 7.0 7.7 5.1 8.5
Standard deviation ± 4.0 ± 7.0 ± 0.12 ± 4.0
-------------------------------------------------------------------------
a Source: Bligh & Taylor (1963).
In the USA, the highest concentration in soft tissues
was found in the large intestine, muscle, and lung. The
median values were approximately 0.15 mg/kg wet weight
(Tipton & Cook, 1963; Tipton et al., 1965; Schroeder et
al., 1972). In the liver and kidney, the median concen-
trations were <0.003 and approximately 0.1 mg/kg wet
weight, respectively. However, tissue values from subjects
from other countries show large differences. The concen-
tration of barium in various tissues was measured in
autopsied subjects from the USA, Africa, the Eastern
Mediterranean, and South-East Asia (Tipton et al., 1965).
For almost all organs examined (aorta, brain, heart,
kidney, liver, and spleen), subjects from Africa, the
Eastern Mediterranean, and South-East Asia were found to
contain higher levels of barium than their counterparts
from the USA. In comparison with the other groups, the
Eastern Mediterranean group showed higher levels in the
lung, and both the Eastern Mediterranean and South-East
Asia groups had higher levels in pancreas and testis.
Median barium concentrations in liver from people in
Africa, the Eastern Mediterranean, South-East Asia, and
Switzerland were 0.05, 0.08, 0.05, and 0.02 mg/kg, re-
spectively. The data on subjects in the USA indicated
increases with age in certain tissues (e.g., the lung and
aorta), whereas the data on subjects from other countries
indicated the opposite, except in the case of the lung
(Perry et al., 1962).
Harrison et al. (1966) found that whole body retention
of barium in humans, 15 days after a single-dose injection
of labelled barium chloride (133BaCl2), was 10.5% of
the initial dose.
In the USA, barium in the tooth enamel of people under
20 years of age has been found to average 4.2 mg/kg dry
weight (Losee et al., 1974), and Cutress (1979) reported a
mean barium concentration of 22 mg/kg (a range of 0.8-432
mg/kg) in the teeth of people less than 20 years old from
13 countries. Miller et al. (1985) reported that the mean
barium/calcium ratio in teeth was five times higher in 34
children from one community exposed to drinking-water con-
taining an average concentration of 10 mg/litre than that
in 35 children from a similar community with much lower
levels of barium in the drinking-water (0.2 mg/litre).
Normal levels of barium in hair are generally 1-2 mg/kg
(Creason et al., 1975, 1976).
According to Schroeder & Mitchener (1975b), barium has
been identified in all samples taken from stillborn babies
and children up to one year of age, implying that barium
can cross the placental barrier and be transported in the
maternal milk.
6.3. Elimination and excretion
The elimination of either injected or ingested barium
in both humans and animals occurs principally in the
faeces rather than in the urine (Harrison et al., 1967;
Domanski et al., 1969; Tipton et al., 1969; Gutwein et
al., 1974; Clary & Tardiff, 1974).
6.3.1. Laboratory animals
In young rats given an intraperitoneal dose of
carrier-free 140Ba, 18.4% (average of four rats) of the
dose had been recovered in the gastrointestinal tract and
faeces 4 h after dosing and 5.8% in urine. After 24 h, the
corresponding values in three rats were 22.7 and 6.6%.
Thus, there was a change from an initial rapid clearance
to a slower phase (Bauer et al., 1956). The biological
half-time for barium in the bone of mice seems to be 100
days (Dencker et al., 1976), while Clary & Tardiff (1974)
estimated the value in the bone of rats to be 90-120 days.
According to Domanski et al. (1964), 34.8% of the initial
dose was found in rats 16 days after a single-dose injec-
tion of barium chloride. In lactating cows, excretion in
milk during the first 8 days after dosing was 0.6% of an
oral dose and 10% of an intravenously administered dose
(Garner et al., 1960). Thomas et al. (1973) reported that
in rats barium sulfate disappeared from the injection site
with a half-life of 26 days; beyond 100 days the disap-
pearance of barium from bone was similar for both soluble
and poorly soluble compounds, the half-life being 460
days.
Gutwein et al. (1974) exposed 14 rats for 10 h to com-
bustion products from fuel to which a barium-containing
smoke-suppressant additive (approximately 20% 133BaSO4)
was added. Six animals were then killed after radioactive
counting. The remaining eight were killed 3-24 days after
exposure. Most barium was eliminated via the faeces. The
elimination from the lungs was rapid with >50% of the
initial lung burden being eliminated during the first 3
days.
6.3.2. Humans
The elimination of barium occurs in both the faeces
and the urine, and varies with the route of administration
and the solubility of the compound. Within 24 h, 20% of an
ingested dose (solubility not specified) appeared in the
faeces and 5-7% was excreted in the urine (Venugopal &
Luckey, 1978). Furthermore, barium that had been absorbed
and transported by the plasma was found to have been
almost entirely cleared from the bloodstream within 24 h
(Browning, 1969).
In healthy human beings in a state of barium equilib-
rium (virtually all of the intake occurring by mouth),
approximately 91% of the total output was found in the
faeces, 6% in sweat, and 3% in urine (Schroeder et al.,
1972).
In a study by Harrison et al. (1966), the excretion
via the faeces and the urine was measured for 10 days in a
healthy 60-year-old man given an intravenous injection of
133Ba. The barium elimination 3-6 h after administration
was measured in saliva and seminal fluid, yielding values
of 0.22-0.33 and 0.81% of the dose, respectively. The per-
centage of the injected dose eliminated via the faeces and
the urine was 20% after 24 h, 70% after 3 days, and 85%
after 10 days. The ratio of faecal to urinary barium was
9.0 after 8 days.
6.4. Metabolism
The mechanisms by which barium is deposited in body
tissues are not well characterized. However, the general
patterns of uptake show similarities to those of calcium
and strontium.
6.4.1. Laboratory animals
In a metabolic study, Bauer et al. (1956) administered
intraperitoneal injections of 140Ba and 45Ca to young
rats. The results indicated that there was no difference
in the metabolism of the two cations. Barium was trans-
ferred more rapidly than calcium from the exchangeable to
the non-exchangeable fractions of bone, but these differ-
ences were not significant. In addition Bligh & Taylor
(1963) noted age-related changes in metabolism (Table 9).
7. EFFECTS ON ORGANISMS IN THE ENVIRONMENT
7.1. Microorganisms
7.1.1. Viruses
Various studies have shown that barium can directly
influence the physico-chemical properties of viruses as
well as their infectivity. At low temperature (5 °C) and
concentration (10 mmol/litre), the Ba2+ ion, like Mg2+ or
K+, causes depolymerization of tobacco mosaic virus
protein (McMichael & Lauffer, 1975). Barium and other
divalent cations prevent antibiotics such as streptomycin
and kanamycin from inhibiting the multiplication of
tobacco mosaic virus in protoplasts (Kassanis et al.,
1975).
Barium is an effective divalent cation in promoting
phage R17 infection (Paranchych, 1966). Divalent cations
are essential for the penetration of the phage RNA into
the host cell. Ba2+ (at concentrations of 0.5-20 mmol per
litre) and other divalent cations, e.g., Ca2+, Sr2+,
and Mn2+, prevented the haemolysis caused by the infec-
tion of chicken erythrocytes with Sendai virus (Toister &
Loyter, 1970). These cations may affect virus structure.
The calcium ion was reported to be essential for cell
fusion by the haemagglutinating virus of Japan (HVJ). When
Ca2+ was absent, the cells were lysed, not fused, by the
virus (Koshi, 1966). Ba2+ in equimolar concentration was
found to replace Ca2+ for this activity.
7.1.2. Bacteria
A number of inorganic elements have been found to be
constituents of microorganisms. Not only are these
elements firmly bound in various ionic forms and involved
in metabolic processes, but they also have a stabilizing
effect on the structural integrity of cellular membranes.
Spectrochemical analyses of bacterial ash have shown the
presence of barium in the following species: Salmonella
paratyphi, Salmonella typhosa, Shigella flexnerii,
Shigella dysenteriae, Mycobacterium tuberculosis, and
Vibrio cholerae (Kovalskii et al., 1965). The content of
barium was found to be higher in most of the following
bacteria than in higher plants: Escherischia coli, Bacil-
lus cereus, Sphaerotilus natams, and Micrococcus roseus
(Rouf, 1964).
Barium, like other divalent cations, maintains the
organization and structure of the bacterial cell wall.
Addition of Ba2+ to osmotically fragile cells of
Pseudomonas aeruginosa (produced by treatment with EDTA
and lysozyme) restored them to an osmotically balanced
state (Asbell & Eagon, 1966). The function of certain
envelope components in Achromobacter is apparently highly
dependent on divalent cations, including Ba2+, and the
integrity of the permeability barrier and stability of the
envelope are affected at low ion concentrations (Ledebo,
1976). It has been postulated that Ba2+ inhibits phago-
cytosis of bacterial cells, thereby contributing to its
cell wall stability. This has become the basis for using
barium sulfate in the animal model of intra-abdominal
sepsis (Bartlet et al., 1978).
7.1.3. Inhibition of growth
Growth studies have demonstrated that, in general,
barium is toxic to bacteria, fungi, mosses, and algae. A
low concentration of Ba2+ (10-100 µmol/litre) was toxic
for the growth of Nitrobacter agilis (Tandon & Mishra,
1968). However, mutants of Aspergillus nidulans have been
isolated that can grow in toxic concentrations of Ba2+ and
other divalent cations. In general, the resistance of the
mutants to the metal ions is the result of modified intra-
cellular metabolism rather than defective transport
(Elorza, 1969). Ba2+ at concentrations of 100 µmol/litre
not only inhibited the growth of Azotobacter but also
reduced slime formation and pigmentation (Dejong & Roman,
1971).
The membrane potential of the ciliate Paramecium is
sensitive to intra-cellular calcium (Brehm et al., 1978).
Ba2+, like Ca2+, spontaneously changes the membrane
potential of Paramecium caudatum, making it resemble the
long-lasting potential found in cardiac muscle fibres and
smooth muscle cells. Upon replacement of calcium ions with
barium ions, the normal swimming behaviour of Paramecium
multimicronucleatum in an essential mineral solution
(200 µmol Ca2+/litre) changed into continuous avoidance
reactions (Kinosita et al., 1964; Yarbrough & O'Kelley,
1962).
The toxic effects of Ba2+ and other divalent cations
to Paramecium has been found to increase in alkaline and
decrease in acid solutions. The effect was most noticeable
at the isoelectric point of the cell surface (Grebecki &
Kuznicki, 1963). The observation that an increase in Ba2+
concentration increased the staining of Escherischia coli
and Shigella ellipsoideus with the anionic fluorochrome,
uranin, supports the earlier finding (Kononenko &
Chaikina, 1970).
Den Dooren de Jong (1965) reported that the highest
concentration of barium tolerated by cultures of
Chlorella vulgaris without affecting growth was 4 mg per
litre and the lowest inhibitory concentration was 8 mg per
litre. Problems with the precipitation of barium from the
culture solution as the sulfate suggested to the author
that the above results might have been artificially high.
Devi Prasad (1984) found that barium inhibited calcifi-
cation of the freshwater green alga Gloeotaenium at a
concentration of 50 mg/litre.
7.1.4. Specific effects
The divalent barium ion has a number of specific
effects, mostly toxic or inhibitory to cellular processes,
on different species of bacteria and fungi. Barium in-
hibits the lipolytic activity of the intact cells of
Mycobacterium rubrum and is a potent inhibitor for
Actinomyces streptomycini (Lebedena et al., 1976). The
Ba2+ ion has been shown to inhibit the dehydrogenase
activities of resting cells of Proteus vulgaris (Lilov &
Zahn, 1967) and to inhibit flocculation in Saccharomyces
cerevisiae (Taylor & Orton, 1973).
The divalent barium ion may cause dissociation of the
polyribosome-mRNA complex in Paramecium aurelia and a
marked decrease in the amount of monoribosomes (Reisner et
al., 1975).
The production of aflatoxins by Aspergillus is affec-
ted by the Ba2+ ion (Lee et al., 1966, Gupta et al.,
1975). Similarly, the production of alpha-amylase was
increased by 65% in Baccillus cereus mycoides by barium
chloride (Yoshiyuki & Yoshimasha, 1975).
The Ba2+ ion has been reported to affect the develop-
ment of germinating bacterial spores (Rode & Foster, 1966;
Foerster & Foster, 1966).
7.2. Aquatic organisms
7.2.1. Aquatic plants
Wang (1986) reported a 96-h EC50 of 26 mg barium per
litre in Lemma minor in deionised water. However, in river
water the barium showed no toxic effect on growth of the
duckweed. Further experiments showed that the effect was
entirely due to precipitation of barium from the river
water as sulfate and, therefore, reduced bioavailability
to the plant. Stanley (1974) investigated the toxic effect
on the growth of Eurasian water milfoil Myriophyllum
spicatum. Root weight was the most sensitive parameter
measured and showed a 50% reduction, relative to controls,
at a barium concentration of 41.2 mg/litre.
7.2.2. Aquatic animals
Details of studies on the lethal effects of barium
salts to aquatic invertebrates and fish are given in Table
10.
LeBlanc (1980) exposed water fleas (Daphnia magna)
in a 48-h test to various concentrations of barium and
calculated the no-observed-effect level (NOEL) to be 68
mg/litre. In contrast, Biesinger & Christensen (1972)
reported 48-h and 21-day LC50 values of 14.5 and 13.5
mg/litre, respectively. They also measured the repro-
ductive performance of the daphnids during the 21-day
tests and reported 16% impairment of reproduction at 5.8
mg barium/litre and 50% impairment at 8.9 mg/litre. In the
same study, a reduction in average weight was also ob-
served. The 30-day LC50 values for two species of cray-
fish were comparable to the 96-h values (Boutet &
Chaisemartin, 1973).
Heitmuller et al. (1981) reported a no-observed-effect
level in the sheepshead minnow of 500 mg/litre.
Table 10. Toxicity of barium to aquatic organisms
---------------------------------------------------------------------------------------------------------
Organism Lifestage/ Stat/ Temperature pH Hardness Duration LC50 Reference
size flowa ( °C) (mg/litre) (mg/litre)
---------------------------------------------------------------------------------------------------------
Water flea <24 h old stat 21-23 7.4-9.4 173 24 h >530 LeBlanc
(Daphnia magna) <24 h old stat 21-23 7.4-9.4 173 48 h 410 (1980)
(fresh water) (320-530)
7.4-8.2 44-53 48 h 14.5 Biesinger &
7.4-8.2 44-53 21 days 13.5b Christensen
(12.2-15.0) (1972)
Crayfish flow 15-17 7.0 96 h 78 Boutet &
(Orconectes limosus) flow 15-17 7.0 30 days 59 Chaisemartin
(fresh water) flow 15-17 7.0 30 days 61b (1973)
Crayfish (Austropot- flow 15-17 7.0 96 h 46 Boutet &
amobius pallipes pallipes) flow 15-17 7.0 30 days 39 Chaisemartin
(fresh water) flow 15-17 7.0 30 days 43b (1973)
Sheepshead minnow 8-15 mm stat 25-31 10-31c 96 h > 500 Heitmuller
(Cyprinodon variegatus) et al.
(marine water) (1981)
---------------------------------------------------------------------------------------------------------
a stat = static conditions (water unchanged for the duration of the test);
flow = intermittent flow-through conditions.
b test conducted with a food source.
c salinity (o/oo).
7.2.3. Effects of marine drilling muds
Studies have been carried out to assess the environ-
mental impact of offshore drilling on marine organisms.
Barite (barium sulfate) is the principal constituent of
drilling mud used in oil drilling operations. However,
these muds contain metals other than barium. Any adverse
effects on organisms not due to the physical effects of
barite could be the result of the toxicity of metals other
than barium.
Daugherty (1951) exposed a number of unspecified
marine fish, crustaceans, and molluscs to various levels
(as high as 7500 mg/kg) of drilling clay or drilling mud
for an unspecified period of time. No deaths occurred and
the materials were designated as non-toxic. Grantham &
Sloan (1975) reported that sailfin mollies (Poecilia
latipinna) survived a 96-h exposure to a 10% suspension
of barite in both salt water and fresh water.
Togatz & Tobia (1978), and Cantelmo et al. (1979)
observed the development of estuarine communities in sands
mixed with (or covered by) barite. Aquaria containing
specific mixtures (sand only; 1:10 barite-sand mixture;
1:3 barite-sand mixture; and sand covered by 0.5 cm of
barite) were prepared in duplicate and exposed for 10
weeks to flowing estuarine water. The estuarine water
naturally contained planktonic larvae. The mollusc popu-
lation (individuals and species) were significantly
reduced in the aquarium with the barite cover but not in
the aquaria containing the barite mixtures. Annelids were
reduced in all barite treatments. It was not possible to
determine whether these results were due to larval avoid-
ance of barite or to barite toxicity.
Similarly, George (1975) reported reduced biomass and
diversity of fouling organisms on test panels suspended in
a turbidity plume of drilling mud off the Louisiana coast,
USA. However, he suggested that this result stemmed from
the physical, rather than chemical, effects of the sus-
pended material.
7.3. Bioconcentration
Marine concentrations of barium are lowest in nutri-
ent-depleted surface waters and generally increase with
depth. This suggests that barium is incorporated into
organisms in the euphotic zone and is subsequently sedi-
mented and released in deeper waters. Thus, the pattern
of barium distribution in ocean waters is consistent with
the conclusion of various authors that barium is actively
taken up by marine organisms (Wolgemuth & Brocker, 1970;
Chow, 1976; Chan et al., 1977). Wolgemuth & Brocker (1970)
suggested that organisms forming opal (SiO2) are primar-
ily responsible for this phenomenon, but sufficient data
to verify this are not available (Chan et al., 1977).
The content of barium in several types of marine
algae, mollusc shells, and corals has been discussed in
terms of ``accumulation'' or ``discrimination'' (Bowen,
1956). Accumulation (A[Ba]) was defined as the ratio of
the barium concentration in dried tissue to that in water.
Discrimination (D[Ba,Ca]) was defined as the ratio of
barium to calcium in the tissue compared with the ratio of
these two elements in sea water. Algae tend to accumulate
barium with a large discrimination factor, whereas mollusc
shells and corals accumulate somewhat higher amounts but
with a relatively lower discrimination factor.
Studies by Havlik et al. (1980) using different con-
centrations of 133Ba in algal culture media showed that
barium was accumulated in algae. After 15 days exposure,
the uptake by algae was 30-60% of the added amount of
barium at concentrations of 0.04, 0.46, and 4.0 µg/litre
medium. The lower the barium concentration in the medium,
the higher was its relative accumulation in algae. The
amount of barium taken up increased with the length of
exposure. Barium was not incorporated into the organic
components of the protoplasm but was bound primarily to
the cell membrane or some other non-extractable algal
components (Havlik et al., 1980).
Guthrie et al. (1979) compared the levels of barium in
water and sediment from a marine area contaminated with
heavy metals with the levels in various organisms. The
water and sediment concentrations of barium were 7.7
mg/litre and 131.0 mg/kg wet weight, respectively. Of the
organisms analysed (barnacles, crabs, oysters, clams, and
polychaete worms), only barnacles showed higher concen-
trations of barium than that of the water (40.5 mg/kg wet
weight). Stary et al. (1984) investigated the accumulation
of barium ions (as 133Ba) into cells of the algae
Scenedesmus obliquus as a function of pH. Accumulation
increased with increasing pH between pH 4 and 7, reaching
a plateau at pH 7 and remaining constant over the range pH
7 to 9. The initial concentration of barium in the culture
medium was 10-6 mol/litre. The Km (affinity constant)
for the accumulation of barium was calculated to be 4.8.
Barium has also been detected in the ash of Alaskan/
Arctic mosses (Rastorfer, 1974).
8. EFFECTS ON EXPERIMENTAL ANIMALS AND IN VITRO SYSTEMS
8.1. Acute exposure
8.1.1. Oral route
The acute toxicity of various barium compounds is
shown in Table 11, where doses are expressed either as
LD50 or as the lowest lethal dose (as reported in RTECS
(1985). Additional information regarding the observed non-
lethal acute effects of barium is reported in Table 12.
8.1.2. Inhalation route
To assess the possible hazard of metal fumes resulting
from certain metal arc-welding and other metal processing
operations, Hicks et al. (1986) carried out inhalation
studies in anaesthetized guinea-pigs. Collected particu-
late material from fumes generated by manual arc-welding
(with electrodes using barium fluoride or carbonate) was
extracted with dilute hydrochloric acid to give a solution
containing barium. Aerosols generated from the barium fume
extract were inhaled intratracheally by mechanical venti-
lation and were found to cause bronchoconstriction to the
same extent as the inhalation of pure barium chloride
(90 µg/m3 per min).
8.1.3. Parenteral administration
In studies by Syed & Hosain (1972), the intravenous
LD50 for barium chloride in ICR white mice was 19.2 mg
barium/kg, and the values for barium nitrate and acetate
were similar. These values were approximately double those
reported for Swiss-Webster mice.
Roza & Berman (1971) found that barium chloride in-
fused intravenously into anaesthetized dogs caused ectopic
ventricular contractions, skeletal muscle paralysis, sali-
vation, and, finally, respiratory paralysis and ventricu-
lar fibrillation. These effects were due to a prompt and
substantial hypokalaemia and could be prevented or
reversed by potassium administration. This barium-induced
hypokalaemia was probably not due to potassium losses in
the gastrointestinal tract or urine. The authors suggested
that potassium accumulated in the intracellular compart-
ment, since the red blood cell potassium level was elev-
ated by barium chloride infusion.
