Barium Guideline

ölçüsü94.92 Kb.

January 1990

(edited September 1990)



The maximum acceptable concentration (MAC) for barium in drinking water is 1.0 mg/L (1000 

µ g/L).

Identity, Use and Sources in the


Barium is present as a trace element in both igneous

and sedimentary rocks. Although it is not found free in



 barium occurs in a number of compounds, most

commonly barite (BaSO


) and, to a lesser extent,

witherite (BaCO



Barium compounds have a wide variety of

industrial applications. They are used in the plastics,

rubber, electronics and textiles industries. Barium

compounds are used in ceramic glazes and enamels, in

glass making and paper making, as a lubricant additive

and in pharmaceuticals and cosmetics.


 Barite is used

extensively in the oil and gas industry as a wetting agent

for drilling mud.


 Domestic consumption of barite in

Canada in 1984 was 78 565 tonnes, 90% of which was

used in oil and gas well drilling.


 Witherite is used in the

production of optical glasses, in brick making, in

case-hardening of steel and as a rodenticide. Organo-

metallic compounds containing barium have been used

in diesel fuel to reduce black smoke emissions from

diesel engines.


The acetate, nitrate and halide salts of barium are

soluble in water, but the carbonate, chromate, fluoride,

oxalate, phosphate and sulphate salts are quite insoluble.

The aqueous solubility of barium compounds increases

as the pH decreases.


 Organometallic barium

compounds are ionic and are hydrolysed in water.



concentration of barium ions in natural aquatic systems

will be limited by naturally occurring anions, such as

sulphates and carbonates, and by the possible adsorption

of barium ions onto metal oxides and hydroxides.



Barium levels were determined in 122 munici-

palities in 10 provinces in samples of raw, treated and

distributed drinking water serving approximately 36%

of the Canadian population.


 The provincial median

concentrations of barium in distributed water ranged

from not detectable (

0.005 mg/L) in British Columbia,

Newfoundland, Nova Scotia and Quebec to 0.084 mg/L

in Alberta. The Canada-wide median concentration was

0.018 mg/L. The maximum level of barium in a sample

of distributed water was 0.602 mg/L, measured at a site

in Ontario. Barium levels in raw water were not

significantly different from those in treated water.

Barium is generally present in air in particulate

form, and its presence is attributed mainly to industrial

emissions, specifically the combustion of coal and diesel

oil and waste incineration. No data on concentrations of

barium in ambient air in Canada have been found. In the

United States, concentrations have been found to range

from 0.0015 to 0.95 






Most foods contain less than 0.002 mg/g of



 The major dietary sources of barium in the

United States are milk, potatoes and flour.


 Some cereal

products and nuts tend to contain high amounts of

barium; for example, pecans contain 0.0067 mg/g,

peanuts 0.0021 mg/g, bran flakes 0.0039 mg/g and

Brazil nuts up to 4 mg/g.


 Certain species of plants

accumulate barium when grown in barium-rich soil.


The International Commission on Radiological

Protection (ICRP) reported that the long-term mean

dietary barium intake for four individuals, including

both food and fluids, was 0.9 mg/d, with a range of 0.44

to 1.8 mg/d.


 In a survey by Schroeder et al. of the diets

of five adults over 30 to 347 days, the mean daily intake

of barium from food was 1.2 mg, with a range of 0.65 to

1.8 mg.

13  Owing to the lack of data on barium levels in

Canadian foodstuffs, it is difficult to estimate daily

intake of barium in the diet. However, on the basis of the

data reported by the ICRP


 and Schroeder et al.,



mean intake of barium by Canadians from this source is

estimated to be approximately 1 mg/d.

Assuming average daily water consumption to be

1.5 L and based on the median concentration of barium

found in a national survey of Canadian drinking water

(0.018 mg/L),


 the barium intake from drinking water

for most Canadians would be approximately 0.03 mg/d.

For individuals consuming drinking water containing

the highest barium concentration measured in the


national survey (0.6 mg/L),


 the maximum daily intake

of barium in drinking water would be 0.9 mg. At the

levels of barium measured in U.S. air,


 intake of barium

through inhalation would be negligible compared with

the amount ingested.

