This report contains the collective views of an international group of
    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

         The International Programme on Chemical Safety (IPCS) is a
    joint venture of the United Nations Environment Programme, the
    International Labour Organisation, and the World Health
    Organization. The main objective of the IPCS is to carry out and
    disseminate evaluations of the effects of chemicals on human health
    and the quality of the environment. Supporting activities include
    the development of epidemiological, experimental laboratory, and
    risk-assessment methods that could produce internationally
    comparable results, and the development of manpower in the field of
    toxicology. Other activities carried out by the IPCS include the
    development of know-how for coping with chemical accidents,
    coordination of laboratory testing and epidemiological studies, and
    promotion of research on the mechanisms of the biological action of

    WHO Library Cataloguing in Publication Data


        (Environmental health criteria ; 107)


        ISBN 92 4 157107 1        (NLM Classification: QV 618)
        ISSN 0250-863X

         The World Health Organization welcomes requests for permission
    to reproduce or translate its publications, in part or in full.
    Applications and enquiries should be addressed to the Office of
    Publications, World Health Organization, Geneva, Switzerland, which
    will be glad to provide the latest information on any changes made
    to the text, plans for new editions, and reprints and translations
    already available.

    (c) World Health Organization 1990

         Publications of the World Health Organization enjoy copyright
    protection in accordance with the provisions of Protocol 2 of the
    Universal Copyright Convention. All rights reserved.

         The designations employed and the presentation of the material
    in this publication do not imply the expression of any opinion
    whatsoever on the part of the Secretariat of the World Health
    Organization concerning the legal status of any country, territory,
    city or area or of its authorities, or concerning the delimitation
    of its frontiers or boundaries.

         The mention of specific companies or of certain manufacturers'
    products does not imply that they are endorsed or recommended by the
    World Health Organization in preference to others of a similar
    nature that are not mentioned. Errors and omissions excepted, the
    names of proprietary products are distinguished by initial capital



     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


     2.1. 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
         AAS - direct aspiration method
         AAS - furnace technique
         AAS - ICP
          2.5.2. Analytical methods used for special applications
         Mass spectrometry
         X-ray fluorescence spectrometry
         Neutron activation analysis


     3.1. Natural occurrence
     3.2. Man-made sources
          3.2.1. Production levels, processes, and uses


     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


     5.1. Environmental levels
          5.1.1. Air
          5.1.2. Water
         Surface waters
         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


     6.1. Absorption
          6.1.1. Inhalation route
         Laboratory animals
          6.1.2. Oral route
         Laboratory animals
          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


     7.1. 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


     8.1. 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


     9.1. General population exposure
          9.1.1. Acute toxicity - poisoning incidents
          9.1.2. Short-term controlled human studies
          9.1.3. Epidemiological studies
         Cardiovascular disease
         Other effects
     9.2. Occupational exposure
          9.2.1. Effects of short- and long-term exposure
     9.3. Carcinogenicity of barium chromate


     10.1. Evaluation of human health risks
          10.1.1. Exposure levels
          General population
          Occupational - air exposures
          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












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

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


Dr B.H. Chen, International Programme on Chemical Safety,
   World Health Organization, Geneva, Switzerland

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.


    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).


    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.


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


1.1.  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-

    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

    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

    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-

    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-

    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

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.


2.1.  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

    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
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                    
a  Source: RTECS (1985).
Table 2.  Physical and chemical properties of bariuma
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
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
                            Relative    Relative   Solubility    Melting       Boiling
Compound                    molecular   density    in waterb     pointc        point
                            mass                                 (°C)          (°C)
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            -
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-

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. 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. 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. 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 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). 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). 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).


3.1.  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,

    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

    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,

    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-

    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

    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-

    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-

    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
Barium compound                               Uses
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

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.)
Barium compound                               Uses
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

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

Perchlorate              In explosives; in rocket fuels (experimentally); in the determi-
                         nation of ribonuclease; as an absorbent of water in C and H analy-

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.)
Barium compound                               Uses
Selenide                 In photocells; in semiconductors

Silicate                 In refining sugar from molasses

Sodium niobate           In lasers, electro-optical modulators, and optical parametric

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

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

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
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,

    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.,


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

    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

    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-

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.