8.1.4. Topical route
In rabbits, barium nitrate causes mild skin irritation
(24-h exposure) and severe eye irritation (24-h exposure)
(RTECS, 1985).
Table 11. Acute toxicity of various barium compounds in
laboratory animalsa
--------------------------------------------------------------
Compound Species Route Doseb (mg/kg
body weight)
--------------------------------------------------------------
Barium acetate ICR mouse iv LD50 = 23.3c
Barium carbonate rat oral LD50 = 418
rat oral LD50 = 800d
mouse iv LLD = 20
mouse oral LD50 = 200
mouse ip LD50 = 50
dog oral LLD = 400
Barium chloride rat oral LD50 = 118
rat sc LD50 = 178
rat iv LLD = 20
mouse oral LLD = 70
mouse ip LD50 = 54
mouse sc LLD = 10
mouse iv LD50 = 12
ICR mouse iv LD50 = 19.2c
dog oral LLD = 90
rabbit oral LLD = 170
rabbit sc LLD = 55
guinea-pig oral LLD = 76
guinea-pig sc LLD = 55
frog sc LLD = 910
Barium fluoborate rat oral LLD = 250
Barium fluoride rat oral LD50 = 250
mouse ip LD50 = 29.9
frog sc LLD = 1540
Barium nitrate rat oral LD50 = 355
mouse sc LLD = 10
mouse iv LD50 = 8.5
ICR mouse iv LD50 = 20.1c
Barium oxide mouse sc LD50 = 50
Barium peroxide mouse sc LD50 = 50
Barium polysulfide rat oral LD50 = 375
Barium silicofluoride rat oral LD50 = 175
Barium sulfide rat oral LD50 = 640
Barium sulfonates rat oral LD50 = 3000
Barium zirconium oxide rat oral LD50 = 1980
rat ip LD50 = 420
--------------------------------------------------------------
a Source: RTECS (1985) except where stated otherwise.
b LLD = Lowest lethal dose: the lowest dose (other than
LD50) of a substance introduced by any route (except
inhalation), over any given period of time in one or more
divided portions, which has caused death in human beings or
animals (RTECS, 1985).
c Source: Syed & Hosain (1972); the concentrations given are
those of the Ba2+ ion.
d Source: Windholz (1983).
8.2. Short-term exposures
8.2.1. Inhalation route
The effects of short-term exposure to barium compounds
in animals are summarized in Table 12. Tarasenko et al.
(1977) carried out a series of subchronic experiments with
rats to measure the effects of inhalation exposure to
barium (as barium carbonate dust). Male rats exposed to
barium carbonate at concentrations of 1.15 and 5.2 mg/m3
for 4 months, 6 days/week, 4 h/day, experienced decreased
weight gain, blood sugar, and haemoglobin, as well as
leucocytosis and thrombopenia in the high-dose group.
Increase in arterial pressure was also noted. No adverse
effects were reported in the low-dose group. In a second
study, male rats exposed to barium carbonate (22.6 mg/m3)
for one cycle of spermatogenesis showed a decrease in
spermatozoids, sperm motility, and osmotic resistance.
There was also a significant increase in the number of
ducts with desquamative epithelium and a reduction in the
number of ducts with 12th-stage meiosis. The authors
indicated that similar spermatogenic changes were observed
in male rats exposed for 4 months at 5.2 mg/m3.
Inhalation exposure of female rats to barium carbon-
ate (3.1 or 13.4 mg/m3) produced a shortening of the
oestrous cycle and changes in ovary morphology. In
addition, females exposed to 13.4 mg/m3 had increased
mortality and underdeveloped offspring (Tarasenko et al.,
1977).
Table 12. Effects of acute and chronic exposure to barium compounds in experimental animals
---------------------------------------------------------------------------------------------------------
Compound Species Concentration Route Duration Observation Reference
---------------------------------------------------------------------------------------------------------
Barium rat 1, 10, 100 oral 16 months depressed cardiac rates and Perry et al.
chloride mg/litre (water) excitability; decreased (1985)
cardiac ATP,
phosphocreatine, and
phosphorylation potential
rat 1, 10, 100 oral 16 months increased systolic pressure, Perry et al.
mg/litre (water) decreased conductivity and (1985)
conduction
rat 100 mg/litre oral 16 months induced disturbances of Kopp et al.
(water) myocardial contractility, (1985)
hypersensitivity to
phenobarbital and shortening
cardiac muscle fibre
velocity
mouse 2, 6.6, 20 ip CNS effects; convulsive Peyton & Boro-
mg/kg corneal electroshock; witz (1978)
sensitivity increased after
0.5 h; decrease in
electroshock sensitivity at
24 h
pig 1.7 mg/kg iv 20 min cardiovascular toxicity; Pento (1979)
per min infusion bradycardia
dog 0.5-2.0 µmol/ iv 10-100 min stimulation of cardiac, Roza & Berman
kg per min infusion smooth, and skeletal muscles (1971)
manifested by arrhythmia,
diarrhoea, and skeletal
muscle twitching;
hypokalaemia, hypertension,
direct stimulation of
arterial smooth muscle
Table 12 (contd.)
---------------------------------------------------------------------------------------------------------
Compound Species Concentration Route Duration Observation Reference
---------------------------------------------------------------------------------------------------------
Barium
carbonate dog initial: iv accelerated ventricular Foster et al.
3.6-64.7 µmol/ infusion 2-10 min escapes; tachycardia (1977)
kg per min;
thereafter:
0.5-1.0
µmol/kg per min
rat 33.4 mg/m3 inhalation hematopoietic differences; Tarasenko et
and reduction in detoxifying al. (1977)
rabbit function in liver;
desquamative bronchitis
rat 5.2 mg/m3 inhalation 4 h/day pronounced general toxic Tarasenko et
6 days/week effect and influence on al. (1977)
4 months mineral metabolism and PNS
rat 22.6 mg/m3 inhalation not stated disturbance of Tarasenko et
spermatogenesis; fewer al. (1977)
viable sperm cells
rat 5.2 mg/m3 inhalation 4 months disturbance of Tarasenko et
Barium spermatogenesis al. (1977)
acetate
rat 3.1 and 13.4 inhalation 4 months disturbance of oestrous Tarasenko et
mg/m3 cycle and ovary morphology al. (1977)
rat 26 mg/kg oral 29 days increased mortality of Tarasenko et
before offspring; embryotoxic al. (1977)
conception effects
and during
entire
pregnancy
Table 12 (contd.)
---------------------------------------------------------------------------------------------------------
Compound Species Concentration Route Duration Observation Reference
---------------------------------------------------------------------------------------------------------
rat 5 mg/litre oral 540 days slightly increased mortality Schroeder &
(water) in females; increase in Mitchener
growth after 150 days over (1975a)
controls
mouse 5 mg/litre oral 540 days longevity slightly reduced Schroeder &
(water) in males, but weight not Mitchener
significantly affected; no (1975b)
change in prevalence of
tumours, oedema, or
blanching of incisor teeth
-----------------------------------------------------------------------------------------------------------------------------
8.2.2 Oral route
To assess adverse effects resulting from exposure to
high levels of barium in drinking-water, Borzelleca et al.
(1988) administered, by gavage, barium chloride (30, 100,
or 300 mg/kg body weight for 1 day or 100, 145, 209, or
300 mg/kg body weight for 10 days) to male and female
Sprague-Dawley rats. In the 1-day exposure study,
decreases in body weight and liver/brain weight ratios and
an increase in kidney weight were found at 300 mg/kg. In
animals exposed for 10 days, there was a decrease in the
survival rate of females given 300 mg/kg. Reductions in
ovary/brain ratios and blood urea nitrogen (BUN) levels
were also reported for females. In males, the BUN levels
were decreased at 300 mg/kg. No other effects were
reported.
In studies by Tardiff et al. (1980), barium chloride
was added to tap water at concentrations of 0, 10, 50, and
250 mg barium/litre and fed to 4-week-old Charles River
rats (30 of each sex per group). A commercial diet con-
taining an average barium concentration of 6.6 ± 0.5 µg/kg
was given, approximating to a background daily dose of
0.5 µg barium/kg body weight. At 4, 8, and 13 weeks of
exposure, five rats of each sex from each dosage level
were killed, biochemical and haematological parameters
were measured, and histopathological examinations were
performed. No clinical signs of toxicity were manifested
during the exposure to barium chloride. Throughout the
duration of the study, the body weights of treated animals
were similar to the control values. No statistically sig-
nificant differences between exposed and control animals
were observed for any of the haematological or biochemical
parameters measured; values for all animals were within
normal limits during the course of the study. No gross or
microscopic abnormalities were found in the liver, kid-
neys, spleen, heart, brain, muscle, femur, or adrenals.
The relative weight of adrenals in male rats treated for 8
(but not 13) weeks at 50 and 250 mg/litre decreased sig-
nificantly. The relative weight of adrenals in female rats
after 13 weeks of exposure to 10, 50, or 250 mg/litre was
slightly decreased. The effect did not appear to be dose-
or duration-related in either sex.
In a series of studies, McCauley et al. (1985) inves-
tigated the histological and cardiovascular effects on
rats exposed to barium chloride in drinking water. Male
Sprague-Dawley rats (6 per group) were exposed to 0, 1,
10, 100, or 250 mg barium/litre in their drinking-water
for 36 weeks or to 0, 1, 10, 100, or 1000 mg/litre for 16
weeks. No histopathological abnormalities were observed in
any of the tissues examined. There were no significant
trends toward hypertension in any of the animals treated
with 100 mg/litre. Transient changes in blood pressure
were reported, but these were not considered to be dose-
or duration-related. Similarly, no significant histologi-
cal or cardiovascular effects were observed in female
Sprague-Dawley rats exposed to 0 or 250 mg barium/litre
for 46 weeks. However, animals receiving 1000 mg barium
per litre did exhibit ultrastructural changes in the kid-
ney glomeruli, including basement membrane thickening,
epithelial foot process fusion, and the presence of myelin
figures. No other effects were reported at any dose levels
for males or females.
8.3 Long-term exposure
8.3.1 Inhalation route
No pertinent data regarding chronic inhalation ex-
posure to barium have been found in the available litera-
ture.
8.3.2 Oral route
The effects of chronic exposure to barium compounds in
experimental animals are summarized in Table 12. McCauley
et al. (1985) studied the effects on male Sprague-Dawley
rats of exposure to drinking-water containing 0, 10, 100,
or 250 mg barium per litre for 68 weeks. Rats exposed to
250 mg/litre for 5 months were then challenged with an
arrhythmagenic dose of L-noradrenaline (5 µg/kg iv).
Barium-treated animals demonstrated no significant histo-
logical changes in 34 tissue types examined, and no
changes in body weight or food and water consumption were
reported. No increase in the incidence of tumours was
reported. All tumours were benign and uniformly distri-
buted. The rats challenged with L-noradrenaline demon-
strated no significant ECG changes when compared to con-
trols. However, the heart rate of treated animals was
significantly lower 4 min after the injection, but
returned to normal within 60 min.
Schroeder & Mitchener (1975a) studied the effects of
lifetime exposure to barium acetate (0 or 5 mg/litre) in
the drinking-water and low-trace-element diets of weanling
Long-Evans rats (52 of each sex). Animals were weighed at
weekly intervals initially, monthly for 1 year, and
finally at 3-month intervals. Barium had no significant
effect on the growth of males, but significantly increased
growth rates were seen in females aged 120 days in 4 of
the 16 measurements. Proteinuria was observed in barium-
exposed males to a greater extent than it was in the con-
trols. No differences were found in serum glucose, choles-
terol, or uric acid concentrations between exposed rats
and controls.
Using the same exposure details, Schroeder & Mitchener
(1975b) conducted a second lifetime study on Swiss mice
(42 males, 36 females). No effects were observed on growth
rate or body weight except in the case of female mice who
weighed slightly less than controls at 30 days. At 60
days, there was no difference between the weights of con-
trol and treated mice. No effects on gross pathology or
histopathology were observed. Longevity (defined as the
mean age at death of the last surviving 10% of animals)
was slightly reduced (P <0.025) in treated males (815 days
versus 920 for controls), but the average age at death did
not differ (548 days, treated mice; 540 days, control mice).
Perry et al. (1983, 1985) maintained female weanling
Long-Evans rats in a ``low contamination'' environment on
a control diet low in trace metals for 16 months.
Drinking-water was deionized and fortified with five
essential trace metals, and 0, 1, 10, or 100 mg barium per
litre (as barium chloride) was added. Based on water con-
sumption data, average daily doses of 0.051, 0.51, and 5.1
mg/kg were calculated. Barium produced no change in growth
rate, and no evidence of toxicity was detected. The
indirect systolic pressure of unanaesthetized rats was
measured in triplicate at 1, 2, 4, 8, 12, and 16 months
(Perry et al., 1983, 1985). The average systolic pressure
was significantly increased (P <0.001) after exposure to
100 mg barium/litre for 1 month, and after exposure to 10
mg/litre (P <0.025) for 8 months. Average increases at 1,
12, and 16 months for the highest dose were 1.6, 2.13, and
2.13 kPa (12, 16, and 16 mmHg), respectively. With the
10-mg/litre dose, increases of 0.8, 0.93, and 0.53 kPa (6,
7, and 4 mmHg) were observed at 8, 12, and 16 months,
respectively. At the highest dose there was a decrease at
16 months in cardiac ATP, phosphocreatine, and phosphory-
lation potential, and an increase in ADP levels. Kopp et
al. (1985) analysed the in vivo myocardial excitability,
contractility, and metabolic characteristics of the
highest-dose rats at 16 months and observed significant
barium-induced disturbances in myocardial contractility.
The most distinctive effect demonstrated was a hypersensi-
tivity of the cardiovascular system to sodium pentobarbi-
tal. Under barbiturate anaesthesia, virtually all of the
myocardial contractile indices were depressed signifi-
cantly in barium-exposed rats. The lack of a similar
response to ketamine and xylazine anaesthesia indicated
that the cardiovascular actions of sodium pentobarbital in
barium-treated rats were linked specifically to this
anaesthetic and were not representative of a generalized
anaesthetic response. The contractile element shortening
velocity of the cardiac muscle fibres was significantly
slower in barium-treated rats relative to the control
rats. Similarly, significant disturbances in myocardial
energy metabolism were detected in the barium-exposed
rats. These disturbances were consistent with the reduced
contractile element shortening velocity. In addition, the
excitability of the cardiac conduction system was de-
pressed preferentially in the atrioventricular nodal
region of hearts from barium-exposed rats. Overall, the
altered cardiac contractility and excitability character-
istics, the myocardial metabolic disturbances, and the
hypersensitivity of the cardiovascular system to the
sodium pentobarbital suggest the existence of a previously
undescribed cardiomyopathic disorder induced by chronic
barium exposure.
8.4 Reproduction, embryotoxicity, and teratogenicity
8.4.1 Reproduction
Inhalation exposure of male rats to barium carbonate
(22.6 mg/m3 for one spermatogenic cycle or 5.2 mg/m3 for
4 months) resulted in a decrease in spermatozoids and a
reduction in the number of ducts with 12th stage necrosis.
Females exposed to barium carbonate (3.1 or 13.4 mg/m3)
experienced a shortening of the oestrous cycle and
increased mortality, and their pups were underdeveloped
(Silayev & Tarasenko, 1976; Tarasenko et al., 1977).
Other reproductive effects observed for various barium
compounds, as reported in RTECS (1985), are listed in
Table 13.
8.4.2 Embryotoxicity and teratogenicity
Barium fluoride orally administered (at 0.03-0.1 of
the LD50 value) to rats on the first days of gestation
decreased the percentage of 5-day-old embryos in the
blastomeric stage and newborn birth weights (Popova &
Peretolcyina, 1976). In addition, the death rate in new-
born rats was higher than normal. No teratogenic effects
were reported. Since fluoride inhibits many biochemical
processes, the results may reflect the presence of fluor-
ide rather than barium. Tarasenko et al. (1977) exposed
rats to barium carbonate (3.1 and 13.4 mg/m3), for 24
days before conception and during gestation, and observed
an increase in the mortality of the fetuses and low birth
weights but no teratogenesis.
Ridgeway & Karnofsky (1952) examined the terato-
genicity of barium by injecting 20 mg barium chloride into
the yolk sac of developing chick embryos. When the injec-
tion was made on day 8 of development, developmental
defects were observed in the toes. In contrast, no effects
were seen when the injection was made on day 4 of develop-
ment.
Table 13. Reproductive effects of barium compoundsa
---------------------------------------------------------------------------------------------------------
Compound Route Species Sex Exposure data Effects on
---------------------------------------------------------------------------------------------------------
Barium carbonate inhalation rat male 1.15 mg/m3 per 24 h for spermatogenesis; testes, epi-
16 weeks prior to mating; didymis, sperm duct
lowest toxic dose
Barium carbonate inhalation rat female 3.13 mg/m3 per 24 h for oogenesis; ovaries, fallopian
16 weeks prior to mating; tubes
lowest toxic dose
Barium iron inhalation rat male 0.76 mg/m3 per 24 h for spermatogenesis
oxide 17 weeks prior to mating;
lowest toxic concentration
Barium chloride intratracheal rat male 16.7 mg/kg 1 day prior to testes, epididymis, sperm
mating; lowest toxic dose duct
---------------------------------------------------------------------------------------------------------
a Source: RTECS (1985).
8.5 Mutagenicity and related end-points
Nishioka (1975) reported that barium chloride produced
no increase in the mutation frequency in repair-deficient
strains of Bacillus subtilis. Using synthetic polynucleo-
tide templates and purified DNA polymerases, Ba2+ was
found to have no effect on DNA synthesis, although other
metals such as Cd2+, Co2+, Ni2+, and Pb2+ did de-
crease the fidelity of DNA synthesis and were categorized
as potential mutagens (Sirover & Loeb, 1976a,b).
8.6 Tumorigenicity and carcinogenicity
Schroeder & Mitchener (1975a,b) examined the long-term
effects of barium and several other metals on rats and
mice. Groups of Long-Evans rats (52 of each sex) and CD
mice (54 of each sex) were given 0 or 5 mg barium/litre in
their drinking-water throughout their life. The incidence
of tumours in treated animals was not significantly dif-
ferent to that of control animals. It was concluded that
under these conditions barium was not carcinogenic.
Barium chromate has been evaluated in monographs on
chromium and chromium compounds (IARC, 1973; IARC, 1980;
IARC, 1987). Barium chromate has been tested for carcino-
genicity in rats by intrabronchial, intramuscular, and
intrapleural administration. No lung tumours were produced
after intrabronchial implantation, but the other exper-
iments were considered inadequate to evaluate carcino-
genicity. IARC considered that there is sufficient
evidence for the carcinogenicity of hexavalent chromium
compounds in animals and humans (Group 1: carcinogenic to
humans). This evaluation applied to the group of chemicals
as a whole and not necessarily to each individual chemical
within the group (IARC, 1987).
8.7 Special studies
8.7.1 Effects on the heart
The studies of Slavicek (1972), Katzung & Morgenstern
(1976), Foster et al. (1977), Meier & Katzung (1978),
Shine et al. (1978), and Pento (1979) have presented
evidence of the detrimental effect of barium on ventricu-
lar automacity and the pacemaker current in the heart.
Infusion of barium chloride into anaesthetized dogs
produced premature ventricular contractions or ventricular
tachycardia (Roza & Berman, 1971). These effects were
accompanied by hypokalaemia, and the administration of
potassium prevented or reversed the arrhythmias. However,
the increased blood pressure also associated with barium
infusion was not blocked by potassium administration.
Kidney removal or the administration of phentolamine, a
blocking agent of alpha-catecholamine receptors, did not
reverse the hypertension. Presumably, barium acts directly
on vascular smooth muscle to cause hypertension.
More recent studies by Perry et al. (1983, 1985), Kopp
et al. (1985), and Hirano & Hiraoka (1986) have shown that
barium decreases cardiac contractility and excitability,
and produces automaticity of ventricular muscles in rats
and guinea-pigs. Barium chloride (2 mmol/litre) induced
slow diastolic dipolarization and reduced membrane poten-
tial in the right ventricle of guinea-pigs (Hirano &
Hiraoka, 1986).
8.7.2 Vascular effects
Using spirally cut strips of rabbit thoracic aorta
suspended in a physiological test-chamber, Perry et al.
(1967) tested responsiveness to various concentrations of
barium ions. A slow, steady contraction was induced, which
averaged 5% at 10-4 mol/litre and increased to 26% at
10-3 mol/litre.
Using intra-arterial barium chloride, Perry & Yunice
(1965) demonstrated a pressure response in Sprague-Dawley
rats. Barium-injected rats (6 per group) showed an aver-
age increase of 0.27 kPa (2 mmHg) in diastolic pressure
after the administration of 0.1 mg Ba2+/kg body weight.
After 10 min, 1 mg Ba2+/kg body weight was injected. Ten
minutes later, an additional 10 mg Ba/kg body weight was
injected. Diastolic pressure increased by 3.2 kPa (24
mmHg) (P <0.01) with the 1 mg/kg injection, and by 7.47
kPa (56 mmHg) (P <0.01) with the 10 mg/kg injection.