Based on the above considerations, the mean daily

intake of barium from food, water and air in Canada is

estimated to be slightly more than 1 mg/d. Of this, food

represents the primary source of barium for the non-

occupationally exposed Canadian population. However,

in cases where barium levels in drinking water are high

(0.6 mg/L), drinking water may contribute significantly

to barium intake (approximately 50%).

Analytical Methods and Treatment


Barium concentrations in water may be determined

by atomic absorption spectroscopy (AAS), either by

direct aspiration into an air–acetylene flame or by

atomization in a furnace. The detection limit for the

furnace technique is much lower than that for the direct

aspiration procedure (2


g/L vs. 100 




 Barium in

water may also be determined by inductively coupled

plasma atomic emission spectrometry; detection limits

for this method of analysis are reported to be equivalent

or superior to those for flame AAS for most elements.


Based upon data collected in a Canadian national

survey, relatively little, if any, soluble or insoluble

barium is removed by conventional water treatment



 Processes effective in removing barium from

drinking water include ion exchange (93 to 98%), lime

softening (>90%) and the reverse osmosis membrane

technique (>90%); efficiency of removal varies,

depending upon levels in the raw water.


Health Effects

Barium is not considered to be an essential element

for human nutrition.


The degree of absorption of barium from the lungs

and gastrointestinal tract depends on the solubility of the

compound, the animal species, the contents of the

gastrointestinal tract, diet and age. Soluble barium salts

are absorbed most readily. Recent data from studies in

rats and man indicate that insoluble barium compounds

may also be absorbed to a significant extent.


Gastrointestinal absorption of barium in rats was found

to decrease with age (85% in rats 14 to 18 days old vs. <10% in rats 60 to 70 weeks old) and was greater in

fasted rats than in fed rats.


Barium is rapidly distributed in blood plasma,

principally to the bone.


 The whole body content of

barium in man is approximately 22 mg, of which 93% is

found in the bone and connective tissues, with smaller

amounts being present in the fat, skin and lungs.



rats administered drinking water containing 0 to

250 mg/L barium as barium chloride for four, eight or

13 weeks, the concentration of barium in the bone was

proportional to dose but not to duration of exposure.



has also been reported that barium crosses the placental

barrier in humans, based on the determination of barium

content of infant and stillborn foetal tissues.


Miller et al.


 reported that the ratio of barium to

calcium in the teeth of 34 children exposed in one

community to drinking water containing high

concentrations of barium (10 mg/L) was five times

higher than that for 35 children from another community

exposed to lower levels (0.2 mg/L). The two

communities were similar with respect to population,

ethnic composition and socioeconomic status.

The principal route of excretion of barium in

humans and animals is faecal;


 20% is excreted in the

faeces and 7% is excreted in the urine within 24 hours.


Soluble barium salts are highly acutely toxic. At

high concentrations, barium causes strong

vasoconstriction by its direct stimulation of arterial

muscle, peristalsis due to the violent stimulation of

smooth muscle, and convulsions and paralysis following

stimulation of the central nervous system.



on the dose and solubility of the barium salt, death may

occur in a few hours or a few days. The acute lethal oral

dose of barium chloride for humans has been estimated

to be between 3 and 4 g; the acute toxic dose is 0.2 to

0.5 g.

23  Repeated exposures to barium chloride in table

salt are believed to have caused recurrent outbreaks of

“Pa-Ping” disease (a transient paralysis resembling

familial periodic paralysis) in the Szechwan province of



The prevalence of dental caries was reported to be

significantly lower in 39 children from one community

ingesting drinking water with a barium concentration of

8 to 10 ppm than in 36 children from another

community ingesting drinking water with much lower

barium concentrations (<0.3 ppm).


 There was no

statistically significant relationship between the

prevalence of dental caries and age, sex, presence of

detectable mottling, use of water softener or income.