5.1.  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              
Lakehurst (NJ), Paulsboro (NJ)      100           0             0            0              
a  Source: Tabor & Warren (1958) 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)     
------------------------------------------------------------------------   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). 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,

    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

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

Table 7.  Barium contents of some common foodsa
          Food                                     Barium content
                                                     (mg/100 g)
Beverages and dietary concentrates
     Chocolate syrup                                    0.17
       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
       Rye                                              0.062
       White                                            0.051
       Whole wheat                                      0.11
     Bran flakes, 40%                                   0.39
     Cheerios (cereal)                                  0.13
     Corn flakes (cereal)                               0.04
       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

     American                                           0.12
     Cottage, creamed                                  <0.04
     Swiss                                              0.22

     Whole                                              0.76
     White                                             <0.01
     Yolk                                               0.058

     Nonfat solids                                     <0.08
     Whole                                             <0.01
     Skim                                              <0.01
     Buttermilk                                        <0.01
Ice cream, vanilla                                     <0.01
Sherbet, orange                                        <0.01

Fruits and fruit juices
       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
       Fresh, with peel                                <0.05
       Juice, canned                                    0.023
       Juice, canned                                   <0.008
         Fresh, skinless                               <0.01
         Canned, drained                               <0.01
       Juice, frozen, reconstituted                    <0.008
       Sections, skinless                              <0.008
       Crushed, canned, drained                         0.014
       Juice, canned                                    0.008
     Peach, cling, canned, drained                     <0.01
     Pear, canned, drained                              0.047
       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)

       Butter                                          <0.04
       Salted, blanched                                 0.21
     Pecans                                             0.67
     Walnuts                                            0.072

Sugars and flours
       Brown                                           <0.04
       Powdered                                        <0.04
       White                                           <0.04
     Flour, bleached, enriched                          0.072

     Asparagus spears, frozen, uncooked                <0.02
       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
       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
       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

    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-

    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

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,

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 

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 

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
a  NR = not reported.

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 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. Humans

    There are no quantitative data on the  deposition  and
absorption  of  barium  compounds  through  inhalation  in

6.1.2.  Oral route 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). 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

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

    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

    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

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.,

    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).


7.1.  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.,

    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,

    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,

    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

    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).


8.1.  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.,

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)                          

           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                                           

           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        

carbonate  dog      initial:        iv                       accelerated ventricular        Foster et al.                   
                    3.6-64.7 µmol/  infusion    2-10 min     escapes; tachycardia           (1977)                          
                    kg per min;                                                                                             
                    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)                      
           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                               
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)    
           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

    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-

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-

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

    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.


9.1  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;
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 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

    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. 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

    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

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.


10.1  Evaluation of human health risks

10.1.1  Exposure levels  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).  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.  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

    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.


    Further  research studies on  barium in the  following
areas  of  environmental  and  human  health  effects  are

*   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-

*   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).


    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.


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.

(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.

(1979) Cardiovascular disease death rates in communities with elevated
levels of barium in drinking water.  Environ. Res., 20: 318-324.

(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

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.

(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.

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).

elements in hair, as related to exposure in metropolitan New York.  Clin.
 Chem., 21: 606-612.

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.

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:

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.

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.

from the Chinese atomic test of May 1965, intercepted over the northwestern
United States.  Health Phys., 12: 862-863.

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.

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-

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

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).

 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).

of the Task Group on Reference Man, No. 23. Pergamon Press, Elmsford, New

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.

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.

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,

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.

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.

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

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.

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-

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.

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.

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.

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-

SILINSKY, E.M. (1978) On the role of barium in supporting the asynchronous
release of acetylcholine quanta by motor nerve impulses.  J. Physiol., 274:

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-

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.

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

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.

(1987) Inhibitory effect of barium on human dental caries prevalence.
 Community dent. oral Epidemiol., 15: 6-9.


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

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

    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

    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.


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

    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


    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

*   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).


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

    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-

    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-

    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

    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

    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.


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

    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.


    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

*   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).

    See Also:
       Toxicological Abbreviations
       Barium (HSG 46, 1991)
       Barium (ICSC)