8.7.3 Electrophysiological effects
Experimental evidence indicates that barium can par-
tially mimic calcium in many physiological processes.
Studies by Silinsky (1978) and Erdelyi (1977) examined the
effect of barium on nerve impulse transmission. Acetyl-
choline is a transmitter of nerve impulses and its release
is controlled by calcium ions. When barium replaces the
calcium, release of acetylcholine is stimulated, causing
depolarization of the post-synaptic nerve. The barium-
stimulated in vitro release of acetylcholine does not
appear to have a feedback control mechanism similar to
that involved in calcium regulation, and within 24 h the
acetylcholine pool is depleted. Although barium releases
acetylcholine quanta, it cannot synchronize the release
with the impulsive event. Thus, despite its efficiency in
supporting neurosecretion, barium is unsuitable as a
normal physiological mediator of depolarization-secretion
coupling at the motor nerve end (McLachlan, 1977).
An important biological action of barium is the block-
ade of potassium efflux from cells. The addition of barium
(0.8 mmol/litre) to cell medium resulted in an increase in
the release of noradrenalin from cat spleen tissue
(Kirpekar et al., 1972). Hausler & Haefely (1979) have
shown that when potassium efflux is blocked by barium, de-
polarization is prolonged. This allows for greater cellu-
lar influx of calcium during depolarization and accounts
for the enhanced effect of nerve stimulation in the
presence of barium (Hausler & Haefely, 1979).
Barium can also affect calcium metabolism by blocking
its efflux from cells. Concentrations of 0.3 mmol/litre
inhibited by 41% the ATPase-mediated extrusion of calcium
in bovine adrenomedullary plasma membrane preparations
(Leslie & Borowitz, 1975). Owing to its ability to block
calcium efflux from cells, barium may have widespread
effects in secretory tissues and, possibly, in certain
muscle tissues. In frog sartorious muscle, barium (0.01
mmol/litre) inhibited potassium uptake and efflux sym-
metrically (Henderson & Volle, 1972).
Pappano (1976) studied the electrophysiological action
of barium in chick embryo atria and compared it to that
of calcium. The ability of barium to evoke an action
potential decreased during ontogeny, but barium was more
potent than calcium in generating an action potential.
Based on these findings, the author suggested that barium
can enter the cell by the same mechanism as calcium.
8.7.4 Effects on synaptic transmission and catecholamine release
Calcium is an essential ion in a number of secretory
processes, especially in the release of neurotransmitters
(Rubin, 1970). Barium mimics this action and can evoke the
release of (1) acetylcholine from the neuromuscular junc-
tion (Silinsky, 1978), (2) acetylcholine from the sympath-
etic ganglia (McLachan, 1977), (3) noradrenaline from the
sympathetic nerve terminals (Rubin, 1970), and (4) cate-
cholamines from the adrenal medulla (Douglas & Rubin,
1964a,b; Shanbaky et al., 1978).
The mode of release of neurotransmitter by barium is
distinct from that by calcium. Calcium can evoke the re-
lease of neurotransmitter only when the nerve membranes
are depolarized by nerve impulse. On the other hand,
barium can evoke the release of transmitter without pre-
vious depolarization. Another characteristic of the
barium-evoked release is that it is persistent, while re-
lease by calcium is transitory and terminated by membrane
repolarization.
The action of barium in triggering the release of
catecholamine was examined in detail using cultured bovine
chromaffin cells. Heldman et al. (1989) showed that barium
can enter cells via the voltage-dependent Ca-channels
without previous depolarization. Izumi et al. (1986)
showed that micromolar concentrations of barium can evoke
the secretion of catecholamines after removal of calcium
by a calcium chelating agent. This suggests that barium
can trigger the secretory process by itself, not merely
via the cellular calcium.
8.7.5 Effects on the immune system
According to Kolpakov (1971), immune mechanisms may be
influenced by barium. Rats given barium chloride every
other day for 3-4 weeks showed marked leucocytosis. An iv
injection of 1.5-2.0 ml of blood serum from barium-treated
rats into untreated rats caused a marked increase in leu-
cocytosis. Barium chloride may have enhanced the pro-
duction of leucopoeitins.
Mouse peritoneal macrophages exposed to barium sulfate
for up to 144 h showed marked cytoplasmic vacuolization
with only partial recovery (Rae, 1977).
8.7.6 Ocular system
Studies by Sowden & Pirie (1958) indicated that barium
may play a role in normal vision. Using neutron-activation
analysis, the pigmented parts of eyeballs were found to
contain a higher barium content than the other parts.
Although the precise function of the metal is unknown, it
was suggested that the presence of barium might be essen-
tial for the function and structure of the choroid and for
vision. This may be the only biological role ascribable
to barium.
9. EFFECTS ON MAN
9.1 General population exposure
9.1.1 Acute toxicity - poisoning incidents
There have been several reports of barium poisoning
due to ingestion of barium chloride (Graham, 1934; Allen,
1943, Wang et al., 1989) or barium carbonate (Morton,
1945; Lewi & Bar-Khayim, 1964; Diengott et al., 1964;
Phelan et al., 1984) or due to the diagnostic use of
barium sulfate in gastrointestinal tract studies (Gray et
al., 1989; Ahmed & Hamza, 1989; Feczko et al., 1989).
It has been estimated that the lethal dose of barium
in untreated cases is 3-4 g (66 mg/kg body weight) and the
threshold for a toxic dose is 0.2-0.5 g (Reeves, 1986).
These values apply to the portion absorbed from the gut.
A lethal dose for barium chloride of 11.4 mg/kg has been
reported in RTECS (1985) (Table 14). Barium carbonate and
barium sulfide are also toxic, but act more slowly
(Sollman, 1953).
Table 14. Toxicity of barium compounds to humansa
----------------------------------------------------------------------
Compound Exposure data Effect
----------------------------------------------------------------------
Barium carbonate lowest lethal dose death
= 57 mg/kg
Barium carbonate lowest toxic dose flaccid paralysis without
= 29 mg/kg anaesthesia; paraesthesia;
muscle weakness
Barium chloride lowest lethal dose death
= 11.4 mg/kg
Barium polysulfide lowest toxic dose flaccid paralysis without
= 226 mg/kg anaesthesia; muscle weakness;
dyspnoea
----------------------------------------------------------------------
a Source: RTECS (1985).
Several hundred cases of acute or subacute barium
poisoning occurred in the Kiating district of China, where
table salt contained a large amount of barium (up to 26%).
The victims suffered sudden attacks of paralysis, ranging
from mild to severe, paraesthesia, and cardiac symptoms,
but recovery was usually rapid (Allen, 1943).
Another instance of barium poisoning affected over a
hundred people who had all consumed sausages made with
barium carbonate instead of potato meal (Lewi & Bar-
Khayim, 1964). Of the large number of people affected only
19 were hospitalized. Symptoms ranged from mild vomiting
and diarrhoea to partial paralysis.
Diengott et al. (1964) reported two further cases of
food poisoning resulting from the ingestion of the con-
taminated sausage. In both cases, the patients experienced
severe weakness, diarrhoea, and paralysis. One patient
died suddenly after developing right facial paralysis and
left hemiplegia. The second patient recovered.
Four recent cases of fatal barium poisoning and hyper-
sensitivity have been reported by Ahmed & Hamza, (1989),
Gray et al. (1989), and Feczko et al. (1989). In two of
the cases, death was the result of acute hypersensitivity
reaction following treatment with radioactive barium sul-
fate contrast medium. The remaining two deaths resulted
from acute inflammation of the bronchi and peripheral
airways after accidental inhalation of barium sulfate.
In a reported case of an attempted suicide, the
ingestion of 40 g barium carbonate resulted in a plasma
potassium level of 1.5 mmol/litre (approximately one third
the normal serum potassium level) and induced muscle weak-
ness, respiratory failure, and complete paralysis. Normal
muscular and renal function was regained within 7 days
(Phelan et al., 1984).
The rapid onset of reflex paralysis was reported in a
chrome-plating worker following the inhalation of barium
powder. Complete recovery occurred during the 5-day period
that followed exposure (Shankle & Keane, 1988). Wang et
al. (1989) reported two cases of barium poisoning
resulting from scalding with barium chloride solution. In
both instances cardiac dysfunction was reported and one
patient died due to sudden cardiac arrest.
There are three stages of barium poisoning: a) acute
gastroenteritis; b) loss of deep reflexes with onset of
muscular paralysis; and c) progressive muscular paralysis.
The muscular paralysis seems to be related to severe hypo-
kalaemia. These three stages need not be present in each
patient for barium poisoning to be suspected. In most
cases, recovery is rapid and uneventful. Treatment gener-
ally consists of intravenous infusion of potassium carbon-
ate or lactate and/or oral administration of sodium sul-
fate to precipitate the barium as barium sulfate (Centro
de Informacion Toxicologica, 1972).
Potassium infusion has been used clinically to reverse
the toxic effects of barium. A patient who attempted
suicide by ingesting a commercial depilatory containing
barium sulfide (12.8 g barium were ingested) showed
marked skeletal muscle paralysis and required assisted
respiration. Potassium was infused intravenously as an
antidote and full recovery was achieved within 24 h (Gould
et al., 1973).
9.1.2 Short-term controlled human studies
Wones et al. (1990) administered barium (as barium
chloride) in the drinking-water of 11 healthy male volun-
teers at levels found in the drinking water of some com-
munities in the USA. Subjects ranged in age from 27 to 61
years and had no previous history of diabetes, hyperten-
sion, or cardiovascular disease of any kind. Diets were
strictly controlled throughout the 10-week study. Subjects
were given 1.5 litres/day of distilled and charcoal-fil-
tered water containing no barium for the first 2 weeks,
5 mg/litre for weeks 3-6, and 10 mg/litre for weeks 7-10.
Blood and urine samples as well as morning and evening
blood pressures were measured throughout the study. In
addition, electrocardiograms and 24-h continuous electro-
cardiographic monitoring were performed for 2 consecutive
days at the end of each study period. No change was
reported in blood pressure, total cholesterol, triglycer-
ides, high-density lipoprotein, or low-density lipoprotein
cholesterol levels. Serum potassium and glucose levels, as
well as urinary metanephrine (catecholamine breakdown
product) levels, were also unchanged. No significant ar-
rhythmias were noted during the barium exposure period.
There was, however, an increase in the number of premature
atrial contractions, but this increase was neither stat-
istically nor clinically significant. There was a slight
increase in total serum calcium levels. Blood protein
levels were unchanged. Although this study was limited by
its small sample size and the brief duration of exposure,
the authors concluded that drinking-water levels of 5 and
10 mg/litre barium did not have a significant impact on
the cardiovascular system.
9.1.3 Epidemiological studies
9.1.3.1 Cardiovascular disease
In two limited epidemiological studies, the negative
correlation between barium levels in drinking-water and
cardiovascular mortalities was questionable (Elwood et
al., 1974, and Schroeder & Kraemer, 1974).
Brenniman et al. (1979) conducted a retrospective
study, for the years 1971-1975, of the association between
age- and sex-adjusted cardiovascular death rates and
barium levels in the drinking-water in 16 Illinois (USA)
communities. Comparisons of these death rates were made
between communities that had high barium levels in their
public drinking-water supplies (2.0-10 mg/litre) and com-
munities with low barium levels (<0.2 mg/litre). Study
communities were matched for population, ethnic character-
istics, age distribution, number of persons per household,
number of school years completed, and mean income. The
study showed a high correlation between age-adjusted death
rates from all cardiovascular disease and areas with high
barium levels. However, some of the communities that had
high barium levels also had a 70% change in their popu-
lation between 1960 and 1970. Additionally, there was no
method of controlling removal of barium by home water-
softeners. For these reasons, the finding of an associ-
ation between barium level and death due to ``all cardio-
vascular disease'' and ``heart disease'' must be inter-
preted with caution. Increased death rates caused by
hypertension were examined, as suggested by Calabrese
(1977), and no correlation was found.
As a follow-up to their earlier study, Brenniman et
al. (1981) conducted a cross-sectional study, for the
years 1976-1977, of the association between intake of
elevated barium levels in drinking-water and elevated
blood pressure. One community that had high barium levels
(West Dundee, Illinois, mean barium level of 7.3 mg/litre)
and one community that had low barium (McHenry, Illinois,
mean barium level of 0.1 mg/litre) were studied. All other
drinking-water constituents were nearly identical between
the two communities. In a questionnaire answered by the
participants in this study, information was obtained on
the following variables: age, sex, weight, height, smoking
habits, family history of disease, occupation, and medi-
cation (with special reference to blood pressure medi-
cation). In addition, information was obtained on the
length of residence in the community and the frequency of
use of a water-softener or other home water-treatment
device.
No significant differences in blood pressure were
found between the populations that had high and low barium
intakes. These findings were not altered by adjustment for
home water-softener use, duration of exposure, or medi-
cation for high blood pressure. In addition to these
findings, no differences, with respect to heart disease,
stroke, or kidney disease, were found between the com-
munuties that had high barium levels in drinking-water and
those with low levels. It was concluded that high levels
of barium in drinking-water do not significantly elevate
blood pressure levels in adult males or females.
9.1.3.2 Other effects
The possible correlation between the level of barium
in the drinking-water and human congenital malformations
was discussed in two studies. No association was found by
Schroeder & Kraemer (1974). Morton et al. (1976), using
the methodology of Elwood et al. (1974), found a negative
association between the concentration of barium in the
drinking-water and the presence of malformations in the
central nervous system. However, the data do not allow any
firm conclusions to be drawn.
The prevalence of dental caries was reported to be
significantly lower in 39 children residing in a community
supplied with drinking-water containing high barium con-
centrations (8-10 mg/litre) than in 36 children from a
similar community with drinking-water concentrations of
<3.0 mg/litre (Zdanowicz et al., 1987).
9.2 Occupational exposure
9.2.1 Effects of short- and long-term exposure
It has been known for many years that workers exposed
to finely ground barium salts develop baritosis consisting
of a mixture of very fine punctate and annular lesions and
some slightly larger nodular lesions (Pendergrass &
Greening, 1953). Pronin & Pashkovskii (1973) reported that
cardiac activity disturbances noted in 31 out of 60
workers exposed to barium salts for 3-22 years possibly
reflect the effect of barium on cell potassium levels.
These studies suggest that the heart may be a primary
target for the action of barium in humans. Workers at a
barite factory were monitored for lung deposition of
barium (Doig, 1976). Chest radiographs showed dense
shadows, which slowly disappeared when exposure to barite
ceased. Affected workers showed no symptoms, no abnormal
physical signs, no loss of vital capacity, no interference
with lung function, and no evidence of increased suscepti-
bility to pulmonary infections. NIOSH (1982) conducted an
environmental and medical investigation at a mineral pro-
cessing plant. Barium workers had a significantly higher
incidence of hypertension than did non-barium workers (58%
versus 20%). Barium exposure resulting from the grinding
and mixing of several grades of barium-containing ore
("baryte process") ranged from 0.8 to 1.92 mg/m3, with
a mean of 1.07 mg/m3
Recently, four cases of pneumoconiosis were reported
in barium miners in Scotland (Seaton et al., 1986). Of the
miners who had developed pneumoconiosis, three developed
progressive massive fibrosis, from which two died, and one
developed a nodular simple pneumoconiosis after leaving
the industry. The radiological and pathological features
of the men's lungs were those of silicosis, which was con-
firmed by the high proportions of quartz that were found.
There was a complete absence of barium in the lungs,
suggesting that much of the barium that is inhaled is not
taken into the pulmonary tissues, but remains in alveolar
macrophages and is eventually removed by the mucociliary
mechanism.
NIOSH (1979) investigated the environmental exposures
and health status of workers and residents in the vicinity
of a New York landfill. The investigation included a his-
torical and qualitative environmental evaluation, measure-
ments of occupational exposures to hazardous substances at
three industries near the landfill, and a cross-sectional
medical study of 428 people. In comparison with the data
from the Health and Nutrition Examination Survey of 1971-
1973, participants in the NIOSH study had higher preva-
lences of musculoskelatal symptoms, gastrointestinal
surgery, skin problems, and respiratory symptoms. The
latter was accounted for mainly by workers in the metal
alloy manufacturing industry, where excessive occupational
exposures were found for soluble barium (0.02-1.7 mg/m3).
However, other agents (inorganic lead, zirconium, total
particulates, and UV-visible-IR radiation) were also
present.
9.3 Carcinogenicity of barium chromate
Barium chromate (VI) is the only barium compound for
which there is sufficient evidence that it is a human
carcinogen (IARC, 1980).
IARC (1987) concluded that there is sufficient evi-
dence for the carcinogenicity of hexavalent chromium com-
pounds to animals and humans (Group I: carcinogenic to
humans). This evaluation applied to the group of compounds
as a whole and not necessarily to each individual chemical
within the group.
10. EVALUATION OF HUMAN HEALTH RISKS AND EFFECTS ON THE ENVIRONMENT
10.1 Evaluation of human health risks
10.1.1 Exposure levels
10.1.1.1 General population
The dietary intake of barium, based on data from the
USA, ranges from 300 to 1700 µg/day. The average values
reported by two different sources were 600 and 900 µg/day.
Recent studies from the USA indicate barium levels in
drinking-water ranging from 1 to 20 µg/litre. Based on
this range and assuming a daily consumption of 2 litres of
drinking-water, the intake of barium in drinking-water
would be 2-40 µg/day.
The intake via inhalation is estimated to range from
0.04 to 3.1 µg/day.
The estimated total daily intake of barium in Wales
(United Kingdom) is 1327 µg (food 1240 µg; drinking-
water 86 µg; air 1 µg).
10.1.1.2 Occupational - air exposures
Exposure of metal alloy workers to concentrations
ranging from 0.08 to 1.92 mg/m3 (mean: 1.07 mg/m3) re-
sulted in a high prevalence of hypertension. In a group of
mineral ore processors experiencing musculoskeletal and
respiratory symptoms, barium exposures of 0.02 to 1.7 mg/m3
were reported. Exposures of steel arc welders to concen-
trations ranging from 2.2 to 6.1 mg/m3 have been
measured. These are the highest occupational levels that
have been reported, but no medical studies were con-
ducted.
10.1.1.3 Acute exposures
Barium doses as low as 0.2-0.5 g (3-7 mg/kg body
weight), generally resulting from the ingestion of barium
chloride or carbonate, have been found to lead to toxic
effects in adult humans. In untreated cases, doses of
3-5 g (40-70 mg/kg body weight) were lethal.
10.1.2 Toxic effects; dose-effect and dose-response relationships
The absorption of barium from the gastrointestinal
tract is largely dependent on age and the solubility of
the compound. Less than 10% of the ingested barium is
believed to be absorbed in adults. However, absorption may
be significantly higher in children. Absorbed barium
enters the bloodstream and various soft tissues and is
deposited in the bone. The metabolism of barium is similar
to that of calcium; unlike calcium, however, barium has no
known biological function. Barium can replace calcium in
many physiological processes, and it affects nerve and
muscle activity.
Barium may cause mild skin and severe eye irritation
upon contact. Adverse health effects have been observed
in sensitive individuals (e.g., diuresis patients) fol-
lowing exposure to barium as a medical X-ray preparation
medium. Several cases of barium poisoning have been
reported. Symptoms include acute gastroenteritis, loss of
deep reflexes with onset of muscular paralysis, and pro-
gressive muscular paralysis.
There is no conclusive evidence that barium compounds,
with the exception of barium chromate, are carcinogenic in
humans, nor is there any conclusive evidence that barium
produces reproductive, embryotoxic, or teratogenic effects
in humans.
Early limited epidemiological studies relating ex-
posure to low levels of barium to cardiovascular disease
and mortality were inconsistent and inconclusive. In a
later epidemiological study, no conclusive evidence of
barium-induced effects on blood pressure were revealed.
No effects on blood pressure were identified in a short-
term study in which volunteers consumed increasing levels
of barium up to 10 mg/litre in drinking-water.
Barium inhaled in the workplace has resulted in bari-
tosis. The prevalence of hypertension observed in workers
exposed to high levels of airborne barium was signifi-
cantly higher than in unexposed workers. A dose-related
increase in systolic blood pressure was reported in rats
exposed to concentrations of barium up to 100 mg/litre.
10.1.3 Risk evaluation
On the basis of the available literature, it can be
concluded that, for the general population, barium, at the
usual concentrations found in water (especially drinking-
water), food, and ambient air, does not constitute any
significant health risk. However, for specific subpopu-
lations (elderly or potassium-deficient individuals) and
under special circumstances (high water content, occu-
pational exposure etc.) the potential for adverse health
effects may exist.
10.2 Evaluation of effects on the environment
Barium is present in the soil at an average concen-
tration of 500 µg/g. Concentrations ranging from 0.04 to
37.0 µg/litre and 7.0 to 15 000 µg/litre have been
measured in ocean and fresh waters, respectively. Levels
of barium in the air are generally < 0.05 µg/m3.
Soluble barium compounds are capable of being trans-
ported through the environment and absorbed by organisms.
Barium may accumulate in different parts of the plant.
Barium has been reported to inhibit growth and cellu-
lar processes in microorganisms. It has also been observed
to affect the development of germinating bacterial
spores.
No information on the adverse effects of barium on
terrestrial plants or wildlife has been found. No toxic
effects due to barium have been reported in aquatic plants
at usual concentrations in water. The LC50 values for
fish in fresh water range from 46 to 78 mg/litre. Barium
concentrations of 5.8 mg/litre have been observed to
impair reproduction and growth in daphnids.