The concentrations of other trace elements (i.e.,

magnesium, calcium, strontium and fluoride) in the

water supplies of the two communities were not

markedly different; however, the study population was

small, and dental examinations were not conducted


In several ecological epidemiological studies,

associations between the barium content of drinking

water and mortality from cardiovascular disease have

been observed. For example, based on analysis of

mortality rates in relation to variations in the amounts of

numerous trace elements in drinking water in different

geographical areas, Schroeder and Kramer



Elwood et al.


 reported significant negative correlations

Barium (01/90)


between barium concentrations in drinking water and

mortality from atherosclerotic heart disease and total

cardiovascular disease, respectively. Conversely,

Brenniman et al.


 reported significantly higher sex- and

age-adjusted death rates for “all cardiovascular diseases”

and “heart disease” in an unspecified number of Illinois

communities with high concentrations of barium in

drinking water (

2 to 10 mg/L) than in communities

with low concentrations (0.0 to 0.2 mg/L) for the period

1971 to 1975. Although the communities were matched

for similar demographic and socioeconomic status

characteristics, population mobility varied between the

communities with high and low barium levels (i.e., two

of the communities with high barium concentrations in

drinking water had a considerable increase in population

size over the study period).

The lack of data on exposure of individuals in

populations in the ecological studies described above

and the resulting inability to adjust rigorously for

confounding factors and population mobility limit their

usefulness in assessing cause–effect relationships.

Moreover, the results of the ecological study in Illinois

conducted by Brenniman et al.


 were not confirmed in

a further cross-sectional study by Brenniman and Levy

of cardiovascular disease prevalence in 1175 adult

residents of West Dundee, Illinois (with a mean barium

concentration in drinking water of 7.3 mg/L and a range

of 2.0 to 10.0 mg/L) and in 1203 adult residents of

McHenry (with a mean barium concentration in drinking

water of 0.1 mg/L).


 Blood pressures of all participants

in the study were measured, and data on occurrence of

cardiovascular, cerebrovascular and renal disease and

possible confounding factors were determined by

questionnaires administered by trained survey workers.

(It was not specified whether or not the study was

conducted blindly.) The socioeconomic status and

demographic characteristics of the populations in the

two towns were similar. There were no significant

differences in the prevalence of hypertension, stroke and

heart and kidney disease between the two populations,

even when the use of water softeners, medication,

duration of exposure, smoking and obesity were taken

into account. The authors concluded that blood pressure

in adults does not appear to be adversely affected even

following prolonged ingestion of drinking water

containing more than 7 mg/L barium.

In a recently completed but unpublished clinical

study, 11 “healthy” men were exposed to barium (as

barium chloride) in drinking water: 0 mg/L for two

weeks, 5 mg/L for the next four weeks and 10 mg/L for

the last four weeks.


 Attempts were made to control

several of the risk factors for cardiovascular disease,

including diet, exercise, smoking and alcohol

consumption throughout the study period (although

study subjects were not continuously monitored in this

regard). Based on twice daily monitoring of blood

pressure, periodic monitoring of blood (for total

cholesterol, triglycerides, HDL cholesterol,

apolipoproteins A1, A2 and B and serum potassium,

glucose, calcium and albumin) and urine (for

vanillymandelic acid and total metanephrines),

electrocardiographic monitoring at the end of each

exposure period and liver function tests, there was no

consistent indication of any adverse effects. There was,

however, a trend towards increased serum calcium

between 0 and 5 mg/L that persisted at 10 mg/L, which,

for total calcium, normalized for differences in albumin

level, was statistically significant. The authors suggested

that this increase would not be expected to be clinically

important. The lack of adverse effects observed in this

study may be attributable to the small number of

subjects included or the short period of exposure.