There is a shortage of data for evaluating the risk to
the environment posed by barium. Based on the available
information on the toxic effects in daphnids, it appears
that barium may represent a risk to populations of some
aquatic organisms.
11. RECOMMENDATIONS FOR FURTHER STUDIES
Further research studies on barium in the following
areas of environmental and human health effects are
recommended:
* bioavailability studies, including solubilization and
transport mechanisms;
* hypertension/cardiovascular studies involving the gen-
eral population and occupationally exposed workers,
and related mechanisms of action;
* well-designed epidemiological studies;
* studies on the immunological effects of barium on hu-
mans;
* long-term sublethal aquatic toxicity studies;
* monitoring data on environmental exposure to identify
areas where protective measures are needed;
* assessment of early indicators of high rate of ex-
posure to barium; biomarker studies (e.g., barium con-
tent in hair and urine, serum potassium levels).
12. PREVIOUS EVALUATIONS BY INTERNATIONAL BODIES
The International Agency for Research on Cancer
Working Group (IARC, 1980) evaluated the carcinogenicity
of barium chromate (VI) and concluded that it is a posi-
tive human carcinogen. The carcinogenic property of this
compound, however, has been ascribed to the chromium (VI)
moiety and not to the barium.
REFERENCES
AHMED, A. & HAMZA, H.M. (1989) Barium sulfate absorption and sensitivity.
Radiology, 172: 213-214.
AKIYAMA, T. & TOMITA, I. (1973) Preparation and some properties of chromium
phosphate ion exchanger. J. inorg. nucl. Chem., 35: 2971-2983.
ALLEN, A.S. (1943) Pa Ping of Kiating paralysis. Chin. med. J., 61: 296-301.
ANDERSON, N.R. & HUME, D.N. (1968) The strontium and barium content of sea
water. In: Trace organics in water, Washington, DC, American Chemical
Society, pp. 296-307 (Advances in Chemistry Series No. 73).
AOAC (1984) Official methods of analysis of the Association of Official
Analytical Chemists, 14th ed., Arlington, Virginia, Association of Official
Analytical Chemists.
ASBELL, M.A. & EAGON, R.G. (1966) The role of multivalent cations in the
organization and structure of bacterial cell walls. Biochem. biophys. Res.
Commun. 22(6): 664-671.
AWWA (1985) An AWWA survey of inorganic contaminants in water supplies.
Research and Technology Committee Report. J. Am. Water Works Assoc.,
May: 67-72.
BACON, M.P. & EDMOND, J.P. (1972) Barium at Geosecs III in the South-
west Pacific. Earth planet. Sci. Lett., 16: 66-74.
BARNES, C.D. & ELTHERINGTON, L.G. (1973) Drug dosages in laboratory animals -
A handbook, Berkeley, California, University of California Press, p. 53.
BARNETT, P.R., SKOUGSTAD, M.W., & MILLER, K.J. (1969) Chemical charac-
terization of a public water supply. J. Am. Water Works Assoc., 2: 60-67.
BARTLET, J.G., ONDERDONK, A.B., LOUIE, T., KASPER, D.L., & GORBACH, S.L.
(1978) A review: Lessons from an animal model of intra-abdominal sepsis.
Arch. Surg., 113: 853-857.
BAUER, G.C.H., CARLSSON, A., & LINDQUIST, B. (1956) A comparative study on
the metabolism of 140Ba and 45Ca in rats. Biochem. J., 63: 536-542.
BECKER, D.A. (1976) Environmental sample banking - research and method-
ology. Trace Subst. environ. Health, 10: 353-359.
BERNAT, M., CHURCH, T., & ALLEGRE, C.J. (1972) Barium and strontium
concentrations in Pacific and Mediterranean sea water profiles by direct
isotope dilution mass spectrometry. Earth planet. Sci. Lett., 16: 75-80.
BIESINGER, K.E. & CHRISTENSEN, G.M. (1972) Effects of various metals on
survival, growth, reproduction, and metabolism of Daphnia magna. J. Fish
Res. Board Can., 29: 1691-1700.
BLIGH, P.H. & TAYLOR, D.M. (1963) Comparative studies of the metabolism of
strontium and barium in the rat. Biochem. J., 87: 612-618.
BOLTER, E., TUREKIAN, K.K., & SCHULTZ, D.F. (1964) The distribution of
rubidium, cesium and barium in the oceans. Geochim. Cosmochim. Acta,
28: 1459-1466.
BORZELLECA, J.F., CONDIE, L.W., & EGLE, J.L. (1988) Short-term toxicity
(one- and ten-day gavage) of barium chloride in male and female rats.
J. Am. Coll. Toxicol., 1(5): 675-685.
BOUTET, C. & CHAISEMARTIN, C. (1973) Propriétés toxiques spécifiques des
sels métalliques chez Austropotamobius pallipes pallipes et Orconetes
limosus. C.R. Soc. Biol. Paris, 167: 1933-1938.
BOWEN, H.J.M. (1956) Barium in sea water and marine organisms. J. Mar. Biol.
Assoc. (U.K.), 35: 451-460.
BOWEN, H.J.M. (1966) Trace elements in biochemistry, New York, Academic
Press, p. 19.
BOWEN, H.J.M. & DYMOND, J.A. (1955) Strontium and barium in plants and soils.
Proc. R. Soc. Lond., B144: 355-368.
BRADFIELD, R. (1932) The concentration of cations in clay soils. J. Phys.
Chem., 36: 340-347.
BRADFORD, G.R. (1971) Trace elements in the water resources of California.
Hilgardia, 41(3): 45-53.
BREHM, P., DUNLAP, K., & ECKERT, R. (1978) Calcium-dependent repolar-
ization of paramecium. J. Physiol., 274: 639-654.
BRENDER, D., STRONG, C.G., & SHEPHERD, J.T. (1970) Effects of acetyl-
strophanthidin on isolated veins of dogs. Circ. Res., 26: 547-555.
BRENNIMAN, G.R., NAMEKATA, T., KOJOLA, W.H., CARNOW, B.W., & LEVY, P.S.
(1979) Cardiovascular disease death rates in communities with elevated
levels of barium in drinking water. Environ. Res., 20: 318-324.
BRENNIMAN, G.R., KOJOLA, W.H., LEVY, P.S., CARNOW, B.W., & NAMEKATA, T.
(1981) High barium levels in public drinking water and its association
with elevated blood pressure. Arch. environ. Health, 36: 28-32.
BROOKS, R.R. (1978) Pollution through trace elements. In: Bockris, J.O.M.,
ed. Environmental chemistry, New York, Plenum Press, pp. 429-476.
BROOKS, R.R. (1980) Barium accumulation by demids of the genus Closterium.
Br. Phycol. J., 15: 261-264.
BROWNING, E. (1969) Toxicity of industrial metals, London, Appleton-Century
Crofts.
CALABRESE, E.J. (1977) Excessive barium and radium-226 in Illinois drinking
water. J. environ. Health, 39(5): 366-369.
CALABRESE, E.J., CANADA, A.T., & SACCO, C. (1985) Trace elements and public
health. Annu. Rev. public Health, 6: 131-146.
CANTELMO, F.R., TAGATZ, M.E., & RANGA RAO, K. (1979) Effect of barite on
meiofauna in a flow-through experimental system. Mar. environ. Res.,
2: 301-309.
CARTER, G.A. & WAIN, R.L. (1904) Investigations on fungicides. IX. The
fungitoxicity, phytotoxicity, and systemic fungicidal activity of some
inorganic salts. Ann. appl. Biol., 53: 291-309.
CARTWRIGHT, K., SPECHT, S.A., GILKESON, R.H., GRIFFIN, R.A., & LARSON, T.E.
(1978) Geologic studies to identify the source of high levels of radium and
barium in Illinois ground water supply: A preliminary report, Springfield,
Virginia, US Department of Commerce, Office of Water Research and Technology,
pp. 13, 287, 737.
CASTAGNOU, R., PAOLETTI, C., & LARABEAU, S. (1957) Absorption et répartition
de baryum administré par voie intraveineuse ou par voie orale du rat. C.R.
Acad. Sci., Paris, 24: 2994.
CENTRO DE INFORMACION TOXICOLOGICA (1972) Treatments for poisonings caused
by rodenticides. Antioquia Med., 22: 699-704.
CHAN, L.H., DRUMMOND, D., EDMOND, J.M., & GRANT, B. (1977) On the barium
data from the Atlantic GEOSECS expedition. Deep Sea Res., 24: 613-649.
CHOW, T.J. (1976) Barium in southern California waters: A potential
indicator of marine drilling contamination. Science, 193: 57-58.
CHOW, T.J. & GOLDBERG, E.D. (1960) On the marine geochemistry of barium.
Geochim. Cosmochim. Acta, 20: 192-198.
CHOW, T.J. & PATTERSON, C.C. (1966) Concentration profiles of barium and
lead in Atlantic waters off Bermuda. Earth. planet. Sci. Lett., 1: 397-400.
CHOW, T.J., EARL, J.L., REED, J.H., HANSEN, N., & ORPHAN, V. (1978) Barium
content of marine sediments near drilling sites: A potential pollutant
indicator. Mar. Pollut. Bull., 9: 97-99.
CLARK, F.W. & WASHINGTON, H.S. (1924) The composition of the earth's crust,
Washington, DC, US Department of the Interior (US Geological Survey:
Professional Paper No. 127).
CLARY, J.J. & TARDIFF, R.G. (1974) The absorption, distribution and
excretion of orally administered 133BaCl2 in weanling male rats. Toxicol.
appl. Pharmacol. , 29: 139.
CLAVEL, J.P., LORRILLOT, M.L., BUTHIAU, D., GERBET, D., HEITZ, F., & GALLI,
A. (1987) Intestinal absorption of barium during radiological studies.
Therapie, 42(2): 239-243.
CONARD, R.A. & SCOTT, W.A. (1961) Modification of radiation-induced gastro-
intestinal effects of barium meals. Radiat. Res., 15: 527-531.
CONSIDINE, D.M., ed. (1976) Van Nostrand's scientific encyclopedia, 5th ed.,
New York, Van Nostrand Reinhold Company.
COOPER, W.W., BECK, J.N., CHEN, T.S., & KURODA, P.K. (1970) Radioactive
strontium and barium fallout. Health Phys., 19: 625-632.
CRAWFORD, A.C. (1908) Barium, a cause of the loco-weed disease. US Dept.
Agric. Bur. Plant Ind. Bull., 129: 87.
CRC (1988) CRC Handbook of chemistry and physics, 68th ed., Boca Raton,
Florida, Chemical Rubber Publishing Company (CRC).
CREASON, J.P., HINNERS, T.A., BUMGARNER, J.E., & PINKERTON, C. (1975) Trace
elements in hair, as related to exposure in metropolitan New York. Clin.
Chem., 21: 606-612.
CREASON, J.P., SVENDSGAARD, D., BUMGARNER, J.E., PINKERTON, C., & HINNERS,
T.A. (1976) Maternal-fetal tissue levels of 16 trace elements in 8 selected
continental United States communities. Trace Subst. environ. Health,
10: 53-62.
CUDDIHY, R.G. & GRIFFITH, W.C. (1972) A biological model describing tissue
distribution and whole body retention of barium and lanthanum in beagle dogs
after inhalation and gavage. Health Phys., 23: 621-633.
CUDDIHY, R.G. & OZOG, J.A. (1973) Nasal absorption of CsCl, SrCL2, BaCl2 and
CeCl3 in Syrian hamsters. Health Phys., 25: 219-224.
CUDDIHY, R.G., HALL, R.P., & GRIFFITH, W.C. (1974) Inhalation exposures to
barium aerosols: Physical, chemical and mathematical analysis. Health Phys.,
26: 405-416.
CUFFE, S.T. & GERSTLE, R.W. (1967) Emissions from coal-fired power plants,
Washington, DC, US Department of Health, Education and Welfare, Government
Printing Office (Publication No. 999-AP-35).
CUTRESS, T.W. (1979) A preliminary study of the microelement composition of
the outer layer of dental enamel. Caries Res., 13: 73-79.
DARE, P.R., HEWE, H.P.J., HICKS, R., VAN BEMST, A., ZOBER, A., & FLEISHER,
M. (1984) Barium in welding fume. Ann. occup. Hyg., 28(4): 445-448.
DAUGHERTY, F.M., Jr (1951) Effects of some chemicals used in oil well
drilling on marine animals. Sewage ind. Wastes, 23: 1282-1287.
DAVIS, W.E. (1972) National inventory of sources and emissions: Barium,
boron, copper, selenium and zinc, Washington, DC, US Environmental
Protection Agency, p. 56 (EPA 68-02-0100).
DEJONG, L.E. & ROMAN, W.B. (1971) Tolerance of Azobacter for metallic and
nonmetallic ions. J. Microbiol. Serol., 37: 119-124.
DENCKER, L., NILLSON, A., RONNBACK, C., & WALINDER, G. (1976) Uptake and
retention of 133Ba and 140Ba-140La in mouse tissues. Acta radiol.,
15: 273-287.
DEN DOOREN DE JONG, L.E. (1965) Tolerance of Chlorella vulgaris for metallic
and non-metallic ions. Antonie van Leeuwenhoek, 31: 301-313.
DEVI PRASAD, P.V. (1984) Effect of magnesium, strontium and barium on the
calcification of the freshwater green alga Gloeotaenium. Phykos,
23: 202-206.
DIENGOTT, D., ROZSA, O., LEVY, N., & MUAMMAR, S. (1964) Hypokalemia in
barium poisoning. Lancet, 2: 343-344.
DOIG, A.T. (1976) Baritosis: A benign pneumoconiosis. Thorax, 31: 30-39.
DOMANSKI, T.M., DEPCZYK, D., & LINIECKI, J. (1964) A test of the theory of
alkaline earth metabolism by the behaviour of 133Ba in rats. Phys. Med.
Biol., 11: 461-470.
DOMANSKI, T.M., LINIECKI, J., & WITKOWSKI, D. (1969) Kinetics of calcium,
strontium, barium, and radium in rats. In: Mays, C.W., Jee, W.S.W., & Lloyd,
R.D., ed. Delayed effects of bone seeking radionuclides, Salt Lake City,
Utah, University of Utah Press, pp. 81-103.
DOUGLAS, W.W. & POISNER, A.M. (1962) On the mode of action of acetyl-
choline in evoking adrenal medullary secretion: Increased uptake of calcium
during the secretory response. J. Physiol., 162: 385-392.
DOUGLAS, W.W. & RUBIN, R.P. (1963) The mechanism of catecholamine release
from the adrenal medulla and the role of calcium in stimulus-secretion
coupling. J. Physiol., 167: 288-310.
DOUGLAS, W.W. & RUBIN, R.P. (1964a) Stimulant action of barium on the
adrenal medulla. Nature (Lond.), 203: 305-307.
DOUGLAS, W.W. & RUBIN, R.P. (1964b) The effects of alkaline earths and other
divalent cations on adrenal medullary secretion. J. Physiol., 175: 231-241.
DURFOR, C.M. & BECKER, E. (1964) Public water supplies of the 100 largest
cities in the United States, 1962, Washington, DC, US Department of the
Interior, Government Printing Office (US Geological Survey: Water Supply Paper
No. 1812).
DURUM, W. (1960) Occurrence of trace elements in water. In: Faber, H. &
Bryson, L., ed. Proceedings of the Conference on Physiological Aspects of
Water Quality, Washington, DC, 8-9 September, 1960, Washington, DC, Public
Health Service, Division of Water Supply and Pollution Control, Research and
Training Grants Branch.
DYBCZYNSKI, R. (1972) Effect of resin cross-linking on the cation-exchange
separation of alkali and alkaline earth metals on sulphonic cation exchangers.
J. Chromatogr., 71: 507-522.
EINBRODT, H.J., WOBKER, F., & KLIPPEL, H.G. (1972) [Animal experiments on
the deposit and distribution of barium sulfate in the rat organism after
inhalation.] Int. Arch. Arbeitsmed., 30: 237-244 (in German).
ELLSASSER, J.C., FARNHAM, J.E., & MARSHAL, J.H. (1969) Comparative kinetics
and autoradiography of 45Ca and 133Ba in 10-year-old beagle dogs. J. Bone
joint Surg., 51: 1397-1412.
ELORZA, M.V. (1969) Toxicity of metal ions to Aspergillis nidulans.
Microbiol. Esp., 22: 131-137.
ELWOOD, P.C., ABERNETHY, M., & NORTON, M. (1974) Mortality in adults and
trace elements in water. Lancet, 2: 1470-1472.
EPSTEIN, M.S. & ZANDER, A.T. (1979) Direct determination of barium in sea
and estuarine water by graphite furnace atomic spectrometry. Anal. Chem.,
51: 915-918.
ERDELYI, L. (1977) Synaptic activation of Helix ganglion cells by barium ions.
Molecologia, 16: 93-100.
EVANS, R.B., SNELLING, R.N., & BUCK, F.N. (1973) Assessment of doses in the
western United States from the People's Republic of China nuclear test of
January 7, 1972. Radiat. Data Rep., 2: 77-83.
FAILYER, G.H. (1910) Barium in soils. US Dept. Agric. Bur. Soils Bull., 72:
23.
FASSEL, V.A. & KNISELEY, R.N. (1974) Inductively coupled plasma optical
emission spectrometry. Anal. Chem., 46: 1110A-1120A.
FECZKO, P.J., SIMMS, S.M., BAKIRCI, N. (1989) Fatal hypersensitivity
reaction during a barium enema. Am. J. Radiol., 153: 275-276.
FOERSTER, H.F. & FOSTER, J.W. (1966) Endotrophic calcium, strontium, and
barium spores of Bacillus megaterium and Bacillus cereus. J. Bacteriol.,
91: 1333-1335.
FORSSEN, A. & ERAMETSA, O. (1974) Inorganic elements in the human body. Ba,
Br, Ca, Cd, K, Ni, Pb, Sn, Sr, Ti, Y and Zn in hair. Ann. Acad. Sci. Fenn.
A.V. Med., 162: 1-5.
FORTESCUE, J.A.C., CURTIS, S.A., RICHARDSON, J., & CAMPBELL, J. (1976)
Regional geochemical maps for the east end of the Niagara Pennisula. Trace
Subst. environ. Health, 10: 177-184.
FOSTER, P.R., ELHARRAR, V., & ZIPES, D.P. (1977) Accelerated ventricular
escapes induced in the intact dog by barium, strontium and calcium. J.
Pharmacol. exp. Ther., 200: 373-383.
FRENCH, N.R. (1963) Review and discussion of barium in radioecology,
New York, Reinhold Press.
GARBARINO, J.R. & TAYLOR, H.E. (1979) An inductive-coupled plasma atomic-
emission spectrometric method for routine water quality testing. Appl.
Spectrosc., 33: 220-226.
GARNER, R.J., JONES, H.G., & SAUSOM, B.F. (1960) Fission products and the
dairy cow. Some aspects of the metabolism of the alkaline earth elements
calcium, strontium, and barium. Biochem. J., 76: 572-579.
GEORGE, R.Y. (1975) Potential effects of oil drilling and dumping activities
in marine biota. In: Proceedings of the Conference on Environmental Aspects
of Chemical Use in Well-Drilling Operations, Houston, Texas, May 1975,
Washington, DC, US Environmental Protection Agency, Office of Toxic
Substances, pp. 333-335 (EPA 560/1-75-004).
GOLDBERG, E.D.D & ARRHENIUS, G. (1958) Chemistry of Pacific pelagic sediments.
Geochim. Cosmochim. Acta, 13: 153-212.
GOODENOUGH, R.D. & STENGER, V.A. (1973) Magnesium, calcium, strontium,
barium and radium. In: Bailer, J.D., Jr, Emeleus, H.J., & Trotman-Dickinson,
J., ed. Comprehensive inorganic chemistry, Oxford, Pergamon Press,
pp. 591-664.
GOODMAN, L.S. & GILMAN, A. (1980) The pharmacological basis of therapeutics,
6th ed., New York, The MacMillan Company.
GORMICAN, A. (1970) Inorganic elements in foods used in hospital menus.
J. Am. Diet. Assoc., 56: 397-403.
GOULD, D.B., SORRELL, M.R., & LUPARIELLO, A.D. (1973) Barium sulfide
poisoning. Some factors contributing to survival. Arch. int. Med.,
132: 891-894.
GRAHAM, C.F. (1934) Barium chloride poisoning. J. Am. Med. Assoc.,
102: 1471.
GRANTHAM, C.K. & SLOAN, J.P. (1975) Toxicity study. Drilling fluid chemi-
cals on aquatic life. In: Proceedings of the Conference on Environmental
Aspects of Chemical Use in Well-Drilling Operations, Houston, Texas May 1975,
Washington, DC, US Environmental Protection Agency, Office of Toxic
Substances, pp. 103-110 (EPA 560/1-75-004).
GRAY, C., SIVALOGANATHAN, S., & SIMPKINS, K.C. (1989) Aspiration of high-
density barium contrast medium causing acute pulmonary inflammation - Report
of two fatal cases in elderly women with disordered swallowing. Clin. Radiol.,
40: 397-400.
GREBECKI, A. & KUZNICKI, L. (1963) The influence of external pH on the
toxicity of inorganic ions for P. candatum. Acta Protozool., 1: 157-184.
GUDIKSEN, P.H., CHAKRAVARTI, D., FAIRHALL, A.W., & YOUNG, J.A. (1965) Debris
from the Chinese atomic test of May 1965, intercepted over the northwestern
United States. Health Phys., 12: 862-863.
GUPTA, S.R., PRASANNA, H.R., VISWANATHAN, W., & VENKITASUBRA-
MANIAN, T.A. (1975) Effect of inorganic salts and some biologically
important compounds on the incorporation of acetate-1-14C into aflatoxins
by resting mycelia of Aspergillis parasiticus. Z. Lebensm. Unters. Forsch.,
157: 19-22.
GUTHRIE, R.K., DAVIS, E.M., CHERRY, S., & MURRAY, H.E. (1979)
Biomagnification of heavy metals by organisms in a marine microcosm.
J. environ. Contam. Toxicol., 21: 53-61.
GUTWEIN, E.E., LANDOLT, R.R., & BRENCHLEY, D.L. (1974) Barium retention in
rats exposed to combustion products from diesel fuel containing a barium-
based antismoke additive. J. Air. Pollut. Control Assoc., 24(1): 40-43.
HAMILTON, E.I. & MINSKI, M.J. (1972) Abundance of the chemical element in
man's diet and possible relations with environmental factors. Sci. Environ.,
1: 315.
HANSEN, M. (1958) Constitution of binary alloys, New York, McGraw-Hill Book
Company, Inc.
HARRISON, G.E., CARR, T.E.F., SUTTON, A., & RUNDO, J. (1966) Plasma
concentration and excretion of calcium-47, strontium-85, barium-133 and
radium-223 following successive intravenous doses to a healthy man.
Nature (Lond.), 209: 526-527.
HARRISON, G.E., CARR, T.E.F. & SUTTON, A. (1967) Distribution of radio-
active calcium, strontium, barium and radium following intravenous
injection into a healthy man. Int. J. Radiat. Biol., 13: 235-247.
HAUSLER, G. & HAEFELY, W. (1979) Modification of release by adrenergic
neutron blocking agents and agents that alter the action potential.
In: Paton, D.M., ed. The release of catecholamines from adrenergic neutrons,
New York, Pergamon Press, pp. 185-216.
HAVLIK, B., HANUSOVA, J., & RALKOVA, J. (1980) Hygienic importance of
increased barium content in some fresh waters. J. Hyg. Epidemiol. Microbiol.
Immunol., 24(4): 396-404.
HAWLEY, G.G. (1977) The condensed chemical dictionary, 9th ed., New York,
Van Nostrand Reinhold Company.
HEFFRON, C.L., REID, J.T., & FURR, A.K. (1977) Lead and other elements in
sheep fed colored magazines and newsprint. J. agric. food Chem., 25: 657-660.
HEITMULLER, P.T., HOLLISTER, T.A., & PARRISH, P.R. (1981) Acute toxicity of
54 industrial chemicals to sheepshead minnows (Cyprinodon variegatus). Bull.
environ. Contam. Toxicol., 27: 596-604.
HELDMAN, E., LEVINE, M., RAVEH, L., & POLLARD, H.B. (1989) Barium ions enter
chromaffin cells via voltage-dependent calcium channels and induce secretion
by a mechanism independent of calcium, J. biol. Chem., 264(14): 7914-7920.
HENDERSON, E.G. & VOLLE, R.L. (1972) Ion exchange in frog sartorious muscle
treated with 9-aminoacridine or barium. J. Pharmacol. exp. Ther., 183: 356-
369.
HICKS, R., CALDAS, L.Q., DARE, P.R., & HEWITT, P.J. (1986) Cardio-
toxic and bronchoconstrictor effects of industrial metal fumes containing
barium. Arch. Toxicol., Suppl. 9: 416-420.
HILDEBRAND, S.G., CUSHMAN, R.M., & CARTER, J.A. (1976) The potential
toxicity and bioaccumulation in aquatic systems of trace elements present
in aqueous coal conversion effluents. In: Hemphill, D.D., X, ed., Trace
substances in environmental health, Columbia, Missouri, University of
Missouri.
HIRANO, Y. & HIRAOKA, M. (1986) Changes in K+ current induced by Ba2+ in
guinea pig ventricular muscles. Am. J. Physiol., 251: 24-33.
IARC (1973) Some inorganic and organometallic compounds, Lyon, International
Agency for Research on Cancer, p. 102 (IARC Monographs on the Evaluation of
Carcinogenic Risk of Chemicals to Humans, Vol. 2).
IARC (1980) Some metals and metallic compounds, Lyon, International Agency
for Research on Cancer, p. 205 (IARC Monographs on the Evaluation of the
Carcinogenic Risk of Chemicals to Humans, Vol. 23).
IARC (1987) Chromium and chromium compounds: Chromium metal, trivalent
chromium compounds, hexavalent chromium compounds. In: Overall evaluations
of carcinogenicity: An updating of IARC Monographs Volumes 1 to 42, Lyon,
International Agency for Research on Cancer, pp. 165-168 (IARC Monographs on
the Evaluation of Carcinogenic Risks to Humans, Supplement 7).
ICRP (INTERNATIONAL COMMISSION ON RADIOLOGICAL PROTECTION) (1959)
Recommendations of the International Commission on Radiological Protection.
Report of Committee II, Elmsford, New York, Pergamon Press (ICRP Publication
No. 2).
ICRP (1974) 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, Oxford, New York, Pergamon Press (ICRP Report No. 23).
ICRP (INTERNATIONAL COMMISSION ON RADIOLOGICAL PROTECTION) (1975) Report
of the Task Group on Reference Man, No. 23. Pergamon Press, Elmsford, New
York.
IZMEROV, N.F., SANOTSKY, I.V., & SIDEROV, K.K. (1982) Toxicometric
parameters of industrial toxic chemicals under single exposure, Moscow,
Centre of International Projects, GKNT, p. 23.
IZUMI, F., TOYOHIRA, Y., YANAGIHARA, N., WADA, A., & KOBAYASHI, H. (1986)
Barium evoked release of cuthecholamines from digitonin-premeabilized
adrenal medullary cells. Neuro-Sci. Lett., 69: 172-175.
KASSANIS, B., WHITE, R.F., & WOODS, R.D. (1975) Inhibition of multi-plication
of tobacco mosaic virus in protoplasts by antibiotics and its prevention by
divalent metals. J. gen. Virol., 28: 185-191.
KATZUNG, B.G. & MORGENSTERN, J. (1976) The effects of potassium and barium
on ventricular automaticity and the pacemaker current. Proc. West.
Pharmacol. Soc., 19: 299-302.
KELLEY, K.K. (1933) Contribution to the data on theoretical metallurgy. II.
High-temperature specific-heat equation for inorganic substances, Pittsburg,
Pennsylvania, US Bureau of Mines (Bulletin No. 371).
KINOSITA, H., DRYL, S., & NAITOH, Y. (1964) Spontaneous change in membrane
potential of Paramecium caudatum induced by barium and calcium ions. Bull.
Acad. Pol. Sci. Ser. Sci. Biol., 12: 459-461.
KIRPEKAR, S.M. & MISU, Y. (1967) Release of noradrenaline by splenic nerve
stimulation and its dependence on calcium. J. Physiol., 188: 219-234.
KIRPEKAR, S.M., PRAT, J.C., PUIG, M., & WAKADE, A.R. (1972) Modification of
the evoked release of noradrenaline from the perfused cat spleen by various
ions and agents. J. Physiol., 221: 601-615.
KNOP, W. (1874) Analyses of the Nile sediment. Landwirtsch, Vers.-Stn,
17: 65-70.
KOIRTYOHANN, S.R. & PICKETT, E.E. (1968) The nitrous oxide-acetylene flame
in emission analysis - II. Lithium and the alkaline earths. Spectroclin.
Acta, 23B: 673-685.
KOJOLA, W.H., BRENNIMAN, G.R., & CARNOW, B.W. (1978) A review of environmental
characteristics and health effects of barium in public water supplies. Rev.
environ, Health, 3(1): 79-95.
KOLPAKOV, V.V. (1971) Effect of barium chloride on production of humoral
factors stimulating leukopoiesis. Patol. Fiziol. eksp. Ter., 5(6): 64-66.
KONONENKO, K.I. & CHAIKINA, L.A. (1970) Effect of metal ion in the electric
charge of cells. Biofizika, 15: 1127-1129.
KOPP, J. (1969) The occurrence of trace elements in water. In: Hemphill,
D.D., III, ed. Trace substances in environmental health, Columbia, Missouri,
University of Missouri, pp. 59-73.
KOPP, J.F. & KRONER, R.C. (1967) Tracing water pollution with an emission
spectrograph. J. Water Pollut. Control Fed., 39:1659.
KOPP, J.F. & KRONER, R.C. (1968) A comparison of trace elements in natural
waters, dissolved vs. suspended. Dev. appl. Spectrosc., 6: 339-352.
KOPP, J.F. & KRONER, R.C. (1970) Trace metals in waters of the United States:
A five-year summary of trace metals in rivers and lakes of the United States
(1 October 1962 - 30 September 1967), Cincinnati, Ohio, US Department of the
Interior, Federal Water Pollution Control Administration, Division of
Pollution Surveillance.
KOPP, S.J., PERRY, H.M., Jr., FELIKSIK, J., ERLANGER, M., & PERRY, E. (1985)
Cardiovascular dysfunction and hypersensitivity to sodium pento-barbital
induced by chronic barium chloride ingestion. Toxicol. appl. Pharmacol.,
72: 303-314.
KOSHI, Y. (1966) Mechanism of cell fusion caused by the haemagglutinating
virus of Japan: Requirement of calcium for cell fusion. Nara Joshi Daigaku
Seibutsu Gakkaishi, 16: 25-28.
KOVALSKII, V.V., BOROVIK, T.F., LETUNOVA, S.V., & GINZBURG, E.O. (1965)
Level of trace elements in microorganisms. Mikrobiologiya, 34: 403-406.
LANGE, N.A. (1985) Lange's handbook of chemistry, 10th ed., New York, McGraw
Hill Publishers, pp. 425-427.
LEBEDENA, ZH.D., VOLKOVA, I.M., & RUBAN, E.L. (1976) Effect of metal ions on
the lipolytic activity of M. rubrum and A. streptomycini. Mikrobiologiya,
45:104-110.
LEBLANC, G.A. (1980) Acute toxicity of priority pollutants to water flea
(Daphnia magna). Bull. environ. Contam. Toxicol., 24: 684-691.
LEDEBO, I. (1976) Divalent cations in the envelope of a psychrophilic
Archromobacter. J. gen. Microbiol., 94: 351-358.
LEDERER, C.M., HOLLANDER, J.M., & PERLMAN, I. (1967) Table of the isotopes,
6th ed., New York, John Wiley and Sons.
LEE, E.G.H., TOWNSLEY, P.M., & WALDEN, C.C. (1966) Effects of bivalent
cations on the production of aflatoxins in submerged cultures. J. food Sci.,
31: 432-436.
LESLIE, S.W. & BOROWITZ, J.L. (1975) Inhibition of the adrenal chromaffin
and membrane calcium by caffeine and various divalent anions. Res. Commun.
chem. Pathol. Pharmacol., 11: 413-424.
LETKIEWICZ, F., SPOONER, C., MACULUSO, C., & BROWN, D. (1984) Occurrence of
barium in drinking water, food and oil, Washington, DC, US Environ-
mental Protection Agency, Office of Drinking Water.
LEWI, Z. & BAR-KHAYIM, Y. (1964) Food poisoning from barium carbonate.
Lancet, 2: 342-343.
LILOV, L. & ZAHN, D. (1967) Effects of some cations on the hydrogenase
activity of Proteus vulgaris OX 19. Zentralbl. Bakteriol., 121: 475-478.
LINIECKI, J. & KARNEWICZ, W. (1971) Long term retention of radiobarium and
radiostrontium in rabbits. Nukleonika (Warsaw), 16: 591-604.
LOSEE, F.L., CUTRESS, T.W., & BROWN, R. (1974) Natural elements of the
periodic table in human dental enamel. Caries Res. 8: 123-134.
MCCABE, L. (1974) Problems of trace metals in water supplies - an over-view.
In: Saponzik, A., ed. Proceedings of the 16th Water Quality Conference on
Trace Metals in Water Supplies: Occurrence, Significance and Control,
Urbana, Illinois, University of Illinois, 12-13 February 1974, pp. 1-9.
MCCABE, L.J., SYMONS, J.M., LEE, R.D., & ROBECK, G.C. (1970) Survey of
community water supply systems. J. Am. Water Works Assoc., 62: 670-687.
MCCAULEY, P.T. & WASHINGTON, I.S. (1983) Barium bioavailability as the
chloride, sulfate, or carbonate salt in the rat. Drug chem. Toxicol.,
6: 209-217.
MCCAULEY, P.T., DOUGLAS, B.H., LAURIE, R.D., & BULL, R.J. (1985)
Investigations into the effect of drinking water barium on rats. In:
Advances in modern environmental toxicology, Princeton, New Jersey,
Princeton Publishing Co., Vol. IX, pp. 197-210.
MCHARGUE, J.S. (1913) The occurrence of barium in tobacco and other plants.
Am. Chem. Soc. J., 35: 826-834.
MCLACHLAN, E.M. (1977) The effects of strontium and barium ions at
synapses in sympathetic ganglia. J. Physiol., 267: 497-518.
MCMICHAEL, J.C. & LAUFFER, M.A. (1975) A specific effect of calcium ion on
the polymerization-depolymerization of tobacco mosaic virus protein. Arch.
Biochem. Biophys., 169: 209-216.
MAGILL, W.A. & SVEHLA, G. (1974) Study on the elimination of interferences
in the determination of barium by atomic absorption spectrophotometry.
Z. anal. Chem., 268: 180-184.
MARSH, D.D., ALSBERG, C.L., & BLACK, O.F. (1912) The relation of barium to
the loco-weed disease. US Dept. Agric. Plant Indus. Bull., 246: 67.
MARUTA, T., TAKEUCHI, T., & SUZUKI, M. (1972) Spectrophotometric studies on
5,7-dibromo-8-aminoquinoline chelates of some bivalent transition metals.
Anal. chem. Acta, 58: 452-455.
MEIER, C.F., Jr & KATZUNG, B.G. (1978) Effects of cesium and barium on
depolarization: Induced automaticity in ventricular myocardium. Proc. West.
Pharmacol. Soc., 21: 71-75.
MILLER, R.G., FEATHERSTONE, J.D.B., CARZON, M.E.J., MILLS, T.S., & SHIELDS,
C.P. (1985) Barium in teeth as indicator of body burden. In: Advances in
modern environmental toxicology, Princeton, New Jersey, Princeton Publishing
Company, Vol. 9, pp. 211-219.
MINER, S. (1969) Air pollution aspects of barium and its compounds, Bethesda,
Maryland, Litton Systems, Inc., Environmental System Division, p. 63. (NTIS
PB-188083).
MORROW, P.E., GIBB, F.R., & JOHNSON, L. (1964) Clearance of insoluble dust
from the lower respiratory tract. Health Phys., 10: 543-555.
MORTON, M.S., ELWOOD, P.C., & AVERNETHY, M. (1976) Trace elements in water
and congenital malformations of the central nervous system in South Wales.
Br. J. Soc. Med., 30: 36-39.
MORTON, W. (1945) Poisoning by barium carbonate. Lancet, 2: 738-739.
MURPHY, E.W., PAGE, L., & WATT, B.K. (1971) Trace minerals in type A school
lunches. J. Am. Diet. Assoc., 59: 115-122.
NADKARNI, R.A. & MORRISON, G.H. (1974) Multi-element analysis of sludge
samples by instrumental neutron activation analysis. Environ. Lett.,
6: 273-285.
NAS (1977) Drinking water and health, Washington, DC, National Academy of
Sciences, Printing and Publication Office.
NIOSH (1976) Health hazard evaluation and determination report. B.F.
Goodrich Company, Koroseal Division, Marietta, Ohio, Cincinnati, Ohio,
National Institute for Occupational Safety and Health, Center for Disease
Control (NIOSH Report No. 75-24-273).
NIOSH (1977) NIOSH manual of analytical methods. Standards program validated
methods. III., Cincinnati, Ohio, National Institute for Occupational Safety
and Health, p. 5198.
NIOSH (1978) Health hazard evaluation determination report: Mark Steel
Corporation, Salt Lake City, Utah, Cincinnati, Ohio, National Institute for
Occupational Safety and Health, Center for Disease Control (NIOSH Report No.
78-93-536).
NIOSH (1979) Health hazard evaluation and technical assistance report:
Kentile Floors Inc., South Plainfield, New Jersey, Cincinnati, Ohio,
National Institute for Occupational Safety and Health, Center for Disease
Control (NIOSH Report No. 78-72-618).
NIOSH (1980) Technical assistance report, Cincinnati, Ohio, National
Institute for Occupational Safety and Health, Center for Disease Control
(NIOSH Report No. 79-022-789).
NIOSH (1982) Health hazard evaluation report: Sherwin Williams Company,
Coffeyille, Kansas, Cincinnati, Ohio, National Institute for Occupational
Safety and Health, Center for Disease Control (NIOSH Report No. HETA/81-356-
1183).
NIOSH (1984) Industrial hygiene survey report of Dorchester Refining Company,
15 September - 5 October, 1981, Cincinnati, Ohio, National Institute for
Occupational Safety and Health, Center for Disease Control (NIOSH Report No.
124-11).
NIOSH (1985) Health hazard evaluation report: General Motors Corporation,
Dayton, Ohio, Cincinnati, Ohio, National Institute for Occupational Safety
and Health, Center for Disease Control (NIOSH Report No. HETA/84-060-1645).
NIOSH (1987a) NIOSH manual of analytical methods. Standards completion
program validated methods. Barium methods 7056, Cincinnati, Ohio, National
Institute for Occupational Safety and Health, Center for Disease Control.
NIOSH (1987b) Health hazard evaluation report: Wellman Dynamics Corporation,
Creston, Iowa, Cincinnati, Ohio, National Institute for Occupational Safety
and Health, Center for Disease Control (NIOSH Report No. HETA/83-015-1809).
NIOSH (1987c) Health hazard evaluation report: International Association of
Fire Fighters, Washington, DC, Cincinnati, Ohio, National Institute for
Occupational Safety and Health, Center for Disease Control (NIOSH Report No.
HETA/85-540-1816).
NISHIOKA, H. (1975) Mutagenic activities of metal compounds in bacteria.
Mutat. Res., 31: 186-189.
PAPPANO, A.J. (1976) Action potentials in chick atria: Ontogenetic changes
in the dependence of tetrodotoxin-resistent action potentials on calcium,
strontium and barium. Circ. Res., 39(1): 99-105.
PARANCHYCH, W. (1966) Stages in phage R17 infection. Virology, 28: 90-99.
PCOC (1966) Pesticide chemical official compendium, Topeka, Kansas,
Association of the American Pesticide Control Officials, Inc., p. 95.
PENDERGRASS, E.P. & GREENING, R.R. (1953) Baritosis: report of a case.
Arch. ind. Hyg. occup. Med., 7: 44-48.
PENTO, J.T. (1979) The influence of barium on calcitonin secretion in the
pig. Pharmacol. Res. Commun., 11: 221-226.
PERRY, H.M., Jr & YUNICE, A. (1965) Acute pressure effects of intraarterial
cadmium and mercuric ions in anesthetized rats. Proc. Soc. Exp. Biol. Med.,
120: 805-808.
PERRY, H.M., Jr., TIPTON, I.H., SCHROEDER, H.A., & COOK, M.J. (1962)
Variability in the metal content of human organs. J. lab. clin. Med.,
60: 245-253.
PERRY, H.M., SCHOEPFLE, E., & BOURGOIGNIE, J. (1967) In vitro production and
inhibition of aortic vasoconstriction by mercuric, cadmium, and other metal
ions. Proc. Soc. Exp. Biol. Med., 124: 485-490.
PERRY, H.M., KOPP, S.Y., ERLANGER, M.W., & PERRY, E.F. (1983) Cardiovascular
effects of chronic barium ingestion. In: Hemphill, D.D., ed. Trace
substances in environmental health, Columbia, Missouri, University of
Missouri, pp. 155-164.
PERRY, H.M., PERRY, E.F., ERLANGER, M.W., & KOPP, S.J. (1985) Barium induced
hypertension. In: Calabrese, E., ed. Inorganics in drinking water and
cardiovascular disease, Princeton, New Jersey, Princeton Publishing Co.,
Chapter 20, pp. 221-229.
PETERSON, D.T. & INDIG, M. (1960) The barium-barium hydride phase system.
J. Am. Chem. Soc., 82: 5645-5646.
PEYTON, J.C. & BOROWITZ, J.L. (1978) Effects of Ba2+ and Cd2+ on convulsive
electroshock sensitivity and 45Ca distribution in brain subcellular fractions
in mice. Toxicol. appl. Pharmacol., 45: 95-103.
PHELAN, D.M., HAGLEY, S.R., & GUERIN, M.D. (1984) Is hypokalaemia the cause
of paralysis in barium poisoning? Br. med. J., 289: 882.
PIERCE, F.D. & BROWN, H.R. (1977) A semi-automated technique for the
separation and determination of barium and strontium in surface waters by
ion exchange chromatography and atomic emission spectrometry. Anal. Lett.,
10: 685-699.