Tardiff et al.


 exposed groups of 30 female and

30 male Charles River rats to 0, 10, 50 or 250 mg/L

barium as barium chloride (equivalent to mean doses of

0, 1.7 and 2.1, 8.1 and 9.7, and 38.1 and 45.7 mg/kg bw

per day for males and females, respectively) in drinking

water for 13 weeks with interim kills (five of each sex)

at four and eight weeks. No adverse histological or

haematological effects were observed; there were also

no effects on serum enzymes or ions, body weight gain

or food consumption. Water consumption was slightly

depressed in the highest dose group (38.1/45.7 mg/kg

bw per day); there was also a slight decrease in adrenal

weights in some dose groups, but it did not appear to be


There were no effects on blood pressure in Sprague-

Dawley rats exposed to 100 ppm barium in drinking

water as barium chloride (equivalent to 15 mg/kg bw per

day, based on the authors’ calculations that 10 ppm was

equal to 1.5 mg/kg bw per day) for up to 20 weeks.



the same series of studies, there were no changes in

blood pressure in hypertension-susceptible Dahl and

uninephrectomized rats exposed for 16 weeks to up to

1000 ppm barium in distilled water or 0.9% saline. At

the highest dose level (1000 ppm), however, there were

ultrastructural changes in the glomeruli of the kidney

discernible by electron microscopy. In addition, no

significant electrocardiographic changes during

L-norepinephrine challenge were observed in Sprague-

Dawley rats ingesting drinking water containing

250 ppm barium for five months.


In a limited study in which the survival, incidence

of tumours upon gross examination at autopsy and

serum levels of cholesterol, glucose and uric acids were

determined in Long-Evans rats exposed for their lifetime

to 5 ppm barium as barium acetate in drinking water,

there was a slight enhancement in growth of females and

a significant increase in proteinuria in males.



should be noted that mortality due to an epidemic of

Barium (01/90)


pneumonia in this study was approximately 35% in

males and 22% in females; there were 52 animals of

each sex per group at the initiation of the study.) In a

similar study in which 5 ppm barium as barium acetate

was administered in drinking water to Charles River CD

mice over their life span, there was a significant

reduction in the survival of males but no effects on body

weight gain, oedema, incidence of tumours or blanching

of incisor teeth based on gross examination at autopsy.


McCauley et al.


 reported no histopathological

effects upon examination of 34 tissues in male and

female Sprague-Dawley rats exposed to 1, 10, 100 or

250 ppm barium as barium chloride in drinking water

for up to 68 weeks.

Perry et al.


 studied the effect of the ingestion of

barium in drinking water on blood pressure in rats.

Groups of female Long-Evans rats were exposed to 1,

10 or 100 ppm barium as barium chloride in drinking

water for one, four or 16 months, equivalent to average

daily barium doses of 0.051, 0.51 and 5.1 mg/kg bw per



 There were no changes in mean systolic pressure

in animals exposed to 1 ppm barium (0.051 mg/kg bw

per day) for one to 16 months. At 10 ppm barium

(0.51 mg/kg bw per day), there were mean increases in

blood pressure of 4 to 7 mmHg by eight months, which

persisted thereafter. In rats receiving 100 ppm barium

(5.1 mg/kg bw per day), there were significant and

persistent increases in mean systolic pressure

(12 mmHg) after only one month, which gradually

increased to a mean of 16 mmHg after 16 months of

exposure. Rates of cardiac contraction, electrical

excitability and high energy phosphate and

phosphorylation potential were decreased. It has been

suggested that the calcium content of the diet in this

study may have been less than the minimum daily

requirement; however, manifestations of calcium

deficiency on growth patterns were not observed.

Increases in systolic pressure of 4 to 7 mmHg are

deemed sufficiently small so as to not constitute an

adverse effect; therefore, 5.1 mg/kg bw per day is

considered to be the lowest-observed-adverse-effect

level (LOAEL), and 0.51 mg/kg bw per day is

considered to be the no-observed-adverse-effect level

(NOAEL). This judgement is consistent with the

opinion of the U.S. Environmental Protection Agency.


Perry et al.


 estimated that a 0.1 to 1% increase in the

clinical appearance of coronary heart disease in the U.S.

population over a six-year period could result from an

increase of 15 mmHg in mean systolic blood pressure.

Wilkins and Calabrese


 suggested that, whereas an

increase in systolic blood pressure of 5 mmHg would

have virtually no short-term clinical implications for

persons 35 years old and younger, a shift of 5 mmHg

may become a difference of nearly 10 mmHg by age 65.

In the United States, an increase of 10 mmHg in systolic

blood pressure at this age would increase the average

risk of a heart attack by 14%.