PIERSON, W.R., TRUEX, T.J., MCKEE, D.E., SHELEF, M., & BAKER, R.E. (1981)
Effects of barium fuel additive and fuel sulfur level on diesel exhaust.
Environ. Sci. Technol., 14(9): 1121-1124.
POPOVA, O.Y.A. & PERETOLCYINA, N.M. (1976) Embryotropic effect of barium
fluoride. Gig. i Sanit., 41: 109-111.
PRONIN, D.A. & PASHKOVSKII, V.G. (1973) Change of the electrical activity of
the heart of workers exposed to barium salts. Gig. Tr. prof. Zabol.,
17: 36-37.
QUAGLIANO, J.V. (1959) Chemistry, Englewood, New Jersey, Prentice Hall, Inc.
RAE, T. (1977) Tolerance of mouse macrophages in vitro to barium sulfate used
in orthopedic bone cement. J. biomed. Mater. Res., 11: 839-846.
RASTORFER, J.R. (1974) Element contents of three Alaskan-Arctic mosses.
Ohio J. Sci., 74: 55-59.
REEVES, A.L. (1979) Barium (toxicity). In: Friberg, L., Nordberg, G.F., &
Velimir, B., ed. Handbook on the toxicology of metals, Amsterdam, Oxford,
New York, Elsevier Science Publishers, pp. 321-328.
REEVES, A.L. (1986) Barium. In: Friberg, L., Nordberg, G.F., & Velimir, B.,
ed. Handbook on the toxicology of metals - Volume II: Specific metals,
Amsterdam, Oxford, New York, Elsevier Science Publishers, pp. 84-93.
REISNER, A.H., BUCHOLTZ, C., & CHANDLER, B.S. (1975) Studies on the
polyribosomes of paramecium. Exp. cell Res., 93: 1-14.
REZINK, R.B. & TOY, P.A. (1978) Source assessment: Major barium compounds,
Dayton, Ohio, Monsanto Research Corporation (NTIS PB-280756).
RIDGEWAY, L.P. & KARNOFSKY, D.A. (1952) The effects of metals on the chick
embryo: Toxicity and production of abnormalities in development. Ann. NY
Acad. Sci., 55: 203-215.
ROBINSON, W.O., WHETSTONE, R.R., & EDGINGTON, G. (1950) The occurrence of
barium in soils and plants. US Dept. Agric. tech. Bull, 1013: 1-36.
RODE, L.J. & FOSTER, J.W. (1966) Influence of exchangeable ions on
germinability of bacterial spores. J. Bacteriol., 91: 1582-1588.
ROUF, M.A. (1964) Spectrochemical analysis of inorganic elements in
bacteria. J. Bacteriol., 88: 1545-1549.
ROZA, O. & BERMAN, L.B. (1971) The pathophysiology of barium: Hypo-kalemic
and cardiovascular effects. J. Pharmacol. exp. Ther., 177: 433-439.
RTECS (1985) Registry of toxic effects of chemical substances. 1983-1984
Cumulative supplement to the 1981-82 edition, Cincinnati, Ohio, National
Institute for Occupational Safety and Health (NIOSH Publication No. 86-103).
RUBIN, R.P. (1970) The role of calcium in the release of neurotransmitter
substances and hormones. Pharmacol. Rev., 22: 389-428.
SCHOFIELD, J.G. & COLE, E.N. (1971) Behaviour of systems releasing growth
hormones in vitro. In: Memoirs of the Society for Endocrinology,
pp. 185-201.
SCHROEDER, H.A. (1970) Barium, Washington, DC, American Petroleum Institute
(Air Quality Monograph No. 70-12).
SCHROEDER, H.A. & KRAEMER, L.A. (1974) Cardiovascular mortality, municipal
water and corrosion. Arch. environ. Health, 28: 303-311.
SCHROEDER, H.A. & MITCHENER, M. (1975a) Life-term studies in rats: Effects
of aluminum, barium, beryllium and tungsten. J. Nutr., 105: 421-427.
SCHROEDER, H.A. & MITCHENER, M. (1975b) Life-term effects of mercury,
methyl mercury and nine other trace metals on mice. J. Nutr., 105: 452-458.
SCHROEDER, H.A., TIPTON, I.H., & NASON, A.P. (1972) Trace metals in man:
strontium and barium. J. chron. Dis., 25: 491-517.
SEATON, A., RUCKELY, V.A., ADDISON, J., & BROWN, W.R. (1986) Silicons in
barium miners. Thorax, 41(8): 591-595.
SHANBAKY, I.O., BOROWITZ, J.L., & KESSLER, W.V. (1978) Mechanism of cadmium-
and barium-induced adrenal catecholamine release. Toxicol. appl. Pharmacol.,
44: 99-105.
SHANKLE, R. & KEANE, J.R. (1988) Acute paralysis from inhaled barium
carbonate Arch. Neurol., 45: 579-580.
SHINE, K.I., DOUGLAS, A.M., & RICCHIUTI, N.V. (1978) Calcium, strontium and
barium movements during ischemia and reperfusion in rabbit ventricle. Circ.
Res., 43: 712-720.
SHREVE, N.R. (1967) Chemical process in industries, 3rd ed., New York,
McGraw-Hill, pp. 357-358, 437-444.
SILAYEV, A.A. & TARASENKO, N.Y. (1976) The effect of barium on the generative
function and its hygienic significance. Gig. Tr. prof., Zabol., 7: 33-
37.
SILINSKY, E.M. (1978) On the role of barium in supporting the asynchronous
release of acetylcholine quanta by motor nerve impulses. J. Physiol., 274:
157-171.
SILLEN, L.G. & MARTELL, A.E. (1964) Stability constants of metalion
complexes, London, Chemical Society, p. 754 (Special Publication No. 17).
SIROVER, M.A. & LOEB, L.A. (1976a) Metal activation of DNA synthesis.
Biochem. Biophys. Res. Commun., 70: 812-817.
SIROVER, M.A. & LOEB, L.A. (1976b) Infidelity of DNA synthesis in vitro:
Screening for potential metal mutagens or carcinogens. Science, 194: 1434-
1436.
SLATER, C.S., HOLMES, R.S., & BYERS, H.G. (1937) Trace elements in the
soils from the erosion experiment stations, with supplementary data on
other soils. US Dept. Agric. tech. Bull., 522: 23.
SLAVICEK, J. (1972) Effect of Ba2+ on contractibility of the isolated right
rat ventricle. Substitution of NaCl for choline of hypertonic sucrose.
Physiol. Bohemoslov., 21: 189-199.
SLAVIN, W. (1984) Graphite furnace AAS - A source book, Norwalk,
Connecticut, Perkin-Elmer Corporation.
SMITH, K.A. (1971a) The comparative uptake and translocation by plants of
calcium, strontium, barium and radium. I. Bertholletia excelsa (Brazil nut
tree). Plant Soil, 34: 369-379.
SMITH, K.A. (1971b) The comparative uptake and translocation by plants of
calcium, strontium, barium and radium. II. Triticum vulgare (wheat). Plant
Soil, 34: 643-651.
SMITH, R.P. & GOSSELIN, R.E. (1976) Current concepts about the treatment of
selected poisonings. Nitrite, cyanide, sulfide, barium, and quinide. Annu.
Rev. Pharmacol. Toxicol., 16: 189-199.
SOLLMAN, T.A. (1953) Manual of pharmacology, Philadelphia, Pennsylvania,
W.B. Saunders Co.
SOWDEN, E.M. & PIRIE, A. (1958) Barium and strontium concentrations in eye
tissue. Biochem. J., 70: 716-717.
SOWDEN, E.M. & STITCH, S.R. (1957) Trace elements in human tissue. II.
Estimation of the concentration of stable strontium and barium in human
bone. Biochem. J., 67: 104-109.
SPRITZER, A.A. & WATSON, J.A. (1964) The measurement of ciliary clearance in
the lungs of rats. Health Phys., 10: 1093-1097.
STANLEY, R.A. (1974) Toxicity of heavy metals and salts to Eurassian
watermilfoil (Myriophyllum spicatum L.). Arch. environ. Contam. Toxicol.,
2: 331-341.
STARY, J., KRATZER, K., & PRASILOVA, J. (1984) The accumulation of radium,
barium and lead in algae. J. radioanal. nucl. Chem., 84: 17-21.
STOCKHAM, J.D. (1971) The composition of glass furnace emissions. J. Air
Pollut. Control. Assoc., 21(11): 713-715.
STOKINGER, H.E. (1981) Chapter 29: The metals. In: Patty's industrial
hygiene and toxicology, 3rd ed., New York, John Wiley and Sons,
Vol. 2A, pp. 1493-2060.
SUBRAMANIAN, K.S. & MERANGER, J.C. (1984) A survey for sodium, potassium,
barium, arsenic, and selenium in Canadian drinking water supplies.
At. Spectrosc., 5: 34-37.
SYED, I.B. & HOSAIN, F. (1972) Determination of LD50 of barium chloride and
allied agents. Toxicol. appl. Pharmacol., 25: 150-152.
TABOR, E.C. & WARREN, W.V. (1958) Distribution of certain metals in the
atmosphere of some American cities. Arch. ind. Health, 17: 145-151.
TANDON, S.P. & MISHRA, M.M. (1968) Activity of nitrifying bacteria in clay-
mineral media. Allahabad, India, University of Allahabad, pp. 1-6
(University of Allahabad Studies, Chemistry Section).
TARASENKO, N.Y., PRONIN, O.A., & SILAYEV, A.A. (1977) Barium compounds as
industrial poisons (an experimental study). J. Hyg. Epidemiol. Microbiol.
Immunol., 21: 361-373.
TARDIFF, R.G., ROBINSON, M., & ULMER, N.S. (1980) Subchronic oral toxicity
of BaCl2 in rats. J. environ. Pathol. Toxicol., 4: 267-275.
TAYLOR, D.M., BLIGH, P.H., & DUGGAN, M.H. (1962) The absorption of calcium,
strontium, barium and radium from the gastrointestinal tract of the rat.
Biochem. J., 83: 25-29.
TAYLOR, N.W. & ORTON, W.L. (1973) Effect of alkaline earth metal salts on
flocculence in S. cerevisiae. J. Inst. Brew. (Lond.), 79: 294-297.
THOMAS, R.G., EWING, W.C., CATRON, D.L., & MCCLELLAN, R.O. (1973) In vivo
solubility of four forms of barium determined by scanning techniques. Am.
Ind. Hyg. Assoc. J., 34: 350-359.
TIPTON, I.H. & COOK, M.J. (1963) Trace elements in human tissue. Part II.
Adult subjects from the United States. Health Phys., 9: 103-145.
TIPTON, I.H., COOK, M.J., STEINER, R.L., BOYE, C.A., PERRY, H.M., Jr, &
SCHROEDER, H.A. (1963) Trace elements in human tissue. Part I. Methods.
Health Phys., 9: 89-101.
TIPTON, I.H., SCHROEDER, H.A., PERRY, H.M., Jr, & COOK, M.J. (1965) Trace
elements in human tissue. Part III. Subjects from Africa, the Near and Far
East and Europe. Health Phys., 11: 403-451.
TIPTON, I.H., STEWART, P.L., & MARTIN, P.G. (1966) Trace elements in diets
nd excreta. Health Phys., 12: 1683-1689.
TIPTON, I.H., STEWART, P.L., & DICKSON, J. (1969) Patterns of elemental
excretion in long term balance studies. Health Phys., 16: 455-462.
TOGATZ, M.E. & TOBIA, M. (1978) Effect of barite (BaSO4) on development of
estuarine communities. Estuarine coastal mar. Sci. 7: 401-407.
TOISTER, Z. & LOYTER, A. (1970) Virus-induced fusion of chicken erythrocytes.
Biochem. biophys. Res. Commun., 41: 1523-1530.
TSAI, F., BUCHANAN, E.B., Jr, & DRAKE, L. (1978) The analysis of sediments
from the Iowa River. Sci. total Environ., 9: 277-285.
TUREKIAN, K.K. (1965) Barium in ocean water profiles. Trans. Am. Geophys.
Union, 46: 168.
UNDERWOOD, E.J. (1977) Trace elements in human and animal nutrition, New
York, Academic Press.
US BUREAU OF MINES (1976) Minerals yearbook, Washington, DC, US Bureau of
Mines.
US EPA (1974) Methods for chemical analysis of water and wastes, Cincinnati,
Ohio, US Environmental Protection Agency, Environmental Monitoring and
Support Laboratory, Environmental Research Center (EPA 625/6-74-003a).
US EPA (1976) Quality criteria for water, Washington, DC, US Environmental
Protection Agency (EPA 440/9-76-023).
US EPA (1979a) Methods for chemical analysis of water and wastes,
Cincinnati, Ohio, US Environmental Protection Agency, Environmental
Monitoring and Support Laboratory, Office of Research and Development
(EPA 600/4-79-020).
US EPA (1979b) Health consequences of sulfur oxides: A report from CHESS,
1970, 1971, Research Triangle Park, North Carolina, US Environmental
Protection Agency, Environmental Research Center.
US EPA (1984) Health effects assessment for barium, Cincinnati, Ohio, US
Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office (Prepared for the
Office of Emergency and Remedial Responsible, Washington, DC)
(EPA 540/1-86-021).
US EPA (1985) Integrated risk information system (IRIS). Reference dose
(RFD) for oral exposure for barium. Online, Cincinnati, Ohio, US
Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office.
VAGT, G.O. (1985) Barite and celesite. In: Canadian minerals yearbook, 1985:
Review and outlook, Ottawa, Mineral Resources Branch, Department of Energy,
Mines and Resources Canada, pp. 10.1-10.4 (Mineral Report No. 34).
VENUGOPAL, B. & LUCKEY, T.D. (1978) Metal toxicity in mammals: Chemical
toxicity of metals and metalloids, New York, Plenum Press.
VOSS, R.L. & NICOL, H. (1960) Metallic trace elements in tobacco. Lancet,
II: 435-436.
WALLACH, J. (1978) Interpretation of diagnostic tests - A handbook synopsis
of laboratory medicines, 3rd ed., Boston, Massachusetts, Little,
Brown and Co.
WANG, W. (1986) The effect of river water on phytotoxicity of Ba, Cd and Cr.
Environ. Pollut., 11: 193-204.
WANG, P.Y., HAN, J.C., CHANG, P.C., & HAN, Y.M. (1989) Occupational
endermatic intoxication of barium - 2 case report. Chim. J. ind. Hyg. occup.
Dis., 7: 86-87.
WATERHOUSE, D.F. (1951) Occurrence of barium and strontium in insects. Aust.
J. sci. Res., B4: 144-162.
WELLS, R.C. (1937) Analyses of rocks and minerals from the laboratory of the
United States Geological Survey, 1914-1936. US geol. Surv. Bull., 878: 134.
WINDHOLZ, M., ed. (1983) The Merck index, 10th ed., Rahway, New Jersey,
Merck and Co., Inc.
WOLGEMUTH, K. & BROECKER, W.S. (1970) Barium in sea water. Earth planet.
Sci. Lett., 8: 372-378.
WONES, R.G., STADLER, B.L., & FROHMAN, L.A. (1990) Lack of effect of
drinking water barium on cardiovascular risk factors. Environ. Health
Perspect., 85: 1-13.
YARBROUGH, J.D. & O'KELLEY, J.C. (1962) Alkaline earth elements and the
avoidance reaction in Paramecium multimicronucleatum. J. Protozool.,
9: 132-135.
YOSHIYUKI, T. & YOSHIMASHA, T. (1975) Enhancement of µ-amylase production.
Japan. Kokai, 160: 477.
ZDANOWICZ, J.A., FEATHERSTONE, J.D.B., EPSELAND, M.A., & CURZON, M.E.J.
(1987) Inhibitory effect of barium on human dental caries prevalence.
Community dent. oral Epidemiol., 15: 6-9.
RESUME ET CONCLUSIONS
1. Résumé
1.1 Identité, état naturel et méthodes d'analyse
Le baryum est un métal alcalino-terreux, de masse
atomique relative 137,34 et de numéro atomique 56. Il
existe sous la forme de sept isotopes stables présents
dans la nature dont le 138Ba est le plus abondant. Le
baryum est un métal mou, blanc jaunâtre, fortement
électro-positif. Il se combine à l'ammoniac, à l'eau, à
l'oxygène, à l'hydrogène, aux halogènes et au soufre en
libérant de l'énergie. Il réagit énergiquement avec
d'autres métaux pour former des alliages. Dans la nature,
on ne le rencontre qu'à l'état combiné, le principal miné-
ral étant la barytine (sulfate de baryum) et la witherite
(carbonate de baryum). Le baryum est également présent en
petites quantités dans les roches ignées et dans le felds-
path et les micas. Il peut également se trouver à l'état
naturel dans les combustibles fossiles ainsi que dans
l'air, l'eau et le sol.
Certains dérivés du baryum comme l'acétate, le nitrate
et le chlorure sont relativement solubles dans l'eau alors
que les autres sels tels que le fluorure, le carbonate,
l'oxalate, le chromate, le phosphate et le sulfate le sont
très peu. A l'exception du sulfate de baryum, la solu-
bilité dans l'eau des sels de baryum augmente à mesure que
le pH diminue.
Le prélèvement d'échantillons aqueux ou gazeux pour le
dosage du baryum s'effectue de la même manière que pour
n'importe quelle autre substance. Les échantillons de
sédiments, de boue ou de terre sont séchés au four ou
frittés. On procède ensuite à une extraction avec de
l'acide chlorhydrique à 1% pour la détermination des
éléments en traces et notamment du baryum. Dans le cas des
échantillons biologiques, on procède à une congélation ou
à une lyophilisation puis on les prépare pour le dosage du
baryum par des techniques d'entraînement à sec.
Les méthodes d'analyse les plus fréquemment utilisées
sont l'absorption atomique et la spectrométrie d'émission
de flamme ou plasma. On a également recours à l'activation
neutronique, à la spectrométrie de masse avec dilution
isotopique et à la fluorescence X.
1.2 Production, usage et sources d'exposition
La barytine est le minerai dont proviennent presque
tous les autres composés du baryum. La production mondiale
de barytine était évaluée à 5,7 millions de tonnes en
1985. On utilise le baryum et ses dérivés dans divers
produits industriels qui vont des céramiques aux lubri-
fiants. Ils entrent également dans la fabrication
d'alliages et peuvent servir de charges pour le papier, le
savon, le caoutchouc, le linoléum. Ils servent aussi à la
fabrication de vannes et à l'extinction des feux de
radium, d'uranium et de plutonium.
Le baryum résultant d'activités humaines est essen-
tiellement d'origine industrielle. Il peut être émis dans
l'environnement à la suite d'activités minières, de raf-
finage ou de traitement de minerais ou de la fabrication
de produits qui en contiennent. Lors de diverses opéra-
tions métallurgiques et industrielles, du baryum peut
également être rejeté dans les eaux résiduaires. Il peut
se déposer sur le sol, par suite de diverses activités
humaines, notamment lors du rejet de cendres volantes et
de l'enfouissement de boues primaires et secondaires. On
estime qu'en 1976, l'extraction et le traitement de la
barytine aux Etats-Unis d'Amérique a entraîné le rejet
d'environ 3200 tonnes de matières particulaires dans
l'atmosphère, les poussières produites par l'utilisation
de barytine lors des forages pétroliers et dans l'indus-
trie pétrolière en représentant environ 100 tonnes. En
1972, on estime que l'industrie du baryum a rejeté aux
Etats-Unis d'Amérique environ 1200 tonnes de matières
particulaires dans l'atmosphère.
Dans l'environnement, le baryum est transporté par
l'intermédiaire de l'air, de l'eau et du sol. Dans
l'atmosphère, il est présent sous forme de particules dont
le transport dépend des conditions atmosphériques et
météorologiques. Dans l'eau, ce transport est conditionné
par les interactions avec d'autres ions, notamment les
ions sulfate, qui régulent et limitent la concentration du
baryum. On connaît mal les transformations subies par le
baryum ainsi que son transport en milieu aqueux.
L'exposition au baryum peut s'effectuer par l'inter-
médiaire de l'air, de l'eau ou des aliments. On n'est pas
très bien renseigné sur les teneurs de l'air en baryum.
Aux Etats-Unis d'Amérique, la concentration habituelle est
estimée à 0,05 µg/m3 au plus. On n'a pas constaté de
corrélation nette entre la teneur de l'air ambiant en
baryum et le degré d'industrialisation, encore que les
concentrations soient plus élevées aux alentours des
usines métallurgiques.
La présence de baryum dans l'eau de mer, l'eau des
rivières et l'eau des puits est attestée et on en trouve
également dans les sédiments et les eaux naturelles en
contact avec des roches sédimentaires. Le baryum est
présent dans presque toutes les eaux superficielles à des
concentrations allant jusqu'à 15 000 µg/litre et il con-
tribue à la dureté de l'eau. Dans l'eau des puits, la con-
centration du baryum dépend de la teneur des roches
environnantes en baryum lessivable. L'eau de boisson en
contient de 10 à 1000 µg/litre encore que dans certaines
régions des Etats-Unis d'Amérique ces concentrations
puissent dépasser 10 000 µg/litre. La qualité de l'eau
distribuée par les municipalités dépend de celle des eaux
de surface et des eaux souterraines et sa teneur en baryum
varie dans de larges proportions selon la dureté de l'eau.
Des teneurs allant de 1 à 20 µg/litre ont été observées
dans l'eau de boisson aux Etats-Unis. Si l'on s'en tient
à ces chiffres et pour une consommation de l'ordre de
2 litres par jour, on obtient un apport quotidien de 2 à
40 µg de baryum.
Selon un certain nombre d'études, l'apport quotidien
d'origine alimentaire se situe entre 300 et 1770 µg avec
d'importantes variations. Il est rare que l'homme consomme
des plantes contenant du baryum en quantité importante ou
du moins la partie de la plante où le baryum s'accumule.
Le noisetier du Brésil constitue une exception, puisque
les concentrations observées vont de 1500 à 3000 µg/g.
Les tomates et le soja concentrent également le baryum
présent dans le sol, le facteur de bio-concentration
allant de 2 à 20.
En général le baryum ne s'accumule pas dans les
plantes ordinaires en quantité suffisante pour intoxiquer
les animaux. Toutefois, on a évoqué la possibilité que
les grandes quantités de baryum (jusqu'à 1260 µg/kg) qui
s'accumulent dans les légumes, la luzerne et le soja
puissent être nocives pour les bovins domestiques.
La teneur en baryum des feuilles de tabac désséchées
est de 105 µg/kg en moyenne, la majeure partie restant
dans les cendres pendant la combustion. Il n'existe pas de
documentation sur la concentration du baryum dans la fumée
de tabac.
Les retombées radioactives constituent une autre
source d'exposition au baryum. Toutefois, grâce à l'inter-
diction des essais nucléaires dans l'atmosphère, la quan-
tité de baryum radioactif présent dans l'environnement a
diminué.
1.3 Cinétique et surveillance biologique
Un individu moyen (70 kg) renferme environ 22 mg de
baryum dans son organisme, qui est en majeure partie
(91%) concentré dans les os. On en trouve des traces dans
divers tissus ou organes tels que l'aorte, le cerveau, le
coeur, le rein, la rate, le pancréas et le poumon. Chez
l'homme, la teneur totale en baryum tend à augmenter avec
l'âge. Les concentrations dépendent de la zone géogra-
phique de résidence des individus. On a trouvé du baryum
dans tous les échantillons de tissus provenant d'enfants
morts-nés, ce qui donne à penser que cet élément est
capable de traverser la barrière placentaire.
Il est difficile d'évaluer l'absorption du baryum
après ingestion car elle dépend d'un certain nombre de
facteurs. Par exemple, la présence de sulfate dans la
nourriture provoque la précipitation du sulfate de baryum.
L'expérimentation animale ainsi qu'un certain nombre de
données limitées concernant l'homme montrent que le baryum
soluble est absorbé au niveau intestinal dans une pro-
portion inférieure à 10% chez l'adulte mais qui peut être
supérieure chez les jeunes. Le baryum est rapidement fixé
par les glandes salivaires et surrénales, le coeur, les
reins, les muqueuses et les vaisseaux sanguins et il finit
par aboutir au squelette. En effet, à l'instar du calcium,
le baryum s'accumule dans les os. Il se dépose de préfé-
rence dans les zones les plus actives de croissance
osseuse, principalement à la surface du périoste. L'âge
et la privation de nourriture sont également des facteurs
importants qui influent sur l'absorption et le dépôt du
baryum. Ainsi les rats âgés absorbent moins cet élément
et présentent des concentrations osseuses inférieures. Le
jeûne augmente en revanche l'absorption du baryum.
Après inhalation, le baryum peut être absorbé au
niveau des poumons ou passer directement dans le courant
sanguin en traversant la muqueuse nasale. Chez le rat,
l'exposition entraîne un dépôt au niveau des os mais
lorsqu'elle se poursuit, le dépôt diminue tant au niveau
des os qu'au niveau des poumons. Les dérivés insolubles
comme le sulfate de baryum s'accumulent dans les poumons
et sont lentement éliminés par l'ascenseur muco-ciliaire.
Le baryum est éliminé dans les urines et les matières
fécales, dans des proportions qui dépendent de la voie
d'administration. Après injection de baryum à des êtres
humains, on a constaté qu'en 24 heures, le baryum était
éliminé à raison d'environ 20% dans les matières fécales
et d'environ 5% dans les urines. Le baryum plasmatique
est presque entièrement éliminé du courant sanguin en
24 heures. Chez l'homme et l'animal, l'élimination du
baryum après ingestion s'effectue plutôt dans les matières
fécales que dans les urines. Après inhalation, le baryum
est lentement éliminé des os et par voie de conséquence de
l'organisme entier. On estime que la demi-vie biologique
du baryum est de 90 à 120 jours chez le rat. Pour assurer
une surveillance biologique satisfaisante de l'exposition
humaine, il conviendrait de contrôler l'élimination du
baryum dans les urines et les matières fécales.
1.4 Effets sur les animaux d'expérience
Chez le rat, on a obtenu des DL50 de 118, 250 et 355
respectivement pour le chlorure, le fluorure et le nitrate
de baryum. Les effets aigus d'une ingestion de baryum con-
sistent notamment en une salivation, des nausées, de la
diarrhée, de la tachycardie, une hypokaliémie, des fibril-
lations musculaires, une paralysie flasque des muscles
squelettiques, une paralysie des muscles respiratoires et
une fibrillation ventriculaire. La paralysie des muscles
respiratoires et la fibrillation ventriculaire peuvent
entraîner la mort. Diverses études ont montré que le
baryum perturbait l'action du centre électrogénique de
l'automatisme cardiaque. En injectant du baryum par voie
intraveineuse à des chiens anesthésiés, on a constaté que
ses effets aigus étaient dus à une hypokaliémie importante
d'instauration rapide qui pouvait être évitée ou abolie
par administration de potassium.
Le baryum provoque une légère irritation cutanée et
une forte irritation oculaire chez le lapin.
Des rats qui avaient bu de l'eau du robinet contenant
jusqu'à 250 mg de baryum par litre pendant 13 semaines
n'ont présenté aucun signe d'intoxication, encore que chez
certains groupes on ait noté une réduction du poids
relatif des surrénales.
Des rats ayant reçu 10 ou 100 mg de baryum dans leur
eau de boisson pendant 16 mois ont présenté une hyperten-
sion, mais la tension artérielle n'était pas modifiée à la
concentration de 1 mg/litre. L'analyse de la fonction du
myocarde au bout de 16 mois à la dose la plus élevée (100
mg de baryum par litre), a révélé que la contractilité et
l'excitabilité cardiaque étaient sensiblement modifiées,
qu'il y avait des perturbations dans le métabolisme du
myocarde et que le système cardio-vasculaire présentait
une hypersensibilité au pentobarbital sodique.
Administré à des rats par voie orale ou par inha-
lation, le carbonate de baryum a excercé des effets nocifs
sur leur fonction de reproduction. En outre, on notait un
taux de mortalité plus élevé chez les ratons nouveau-nés
issus de femelles traitées par du baryum. On possède des
preuves limitées d'un pouvoir tératogène du baryum mais
aucune donnée concluante quant à sa cancérogénicité.
Du fait de ses propriétés chimiques et physiologiques,
le baryum peut entrer en compétition avec le calcium et le
remplacer dans les processus où cet élément intervient
normalement, notamment la libération de catécholamines par
les surrénales et de neurotransmetteurs comme l'acéty-
choline et la noradrénaline.
On ne possède que peu d'informations sur les effets
immunologiques du baryum chez l'animal.
1.5 Effets sur l'être humain
On a signalé plusieurs cas d'intoxication consécutifs
à l'ingestion de dérivés du baryum. Des doses ne dépassant
pas de 0,2 à 0,5 mg de baryum par kg de poids corporel,
qui sont généralement consécutives à l'ingestion de
chlorure ou de carbonate de baryum, ont provoqué des
effets toxiques chez l'adulte. Le tableau clinique d'une
intoxication par le baryum se caractérise par une gastro-
entérite aiguë, la disparition des réflexes tendineux et
l'apparition d'une paralysie musculaire progressive. La
paralysie musculaire paraît liée à une hypokaliémie grave.
Dans la plupart des cas qui ont été signalés, on a
constaté une récupération rapide et sans complications
après traitement consistant dans la perfusion de sels de
potassium (carbonate ou lactate) et/ou l'administration
de sulfate de sodium par voie orale.
Des études épidémiologiques limitées ont été menées
pour étudier l'existence d'une relation éventuelle entre
la concentration du baryum dans l'eau de boisson et la
mortalité par maladies cardiovasculaires; toutefois les
résultats obtenus sont irréguliers, et ne permettent pas
de conclure.
Chez une population exposée à des fortes concen-
trations de baryum dans son eau de boisson, on n'a
constaté aucune augmentation de l'incidence de l'hyperten-
sion, des accidents vasculaires cérébraux ni des maladies
cardiaques ou rénales par rapport à un groupe analogue qui
était exposé à des concentrations plus faibles. Lors d'une
étude de courte durée sur des volontaires, la consommation
d'eau de boisson contenant du baryum n'a pas eu d'effets
sur la tension artérielle.
On a signalé une augmentation de l'incidence de
l'hypertension chez des travailleurs exposés au baryum par
rapport à des travailleurs non exposés. Des cas de
barytose ont été observés chez des individus exposés de
par leur profession à des composés du baryum. Dans un
groupe d'étude constitué de travailleurs exposés au baryum
et de personnes résidant à proximité d'une décharge où se
trouvaient des dérivés du baryum, on a constaté une
fréquence accrue de symptômes musculo-squelettiques,
d'interventions chirurgicales pour affection gastro-intes-
tinale, de problèmes dermatologiques et de symptômes
respiratoires.
On n'a pas constaté d'association concluante entre la
teneur de l'eau de boisson en baryum et l'incidence des
malformations congénitales. Il n'existe aucune preuve
d'une cancérogénicité du baryum.
1.6 Effets sur les êtres vivants dans leur milieu naturel
Le baryum influe directement sur les propriétés
physico-chimiques et sur l'infectiosité de plusieurs virus
ainsi que sur leur aptitude à se multiplier. Il perturbe
également le développement des spores bactériennes en
germination et il excerce un certain nombre d'effets sur
divers micro-organismes, notamment en inhibant les
processus cellulaires.
On connaît mal les effets que le baryum exerce sur les
organismes aquatiques. L'exposition de poissons pendant
30 jours à du baryum n'a eu aucun effet sur leur survie.
Toutefois, lors d'une étude de 21 jours, on a constaté,
chez des daphnies exposées à une dose de 5,8 mg de baryum
par litre, des perturbations de leur fonction de repro-
duction et une moindre croissance. Rien n'indique
cependant que la barytine soit toxique pour les animaux
marins. Toutefois l'exposition à de grandes quantités de
barytine pourrait avoir une influence néfaste sur les
colonies de benthos.
Les végétaux et les invertébrés marins pourraient
accumuler activement le baryum provenant de l'eau de mer.
2. Conclusions et recommandations
Aux concentrations où il se rencontre habituellement
dans l'environnement, le baryum ne présente pas de risque
important pour la population dans son ensemble. Toutefois,
pour certains sous-groupes et dans des conditions de forte
exposition, il faut prendre en compte la possibilité
d'effets nocifs sur la santé.
On possède peu de données qui permettraient d'évaluer
le risque que le baryum représente sur le plan écologique.
Toutefois en s'appuyant sur les données disponibles rela-
tives aux effets toxiques chez les daphnies, il semble que
le baryum constitue une menace pour certains organismes
aquatiques.
Il est nécessaire de procéder à des études épidémio-
logiques ainsi qu'à des recherches sur la biodisponibilité
du baryum et sur sa toxicité pour le système cardiovascu-
laire et le système immunitaire; il faudrait également
disposer de données complémentaires sur sa toxicité
chronique pour la vie aquatique. On aurait besoin de
données plus nombreuses sur l'exposition dans les
ambiances de travail et sur l'utilisation de marqueurs
biologiques afin de pouvoir prendre de meilleures mesures
de protection.
EVALUATION DES RISQUES POUR LA SANTE HUMAINE ET EFFETS SUR L'ENVIRONNEMENT
1. Evaluation des risques pour la santé humaine
1.1 Niveaux d'exposition
1.1.1 Population générale
D'après les données en provenance des Etats-Unis
d'Amérique, l'apport alimentaire de baryum varie de 300 à
1700 µg/jour. Les valeurs moyennes fournies par deux
sources différentes se situent respectivement à 600 et
900 µg/jour.
Des études récentes effectuées aux Etats-Unis
d'Amérique indiquent que l'eau de boisson a une teneur en
baryum qui varie de 1 à 20 µg/litre. Compte tenu de ces
valeurs et en supposant que la consommation quotidienne
d'eau de boisson soit de deux litres, l'apport de baryum
par cette voie serait de 2 à 40 µg/jour.
Par inhalation, l'apport est estimé à 0,04-3,1 µg/jour.
Au Pays de Galles (Royaume-Uni) on estime que l'apport
quotidien de baryum est de 1327 µg (aliments: 1240 µg;
eau de boisson: 86 µg; air: 1 µg).
1.1.2 Exposition respiratoire d'origine professionnelle
Chez des ouvriers métallurgistes exposés à des
concentrations allant de 0,08 à 1,92 mg/m3 (moyenne
1,07 mg/m3) de baryum, on a constaté une forte
prévalence de l'hypertension artérielle. Chez un groupe
d'ouvriers employés au traitement des minerais de baryum
et qui présentaient des symptômes musculo-squelettiques et
respiratoires, on a observé une exposition à des concen-
trations de 0,02 à 1,7 mg/m3. Chez des soudeurs à l'arc,
on a observé des expositions à des concentrations allant
de 2,6 à 6,1 mg/m3. Ce sont les expositions profession-
nelles les plus fortes qu'on ait signalées mais aucune
étude clinique n'a été effectuée.
1.1.3 Exposition aiguë
Des doses ne dépassant pas 0,2 à 0,5 g (3 à 7 mg/kg de
poids corporel), telles qu'elles résultent en général de
l'ingestion de chlorure ou de carbonate de baryum,
entraînent des effets toxiques chez l'adulte. En l'absence
de traitement, des doses de 3 à 5 g (40 à 70 mg/kg de
poids corporel) ont été mortelles.
1.2 Effets toxiques, relations dose-effet et dose-réponse
L'absorption du baryum dans les voies digestives
dépend en grande partie de l'âge et de la solubilité du
composé en cause. On pense que le baryum ingéré est
absorbé dans une proportion inférieure à 10% chez
l'adulte. Toutefois l'absorption peut être sensiblement
plus forte chez l'enfant. Après absorption, le baryum
pénètre dans le courant sanguin, se fixe dans divers
tissus mous et se dépose dans les os. Le métabolisme du
baryum est analogue à celui du calcium; toutefois, con-
trairement à ce dernier, on ne lui connaît aucun rôle
biologique. Le baryum peut remplacer le calcium dans de
nombreux processus physiologiques et il affecte l'activité
nerveuse et musculaire.
Le baryum peut provoquer une légère irritation cutanée
et une forte irritation oculaire. On a observé des effets
indésirables sur la santé chez des sujets sensibles
(malades sous diurétiques) après exposition à du baryum
consécutive à l'absorption d'un milieu de contraste baryté
en vue d'une radiographie. Plusieurs cas d'intoxication
par le baryum ont été signalés. Parmi les symptômes,
figurent une gastroentérite aiguë, la disparition des
réflexes tendineux et l'apparition d'une paralysie muscu-
laire progressive.
Il n'existe aucune preuve concluante que les dérivés
du baryum, à l'exception du chromate, soient cancérogènes
pour l'homme. Rien n'indique non plus avec certitude que
le baryum ait des effets tératogènes ou embryotoxiques ou
des effets nocifs sur la reproduction chez l'homme.
Des études épidémiologiques anciennes, de portée
limitée, et concernant les relations entre l'exposition à
de faibles teneurs en baryum et la morbidité et la
mortalité cardiovasculaires, n'ont pas donné de résultats
concluants. Une étude épidémiologique ultérieure n'a pas
permis non plus de conclure à un effet du baryum sur la
tension artérielle. Lors d'une étude de brève durée au
cours de laquelle des volontaires avaient consommé des
quantités de plus en plus fortes de baryum allant jusqu'à
10 mg/litre (dans leur eau de boisson), on n'a pas
constaté non plus d'effets sur la tension artérielle.
L'inhalation de dérivés du baryum sur les lieux de
travail a donné lieu à des cas de barytose. Chez les
travailleurs exposés à de fortes concentrations de baryum
dans l'atmosphère, on a constaté que l'hypertension
artérielle était plus fréquente que chez les ouvriers non
exposés. On a fait état, chez le rat exposé à des concen-
trations de baryum allant jusqu'à 100 mg/litre, d'une
augmentation de la pression artérielle systolique.
1.3 Evaluation du risque
Sur la base des publications existantes, on peut
conclure qu'aux concentrations où il est généralement
présent dans l'eau (spécialement l'eau de boisson), les
aliments et l'air ambiant, le baryum ne présente pas de
risque important pour la population dans son ensemble.
Toutefois dans certains sous-groupes particuliers (les
sujets âgés ou qui présentent un déficit de potassium) et
dans certaines circonstances particulières (eau fortement
chargée en baryum, exposition professionnelle, etc.), il
peut y avoir un risque d'effets nocifs sur la santé.
2. Evaluation des effets sur l'environnement
Le baryum est présent dans le sol à une concentration
moyenne de 500 µg/g. Dans les océans et les eaux douces,
on a mesuré des concentrations allant de 0,04 à 37 µg/litre
et de 7,0 à 15 000 µg/litre respectivement. Dans l'air,
la concentration du baryum est généralement < 0,05 µg/m3.
Les composés solubles peuvent être transportés dans
l'environnement et absorbés par les divers organismes. Le
baryum peut s'accumuler dans les différentes parties des
végétaux.
D'après certains rapports, le baryum inhiberait la
croissance et les processus cellulaires chez les micro-
organismes. On a également constaté qu'il perturbait la
germination des spores bactériennes.
On ne dispose pas de renseignements sur les effets
nocifs que le baryum exercerait sur les végétaux ou la
faune terrestres. Aucun effet toxique n'a été signalé sur
les végétaux aquatiques aux concentrations habituellement
rencontrées dans l'eau. Pour les poissons d'eau douce, les
valeurs de la CL50 vont de 46 à 78 mg/litre. On a
constaté que des concentrations de baryum égales à
5,8 mg/litre perturbaient la reproduction et la croissance
des daphnies.
On manque de données qui permettraient d'évaluer le
risque que le baryum constitue pour l'environnement. En se
fondant sur les données disponibles concernant les effets
toxiques pour les daphnies, il semble que le baryum re-
présente un risque pour certaines populations d'organismes
aquatiques.
RECOMMANDATIONS EN VUE D'ETUDES COMPLEMENTAIRES
Il est recommandé de procéder à des recherches
complémentaires sur le baryum, à propos de ses effets
écologiques et de ses effets sur la santé humaine, dans
les secteurs suivants:
* études de biodisponibilité, notamment des mécanismes
de solubilisation et de transport;
* études sur l'hypertension et les effets cardiovascu-
laires au niveau de la population dans son ensemble et
des travailleurs exposés de par leur profession; étude
des modes d'action;
* études épidémiologiques bien conçues;
* études sur les effets immunologiques du baryum chez
l'homme;
* études sur la toxicité sublétale à long terme chez les
organismes aquatiques;
* données de surveillance relatives à l'exposition
environnementale afin de recenser les secteurs où des
mesures de protection sont nécessaires;
* évaluation des indicateurs permettant la détection
précoce d'une forte exposition au baryum;
* études sur les marqueurs biologiques (teneur du sys-
tème pileux et des urines en baryum, taux plasmatique
de potassium).
RESUMEN Y CONCLUSIONES
1. Resumen
1.1 Identidad, aparición natural y métodos de análisis
El bario es un metal alcalinotérreo que tiene una masa
atómica relativa de 137,34 y un número atómico de 56.
Existen siete isótopos estables de aparición natural, de
los que el 138Ba es el más abundante. El bario es un
metal blando de color blanco amarillento fuertemente
electropositivo. Se combina con el amoniaco, el agua, el
oxígeno, el hidrógeno, los halógenos y el azufre, liber-
ando energía en esas reacciones. También reacciona fuerte-
mente con los metales para constituir aleaciones metáli-
cas. En la naturaleza, el bario aparece sólo en forma
combinada, siendo las principales formas minerales la
barita (sulfato de bario) y la witherita (carbonato de
bario). El bario se halla también en pequeñas cantidades
en las rocas ígneas y en el feldespato y las micas. Puede
encontrarse como componente natural de los combustibles
fósiles y se halla en el aire, el agua y el suelo.
Ciertos compuestos de bario, como el acetato, el
nitrato y el cloruro, son relativamente hidrosolubles,
mientras que las sales de fluoruro, carbonato, oxalato,
cromato, fosfato y sulfato presentan una solubilidad muy
baja. Con la excepción del sulfato de bario, la solubili-
dad en agua de las sales de bario aumenta al disminuir
el pH.
El muestreo del bario en los medios acuosos y gaseosos
se realiza del mismo modo que en el caso de cualquier otro
material. Las muestras de sedimentos, barro y tierra se
desecan en horno o se sinterizan. Después se extraen las
muestras con HCl al 1% para el análisis de los oligo-
elementos, incluido el bario. Las muestras biológicas se
congelan o liofilizan y se preparan para el análisis del
bario utilizando procedimientos de lavado en seco.