There has been no evidence of the carcinogenicity

of barium in extremely limited lifetime bioassays of rats

and mice exposed to 5 mg/L in drinking water, based on

gross examination only of tumours at autopsy.


Barium chloride did not increase the frequency of

mutation in repair-deficient strains of Bacillus subtilis.


Results were also negative for the induction of errors in

viral DNA transcription in vitro.


It has been reported that the oestrous cycle was

shortened and that the morphological structure of the

ovaries was disturbed in female rats exposed to


±  0.7 mg/m


 and 3.1 


0.16 mg/m



carbonate dust for four months.


 Mortality increased

and body weight gain decreased in the offspring of the

dams in the high dose group; the lability of the

peripheral nervous system decreased, and blood

disorders (erythropenia, leukocytosis, eosinophilia,

neutrophilia) related to the irritant effect of barium on

the bone marrow in two-month-old offspring were also



 In a similar inhalation study in male rats

exposed to 22.6 


 0.6 mg/m


 barium carbonate dust,


deleterious effects on spermatogenesis were reported.

However, data presented in the published account were

insufficient to permit evaluation of the protocols of these


Classification and Assessment

Because there are few data available regarding the

carcinogenicity of barium, it has been classified in

Group VA (inadequate data for evaluation). For

compounds classified in Group VA, the maximum

acceptable concentration (MAC) is derived on the basis

of division of the NOAEL or LOAEL in an animal

species by an uncertainty factor.

In studies in which Long-Evans rats ingested

drinking water containing 100 mg/L (5.1 mg/kg bw per

day) for up to 16 months, there were significant

increases in mean systolic blood pressure (12 mmHg

after one month, 16 mmHg after 16 months), depressed

rates of cardiac contraction, depressed electrical

excitability and decreased high energy phosphate and

phosphorylation potential.


 Increases of 4 to 7 mmHg

in mean systolic blood pressure were observed in rats

exposed to a barium concentration of 10 mg/L

(0.51 mg/kg bw per day) in drinking water after eight

months. In a study with Sprague-Dawley rats, however,

there were no effects on blood pressure following

exposure to barium at 100 ppm in drinking water

(approximately 15 mg/kg bw per day) for 20 weeks.


Barium (01/90)


It has been suggested by some authors that small

increases in mean systolic blood pressure in the human

population similar to those observed in rats by Perry et al.


 (5 to 15 mmHg) could result in significant

increases in clinical cases of coronary heart disease.

However, in the most sensitive epidemiological study

conducted to date, there were no significant differences

in blood pressure or the prevalence of cardiovascular

disease between a population drinking water containing

7.3 mg/L barium and one ingesting water containing

0.1 mg/L barium.


On the basis of the results of the epidemiological

study by Brenniman and Levy,


 in which adverse

effects on blood pressure and increases in the prevalence

of cardiovascular disease were not observed in a

population ingesting water containing a mean concen-

tration of 7.3 mg/L barium, the MAC is derived as





7.3 mg/L

=  0.73 mg/L



7.3 mg/L is the NOAEL in the most sensitive epidemiological study

conducted to date


10 is the uncertainty factor (to account for intraspecies variation).

This value is not substantially different from that

derived on the basis of the results of toxicological

studies in animals, based on the NOAEL of 0.51 mg/kg

bw per day for effects on blood pressure in rats



an uncertainty factor of 10 (


10 for intraspecies



1 for interspecies variation, as the results of a

well-conducted epidemiological study indicate that

humans are less sensitive than rats to barium in drinking


Because the MAC derived above does not differ

greatly from the MAC of 1.0 mg/L included in the 1978

Guidelines, a MAC for barium of 1.0 mg/L has been




U.S. Environmental Protection Agency. Health advisory—Barium.

Office of Drinking Water (1985).


Brooks, S.M. Pulmonary reactions to miscellaneous mineral dusts,

man-made mineral fibers, and miscellaneous pneumoconioses. In:

Occupational respiratory diseases. J.A. Merchant (ed.). U.S.

Department of Health and Human Services. p. 401 (1986).


Vagt, G.O. Barite and celestite. In: Canadian minerals yearbook.