Los métodos de análisis empleados más corrientemente
son la absorción atómica y la espectrometría de llama y
emisión del plasma. También se utilizan la activación
neutrónica, la espectrometría de masa por dilución de
isótopos y la fluorescencia con rayos X.
1.2 Producción, utilizaciones y fuentes de exposición
El mineral barita es el material bruto del que se
extraen casi todos los demás compuestos de bario. La
producción mundial de barita se estimó en 1985 en 5,7
millones de toneladas. El bario y sus compuestos se
emplean en distintos productos industriales que comprenden
desde la cerámica hasta los lubricantes. Se utiliza en la
fabricación de aleaciones, como cargador para papel,
jabón, caucho y linóleo, en la fabricación de válvulas y
como extintor en los incendios provocados por radio,
uranio y plutonio.
Las fuentes antropogénicas de bario son fundamental-
mente industriales. Las emisiones pueden deberse a la
minería, el refino o el tratamiento de minerales de bario
y a la fabricación de productos de bario. El bario aparece
también en las aguas residuales procedentes de la metalur-
gia y de otras industrias. La deposición en el suelo puede
deberse a las actividades humanas, que comprenden la
eliminación de cenizas y el empleo de fangos primarios y
secundarios en el relleno de tierras. Se ha calculado que
en 1976, la minería y el tratamiento del mineral barita en
los Estados Unidos de América liberaron unas 3200 tone-
ladas de partículas en el aire y que los polvos fugitivos
procedentes del uso de barita en la perforación petro-
lífera y en industrias conexas representaron alrededor de
100 toneladas de partículas. En 1972, en los Estados
Unidos de América, la industria química del bario despren-
dió alrededor de 1200 toneladas de partículas en la
atmósfera.
El transporte ambiental del bario se produce por el
aire, el agua y el suelo. El bario atmosférico consiste en
partículas cuyo transporte está regulado por las condi-
ciones atmosféricas y meteorológicas normales. El trans-
porte del bario por el agua está sometido a la interacción
con otros iones, en particular el sulfato, que regula y
limita la concentración de bario. Se dispone de escasa
información acerca de las transformaciones y el transporte
de bario por el agua.
La exposición al bario puede producirse por el aire,
el agua o los alimentos. No se poseen datos suficientes
sobre las concentraciones de bario en el aire. En los
Estados Unidos de América se ha calculado que la concen-
tración habitual es de 0,05 µg/m3 o menos. No se ha
observado una correlación neta entre las concentraciones
ambientales de bario en el aire y la amplitud de la indus-
trialización, aunque pueden producirse mayores concen-
traciones alrededor de las fundiciones.
Se ha probado la presencia de bario en el agua de
mares, ríos y manantiales, y se ha hallado también en
sedimentos y aguas naturales en contacto con rocas sedi-
mentarias. El bario se encuentra en casi todas la aguas
superficiales en concentraciones de hasta 15 000 µg/litro
y contribuye a la dureza del agua. La concentración del
bario en el agua de manantial depende del contenido de
bario lixiviable de las rocas. El agua potable contiene
10-1000 µg/litro, aunque se ha observado que el agua de
ciertas regiones de los Estados Unidos de América presenta
concentraciones superiores a 10 000 µg/litro. Los sumini-
stros municipales de agua dependen de la calidad de las
aguas de superficie y freáticas y, en función de la
dureza, contienen una amplia gama de concentraciones de
bario. Los estudios efectuados en los Estados Unidos de
América muestran que las concentraciones en el agua
potable varían entre 1 y 20 µg/litro. Basándose en esos
datos y suponiendo un consumo de 2 litros por día, la
ingesta diaria sería de 2-40 µg de bario.
En varios estudios se ha calculado una ingesta alimen-
taria diaria de 300 a 1770 µg, con amplias variaciones.
Las personas rara vez comen plantas en las que se halle
el bario en concentraciones notables o partes de la planta
en las que se acumule el bario. El nogal del Brasil es
una excepción, pues se han hallado concentraciones de
1500-3000 µg/g. También se sabe que los tomates y las
habas de soja concentran el bario del suelo, con un factor
de bioconcentración comprendido entre 2 y 20.
Por lo general, el bario no se acumula en las plantas
corrientes en cantidades suficientes para que sea tóxico
para los animales. Sin embargo, se ha señalado que las
altas cantidades de bario (hasta 1260 mg/kg) acumuladas en
las verduras, el alfalfa y las habas de soja pueden produ-
cir problemas en el ganado bovino.
El contenido de bario de las hojas de tabaco secas
alcanza un promedio de 105 mg/kg y es probable que la
mayor parte permanezca en la ceniza en el curso de la
combustión. No se han señalado las concentraciones de
bario en el humo del tabaco.
Otra fuente de exposición al bario es la lluvia radi-
activa. Sin embargo, la adopción de tratados que prohíben
las pruebas en la atmósfera ha reducido la cantidad de
bario radiactivo presente en el medio.
1.3 Cinética y vigilancia biológica
La persona media (70 kg) contiene unos 22 mg de bario,
hallándose la mayor parte (91%) en el esqueleto. Se
encuentran cantidades infinitesimales en varios órganos
como la aorta, el cerebro, el corazón, los riñones, el
bazo, el páncreas y los pulmones. El bario total del
organismo humano tiende a aumentar con la edad. Las
concentraciones observadas en el organismo dependen de la
situación geográfica del individuo. También se ha encon-
trado bario en todas las muestras de recién nacidos, lo
que permite pensar que atraviesa la placenta.
Es difícil evaluar la captación del bario ingerido
porque distintos factores influyen en la absorción. Por
ejemplo, la presencia de sulfato en los alimentos se debe
a la precipitación del sulfato de bario. Los estudios
efectuados en animales de experimentación y los limitados
datos obtenidos en personas muestran que el bario soluble
se absorbe por el intestino hasta el < 10% en los adultos,
pero más en los jóvenes. La captación se produce rápida-
mente en las glándulas salivales y suprarrenales, el
corazón, los riñones, las mucosas y los vasos sanguíneos
y, por último, el esqueleto. Igual que el calcio, el bario
se acumula en los huesos. Se deposita de preferencia en
las zonas más activas del crecimiento óseo, y sobre todo
en las superficies periósticas. Entre otros factores
importantes en la absorción y la deposición figuran la
edad y las restricciones alimentarias. Las ratas de edad
avanzada presentan una disminución de la absorción y de
las concentraciones óseas de bario. El ayuno desencadena
un aumento de la absorción de bario.
El bario inhalado puede absorberse por el el pulmón o
directamente por la mucosa nasal pasando a la corriente
sanguínea. En las ratas, la exposición da lugar a la
deposición en los huesos, pero la exposición continua
origina una disminución de la deposición en los huesos y
los pulmones. Los compuestos insolubles, como el sulfato
bárico, se acumulan en los pulmones y se eliminan lenta-
mente por la acción de los cilios.
El bario se elimina por la orina y la heces, en tasas
que varían conforme a la vía de administración. Una dosis
de bario inyectada al hombre se elimina en 24 horas en un
20% aproximadamente por las heces yen alrededor del 5% por
la orina. El bario plasmático queda eliminado casi por
completo de la corriente sanguínea en 24 horas. La elimi-
nación del bario ingerido en el hombre y los animales se
produce por las heces más que por la orina. Tras la expo-
sición por inhalación, se produce una lenta eliminación
del bario de los huesos y por consiguiente de todo el
organismo. En las ratas se ha calculado que la semivida
biológica del bario es de 90-120 días. Para efectuar una
vigilancia biológica apropiada de la exposición humana
debe observarse la eliminación del bario por la orina y
las heces.
1.4 Efectos en los animales de experimentación
En la rata, los valores de la DL50 oral son de 118,
250 y 355 en los casos del cloruro, el fluoruro y el
nitrato de bario, respectivamente. Entre los efectos
agudos de la ingestión de bario figuran los siguientes:
salivación, náuseas, diarrea, taquicardia, hipopotasemia,
calambres, parálisis fláccida de la musculatura esque-
lética, parálisis de los músculos respiratorios y fibri-
lación ventricular. La parálisis de los músculos respira-
torios y la fibrilación ventricular pueden conducir a la
muerte. En varios estudios se ha demostrado el efecto
nocivo del bario sobre el automatismo ventricular y las
corrientes marcapasos del corazón. La inyección intra-
venosa de bario a perros anestesiados muestra que esos
efectos agudos se deben a la aparición rápida de una
hipopotasemia notable y pueden evitarse o contrarrestarse
por la administración de potasio.
El bario produce irritación moderada de la piel e
intensa de los ojos en el conejo.
En ratas que ingirieron agua del grifo que contenía
hasta 250 mg de bario/litro durante 13 semanas, no se
observaron signos de toxicidad, aunque algunos grupos
presentaron un descenso del peso relativo de las suprar-
renales.
Las ratas que recibieron 10 o 100 mg de bario/litro en
su agua de beber durante 16 meses presentaron hiper-
tensión, pero una concentración de 1 mg/litro no ocasionó
cambio alguno de la tensión arterial. Los análisis de la
función miocárdica a los 16 meses (dosis de 100 mg de
bario/litro) mostraron alteraciones significativas de la
contractilidad y la excitabilidad del corazón, altera-
ciones metabólicas del miocardio e hipersensibilidad del
sistema cardiovascular al pentobarbital sódico.
En las ratas, la administración oral o la inhalación
de carbonato bárico influyeron desfavorablemente en la
reproducción. Además la tasa de mortalidad fue mayor en
las crías recién nacidas de madres tratadas con bario.
Algunos datos muestran la teratogenicidad del bario, pero
no se dispone de indicios concluyentes de cancerogenici-
dad.
El bario posee propiedades químicas y fisiológicas que
le permiten competir con el calcio y sustituirlo en los
procesos en los que este elemento actúa normalmente de
mediador, en particular en los relacionados con la liber-
ación de catecolaminas adrenales y de neurotransmisores,
como la acetilcolina y la noradreladina.
Se dispone de información limitada acerca de los
efectos inmunológicos del bario en los animales.
1.5 Efectos en la especie humana
Se han señalado varios casos de intoxicación por
ingestión de compuestos de bario. Se ha observado que
dosis de bario tan bajas como 0,2-0,5 mg/kg de peso
corporal, resultantes en general de la ingestión de
cloruro o carbonato de bario, producen efectos tóxicos en
el hombre. El cuadro clínico producido por la intoxicación
por bario comprende gastroenteritis aguda, pérdida de los
reflejos profundos con comienzo de parálisis muscular, y
parálisis muscular progresiva. La parálisis muscular
parece guardar relación con la hipopotasemia intensa. En
la mayoría de los casos notificados se produjo una recu-
peración rápida y sin problemas después del tratamiento
consistente en la perfusión de sales de potasio (carbonato
o lactato) y/o en la administración oral de sulfato
sódico.
Se han realizado estudios epidemiológicos limitados
para estudiar la posible relación existente entre las
concentraciones de bario en el agua potable y la mortali-
dad cardiovascular, pero los resultados han sido incohe-
rentes y nada concluyentes.
No se han observado aumentos de la incidencia de la
hipertensión arterial, los accidentes cerebrovasculares o
las enfermedades cardiacas y renales en una población
expuesta a altas concentraciones de bario en el agua de
beber, en comparación con un grupo análogo expuesto a
menores niveles. En un estudio a corto plazo en volun-
tarios humanos, el consumo de bario en el agua de beber no
influyó en la tensión arterial.
Se ha comunicado un aumento de la incidencia de la
hipertensión en trabajadores expuestos al bario, en compa-
ración con los no expuestos. Se ha observado la aparición
de baritosis en personas expuestas profesionalmente a
compuestos de bario. En un grupo estudiado formado por
trabajadores expuestos al bario y personas que vivían
cerca de un lugar rellenado con productos que contenían
bario se observó una mayor prevalencia de síntomas muscu-
loesqueléticos, intervenciones quirúrgicas gastrointesti-
nales, problemas cutáneos y síntomas respiratorios.
No se ha observado ninguna asociación concluyente
entre la concentración de bario del agua de beber y la
incidencia de malformaciones congénitas. No hay indicios
de que el bario sea carcinógeno.
1.6 Efectos en los seres vivos del medio ambiente
El bario influye directamente en las propiedades
fisicoquímicas y en la infecciosidad de varios virus, así
como en su capacidad de multiplicación. Afecta también al
desarrollo de esporas bacterianas en germinación y ejerce
distintos efectos específicos sobre diferentes microorgan-
ismos, incluida la inhibición de los procesos celulares.
Se dispone de escasa información sobre los efectos del
bario en los seres vivos acuáticos. No se han observado
efectos en la supervivencia de peces sometidos a una
exposición de 30 días de duración. Sin embargo, en un
estudio de 21 días se observaron alteraciones de la repro-
ducción y reducción del crecimiento en dafnidos empleando
dosis de 5,8 mg de bario/litro. No se han recogido
indicios que muestren que la barita es tóxica para los
animales marinos. Sin embargo, la exposición a la barita
en grandes concentraciones puede influir desfavorablemente
en la colonización producida por la fauna béntica.
Los vegetales y los invertebrados marinos pueden
acumular activamente bario procedente del agua del mar.
2. Conclusiones y recomendaciones
En las concentraciones halladas normalmente en nuestro
medio ambiente, el bario no plantea ningún riesgo impor-
tante para la población en general. Sin embargo, en el
caso de determinadas subpoblaciones y en condiciones de
alta exposición al bario, deben tomarse en consideración
las posibilidades de efectos adversos en la salud.
Se dispone de escasos datos para evaluar el riesgo del
bario para el medio ambiente. Sin embargo, basándose en
la información disponible sobre los efectos tóxicos del
bario en los dáfnidos, parece que puede representar un
riesgo para las poblaciones de ciertos seres vivos
acuáticos.
Se necesitan estudios epidemiológicos, investigaciones
sobre la biodisponibilidad y la toxicidad cardiovascular e
inmunitaria, e información adicional sobre la toxicidad
acuática crónica. Para establecer mejores medidas de
protección se requieren más datos sobre la exposición en
el lugar de trabajo y el uso de biomarcadores.
EVALUACION DE LOS RIESGOS PARA LA SALUD HUMANA Y DE LOS EFECTOS
SOBRE EL MEDIO AMBIENTE
1. Evaluación de los riesgos para la salud humana
1.1 Niveles de exposición
1.1.1 Población general
La ingesta alimentaria de bario, basada en datos
procedentes de los Estados Unidos de América, es de 300 a
1700 µg/día. Los valores medios notificados por dos
fuentes distintas son de 600 y 900 µg/día.
Recientes estudios estadounidenses muestran que las
concentraciones de bario en el agua potable van de 1 a
20 µg/litro. Basándose en esa gama y suponiendo un
consumo diario de dos litros de agua potable, la ingesta
de bario en el agua de beber sería de 2-40 µg/día.
La entrada de bario por la inhalación se calcula en
0,04 a 3,1 µg/día.
Según las estimaciones efectuadas en Gales (Reino
Unido), la toma diaria total de bario es de 1327 µg (alimen-
tos: 1240 µg; agua de beber: 86 µg; aire: 1 µg).
1.1.2 Exposición al aire del medio laboral
La exposición de los trabajadores en la industria de
aleaciones metálicas a concentraciones comprendidas entre
0,08 y l,92 mg/m3 (media: 1,07 mg/m3) da lugar a una
elevada prevalencia de la hipertensión. En un grupo de
trabajadores de transformación de mineral de bario que
presentaban síntomas musculoesqueléticos y respiratorios
se observaron exposiciones de 0,02 a 1,7 mg/m3. En
soldadores con arco de acero se han medido exposiciones a
concentraciones comprendidas entre 2,2 a 6,1 mg/m3. Son
las mayores concentraciones ocupacionales que se han noti-
ficado, pero no se realizaron estudios médicos.
1.1.3 Exposiciones agudas
Se ha observado que dosis de bario tan bajas como
0,2-0,5 g (3-7 mg/kg de peso corporal), resultantes en
general de la ingestión de cloruro o carbonato de bario,
provocan efectos tóxicos en personas adultas. En casos
sin tratar, dosis de 3-5 g (40-70 mg/kg de peso corporal)
resultaron mortales.
1.2 Efectos tóxicos; relaciones dosis-efecto y dosis-respuesta
La absorción de bario por el tracto gastrointestinal
depende en gran parte de la edad y de la solubilidad del
producto. Se cree que en los adultos se absorbe menos del
10% del bario ingerido. Ahora bien, la absorción puede
ser notablemente mayor en los niños. El bario absorbido
penetra en la corriente sanguínea y en varios tejidos
blandos y se deposita en el esqueleto; el metabolismo del
bario es análogo al del calcio, pero la diferencia estriba
en que el bario no tiene ninguna función biológica cono-
cida. El bario puede sustituir al calcio en numerosos
procesos fisiológicos y afecta a la actividad nerviosa y
muscular.
El contacto con bario puede producir irritación
moderada de la piel e intensa de los ojos. Se han obser-
vado efectos nocivos en personas sensibles (por ejemplo,
enfermos sometidos a diuresis) tras la exposición al bario
como medio de examen radiológico. Se han registrado
algunos casos de intoxicación por bario. Entre los sín-
tomas figuran la gastroenteritis aguda, la pérdida de
reflejos profundos con comienzo de parálisis muscular, y
la parálisis muscular progresiva.
No hay datos concluyentes en el sentido de que los
productos de bario, con excepción del cromato, sean
carcinógenos en el hombre. Tampoco puede afirmarse que el
bario produzca efectos en la reproducción, embriotóxicos o
teratógenos en la especie humana.
Los limitados estudios epidemiológicos iniciales que
establecían una relación entre la exposición a concen-
traciones bajas de bario y la morbilidad y mortalidad
cardiovascular eran incoherentes y nada concluyentes. En
un estudio epidemiológico ulterior no se encontró ningún
dato decisivo que pusiera de manifiesto efectos del bario
en la tensión arterial. Tampoco se observaron esos efectos
en un estudio a corto plazo en el que un grupo de
voluntarios consumió concentraciones crecientes de bario
hasta de 10 mg/litro de agua de beber.
El bario inhalado en el lugar de trabajo ha dado lugar
a baritosis. La prevalencia de la hipertensión en traba-
jadores expuestos a concentraciones altas de bario trans-
portado por el aire fue claramente superior a la observada
en trabajadores que no sufrieron esa exposición. Se señaló
un aumento de la tensión arterial sistólica relacionado
con la dosis en ratas expuestas a concentraciones de bario
de hasta 100 mg/litro.
1.3 Evaluación del riesgo
Basándose en las publicaciones disponibles, puede
llegarse a la conclusión de que la salud de la población
general no corre ningún riesgo significativo por la acción
del bario en las concentraciones halladas habitualmente en
el agua (especialmente el agua de beber), los alimentos y
el aire ambiental. Sin embargo, en el caso de determinadas
subpoblaciones (ancianos o personas con deficiencia de
potasio) y en circunstancias particulares (concentración
elevada en el agua, exposición profesional, etc.) puede
haber posibilidades de efectos adversos para la salud.
2. Evaluación de los efectos sobre el medio ambiente
El bario se halla en el suelo a una concentración
media de 500 µg/g. Se han medido concentraciones de 0,04
a 37,0 µg/litro y de 7,0 a 15 000 µg/litro en las aguas
oceánicas y dulces, respectivamente. Las concentraciones
de bario en el aire son en general de < 0,05 µg/m3.
Los compuestos de bario solubles pueden transportarse
por el medio ambiente y ser absorbidos por los seres
vivos. El bario puede acumularse en distintas partes de
las plantas.
Se ha señalado que el bario inhibe el crecimiento y
los procesos celulares de los microorganismos. Se ha
observado también que influye en el desarrollo de las
esporas bacterianas en germinación.
No se han hallado datos sobre los efectos adversos del
bario en las plantas terrestres o los animales silvestres.
En las plantas acuáticas no se han registrado efectos
tóxicos debidos al bario en las concentraciones habituales
en el agua. Los valores de CL50 para los peces de agua
dulce son de 46 a 78 mg/litro. Se ha observado que las
concentraciones de bario de 5,8 mg/litro alteran la repro-
ducción y el crecimiento de los dáfnidos.
Faltan datos para evaluar el riesgo que supone el
bario para el medio ambiente. Basándose en la información
disponible sobre los efectos tóxicos en los dáfnidos,
parece que el bario puede representar un riesgo para las
poblaciones de ciertos seres vivos acuáticos.
RECOMENDACIONES PARA ULTERIORES ESTUDIOS
Se recomiendan investigaciones ulteriores sobre el
bario en los siguientes sectores de los efectos en el
medio ambiente y la salud humana:
* estudios de biodisponibilidad, que comprendan los
mecanismos de solubilización y transporte;
* estudios sobre hipertensión/enfermedades cardiovascu-
lares, que abarquen la población general y los
trabajadores expuestos por razones profesionales, y
mecanismos de acción conexos;
* estudios epidemiológicos bien planeados;
* estudios sobre los efectos inmunológicos del bario en
el hombre;
* estudios sobre la toxicidad acuática subletal a largo
plazo;
* datos de vigilancia sobre la exposición ambiental para
determinar los sectores en los que se necesitan medi-
das protectoras;
* evaluación de indicadores iniciales de alta tasa de
exposición al bario; estudios de marcadores biológicos
(por ejemplo, contenido de bario en el pelo y la
orina, concentraciones de potasio sérico).