Mineral Resources Branch, Energy, Mines and Resources Canada



Miner, S. Preliminary air pollution of barium and its compounds.

A literature review. Prepared under Contract No. PH 22-68-25

USDHEW, Public Health Service, National Air Pollution Control

Administration, Raleigh, NC (1969).


Cotton, F.A. and Wilkinson, G. Advanced inorganic chemistry:

Comprehensive text. 4th edition. J. Wiley, New York, NY. p. 286



Hem, J.D. Barium. In: Study and interpretation of the chemical

characteristics of natural water. Geological Survey Water-Supply

Paper 1473, U.S. Government Printing Office, Washington, DC.

p. 197 (1970).


Subramanian, K.S. and Méranger, J.C. A survey for sodium,

potassium, barium, arsenic, and selenium in Canadian drinking water

supplies. At. Spectrosc., 5: 34 (1984).


U.S. Environmental Protection Agency. Computer printout:

Frequency distributions by site/year for barium, the results of

samples collected at National Air Surveillance Network sites.

Unpublished, Environmental Monitoring Systems Laboratory (1984),

cited in reference 35.


Gormican, A. Inorganic elements in foods used in hospital menus.

J. Am. Diet. Assoc., 56: 397 (1970).

10. Calabrese, E.J., Canada, A.T. and Sacco, C. Trace elements and

public health. Annu. Rev. Public Health, 6: 131 (1985).

11. Underwood, E.J. Trace elements in human and animal nutrition.

Academic Press, New York, NY. p. 431 (1971).

12. International Commission on Radiological Protection. Report of

the task group on reference man. Pergamon Press, New York, NY


13. Schroeder, H.A., Tipton, I.H. and Nason, P. Trace metals in man:

Strontium and barium. J. Chronic Dis., 25: 491 (1972). 

14. Ontario Ministry of the Environment. The determination of trace

metals in surface waters by ICP–AES. Laboratory Services Branch


15. McCauley, P.T. and Washington, I.S. Barium bioavailability as the

chloride, sulfate, or carbonate salt in the rat. Drug Chem. Toxicol., 6:

209 (1983).

16. Clavel, J.P., Lorillot, M.L., Buthiau, D., Gerbet, D., Heitz, F. and

Galli, A. Intestinal absorption of barium during radiological studies.

Therapie, 42(2): 239 (1987).

17. Taylor, D.M., Bligh, P.H. and Duggan, M.H. The absorption of

calcium, strontium, barium and radium from the gastrointestinal tract

of the rat. Biochem. J., 83: 25 (1962).

18. National Academy of Sciences. Drinking water and health. Vol. 1.

National Research Council, Washington, DC (1977).

19. Tardiff, R.G., Robinson, M. and Ulmer, N.S. Subchronic oral

toxicity of BaCl


 in rats. J. Environ. Pathol. Toxicol., 4: 267 (1980).

20. Miller, R.G., Featherstone, J.D.B., Curzon, M.E.J., Mills, T.S. and

Shields, C.P. Barium in teeth as indicator of body burden. In:

Advances in modern environmental toxicology. Vol. IX. Princeton

Publishing Co., Princeton, NJ. p. 211 (1985).

21. Ohanian, E.V. and Lappenbusch, W.L. Problems associated with

toxicological evaluations of barium and chromium in drinking water.

Office of Drinking Water, U.S. Environmental Protection Agency


22. Stockinger, H.E. The metals. In: Patty’s industrial hygiene and

toxicology. Vol. II(A). G.D. Clayton and F.E. Clayton (eds.). J.

Wiley, New York, NY. p. 1531 (1981).

23. Reeves, A.L. Barium. In: Handbook on the toxicology of metals.

L. Friberg, G.F. Nordberg and V.B. Vouk (eds.). Elsevier/North

Holland Biomedical Press, Amsterdam (1979).

Barium (01/90)


24. Shankle, R. and Keane, J.R. Acute paralysis from barium

carbonate. Arch. Neurol., 45(5): 579 (1988).

25. Zdanowicz, J.A., Featherstone, J.D.B., Espeland, M.A. and

Curzon, M.E.J. Inhibitory effect of barium on human caries

prevalence. Community Dent. Oral Epidemiol., 15: 6 (1987).

26. Schroeder, H.A. and Kramer, L.A. Cardiovascular mortality,

municipal water, and corrosion. Arch. Environ. Health, 28: 303


27. Elwood, P.C., Abernethy, M. and Morton, M. Mortality in adults

and trace elements in water. Lancet, ii: 1470 (1974).

28. Brenniman, G.R., Namekata, T., Kojola, W.H., Carnow, B.W. and

Levy, P.S. Cardiovascular disease rates in communities with elevated

levels of barium in drinking water. Environ. Res., 20: 318 (1979).

29. Brenniman, G.R. and Levy, P.S. Epidemiological study in Illinois

drinking water supplies. In: Advances in modern environmental

toxicology. Vol. IX. Princeton Publishing Co., Princeton, NJ. p. 231


30. Wones, R.G., Stadler, B.L. and Frohman, L.A. Lack of effect of

drinking water barium on cardiovascular risk factors. Study

conducted by the University of Cincinnati College of Medicine for

the U.S. Environmental Protection Agency (unpublished) (1989).

31. McCauley, P.T., Douglas, B.H., Laurie, R.D. and Bull, R.J.

Investigations into the effect of drinking water barium on rats. In:

Advances in modern environmental toxicology. Vol. IX. Princeton

Publishing Co., Princeton, NJ. p. 197 (1985).

32. Schroeder, H.A. and Mitchener, M. Life-term studies in rats:

Effects of aluminum, barium, beryllium and tungsten. J. Nutr., 105:

421 (1975).

33. Schroeder, H.A. and Mitchener, M. Life-term effects of mercury,

methyl mercury and nine other trace elements on mice. J. Nutr., 105:

452 (1975).

34. Perry, H.M., Jr., Kopp, S.J., Erlanger, M.W. and Perry, E.F.

Cardiovascular effects of chronic barium ingestion. Trace Subst.

Environ. Health, 16: 155 (1983).

35. U.S. Environmental Protection Agency. Drinking water criteria

document for barium. Office of Drinking Water (1985).

36. Wilkins, J.R. and Calabrese, E.J. Health implications of a 5 mm

Hg increase in blood pressure. In: Advances in modern environ-

mental toxicology. Vol. IX. Princeton Publishing Co., Princeton, NJ.

p. 85 (1985).

37. Nishioka, H. Mutagenic activities of metal compounds in

bacteria. Mutat. Res., 31: 185 (1975). Cited in U.S. Environmental

Protection Agency. Health effects assessment for barium (1984).

38. Loeb, L., Sirover, M. and Agarwal, S. Infidelity of DNA synthesis

as related to mutagenesis and carcinogenesis. Adv. Exp. Med. Biol.,

91: 103 (1978). Cited in U.S. Environmental Protection Agency.

Health effects assessment for barium (1984).

39. Tarasenko, N.Y., Pronin, O.A. and Silayev, A.A. Barium

compounds as industrial poisons (an experimental study). J. Hyg.

Epidemiol. Microbiol. Immunol., 21: 361 (1977).

40. Perry, H.M., Jr., Perry, E.F., Erlanger, M.W. and Kopp, S.J.

Barium-induced hypertension. In: Advances in modern environ-

mental toxicology. Vol. IX. Princeton Publishing Co., Princeton,

NJ. p. 221 (1985).

Barium (01/90) 6


content -> dam
dam -> Microsoft Word Soc generalresponse az doc
dam -> Blackberry internet cəMİYYƏTİNDƏ ÜNSİYYƏt standartlari
dam -> Data Mining From a to Z
dam -> From cyber-crime to insider trading, digital investigators are increasingly being asked to
dam -> EnCase Forensic Transform Your Investigations
dam -> Send and retrieve files via ftp/sftp using FileZilla
dam -> Böyük Verilənlər üzrə Elmi Tədqiqat və Təlim Mərkəzinin Yaradılması

Dostları ilə paylaş:

©2018 Учебные документы
Рады что Вы стали частью нашего образовательного сообщества.