Toxicological Review of Barium and Compounds

3.2.  DISTRIBUTION 

The highest concentrations of barium in the body are found in the bone; approximately 

91% of the total body burden is in the bone (WHO, 1990).  Bauer et al. (1956) reported that 

barium accretion rates for whole skeleton, tibia, and incisors were 1.4 - 2.4 times greater than 

accretion rates for calcium.  Reeves (1986) noted that osseous uptake of barium is 1.5 to 5 times 

higher than that of calcium or strontium.  In the bone, barium is primarily deposited in areas of 

active bone growth (WHO, 1990).  The uptake of barium into the bone appears to be rapid.  One 

day after rats were exposed to barium chloride aerosols, 78% of the total barium body burden 

was found in the skeleton; by 11 days postexposure, more than 95% of the total body burden was 

found in the skeleton (Cuddihy et al., 1974). 

The remainder of the barium in the body is found in soft tissues (i.e., aorta, brain, heart, 

kidney, spleen, pancreas, and lung) (WHO, 1990).  High concentrations of barium are sometimes 

found in the eye, primarily in the pigmented structures (Reeves, 1986).  McCauley and 

Washington (1983) found that 24 hours after administration of an oral dose of 

131

BaCl

2

 to dogs, 

131

Ba levels in the heart were three times higher than the concentration in the eye, skeletal 

muscle, and kidneys (concentrations in the eye, muscle, and kidneys were similar).  Additionally, 

the levels in the heart, eye, skeletal muscle, and kidneys were higher than the whole-blood 

concentration, suggesting the ability of soft tissue to concentrate barium. 

3.3.  ELIMINATION AND EXCRETION 

Barium is excreted in the urine and feces following oral, inhalation, and parenteral 

exposure.  The feces are the primary route of excretion.  For an intake level of 1.33 mg/day 

(1.24, 0.086, and 0.001 mg/day from food, water, and air, respectively), approximately 90% of 

the barium is excreted in the feces and 2% in the urine (Schroeder et al., 1972).  Tipton et al. 

(1969) found similar results; in the two men studied, 95%-98% and 2%-5% of the daily barium 

intake was excreted in the feces and urine, respectively.  A physical half-time of 12.8 days was 

estimated in beagle dogs following inhalation exposure to 

140

BaCl

2

 –

140

LaCl

2

 (AMAD of 1.6-2.1 

:

m, 

F

g

 of 2.0) (Cuddihy and Griffith, 1972). 

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4.  HAZARD IDENTIFICATION

4.1.  STUDIES IN HUMANS—EPIDEMIOLOGY, CASE REPORTS, AND CLINICAL 

CONTROLS 

4.1.1.  Oral Exposure 

Wones et al. (1990) administered barium (as barium chloride) in drinking water to 11 

healthy male volunteers (4 African-Americans and 7 Caucasians) whose ages ranged from 27 to 

61 years (mean 39.5 and median 41).  None of the subjects reported taking any medications and 

none had hypertension, diabetes, or cardiovascular disease.  Barium concentrations in the 

drinking water consumed by the subjects prior to the study were not reported.  The subjects were 

given 1.5 L/day of distilled water containing various levels of barium chloride.  No barium was 

added for the first 2 weeks, which served as a control period. For the next 4 weeks, 5 ppm 

barium (0.11 mg/kg-day using 70 kg reference body weight) were added, and 10 ppm barium 

(0.21 mg/kg-day) were added for the last 4 weeks of the study.  Diets were controlled to mimic 

American dietary practices.  Barium content of the diet was not determined, but the authors 

noted that a typical hospital diet provided 0.75 mg/day barium, or 0.011 mg/kg-day using 70 kg 

body weight.  All beverages and food were provided, and subjects were instructed to consume 

only what was provided.  The subjects were instructed to keep their levels of exercise constant 

and to abstain from alcohol.  Smokers were told to maintain their normal smoking habit 

throughout the study.  Systolic and diastolic blood pressures were measured in the morning and 

evening.  Blood was collected at the beginning and periodically throughout the study, including 

four consecutive daily samples at the end of each of the three study periods.  Twenty-four-hour 

urine collections were performed at the end of each study period.  Twenty-four-hour continuous 

electrocardiographic monitoring was performed on 2 consecutive days at the end of each study 

period. 

Blood pressures were not significantly affected by barium exposure at any dose level.  No 

significant alterations in serum calcium levels were observed (9.11, 9.23, and 9.23 mg/dL at the 

0, 5, and 10 ppm exposure levels, respectively).  When the serum calcium levels were 

normalized for differences in albumin levels, a significant increase (p=0.01) was observed (8.86 

vs. 9.03 and 9.01 mg/dL, respectively).  This type of adjustment has been criticized as unreliable 

(Sutton and Dirks, 1986).  Wones et al. (1990) attributed the increase in adjusted serum calcium 

levels to a slight decrease in serum albumin.  The increase in serum calcium levels was 

considered borderline and not clinically significant.  No significant changes were observed in 

plasma total cholesterol, triglyceride; LDL or HDL cholesterol; LDL:HDL ratio; apolipoproteins 

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A1, A2, and B; serum glucose, albumin, and potassium levels; or urinary levels of sodium, 

potassium, vanillylmandelic acid, or metanephrines.  Electrocardiograms revealed no changes in 

cardiac cycle intervals, including the QT interval.  The study authors noted that the lack of 

shortening of the QT interval provided evidence that the slight increase in serum calcium was 

not clinically significant.  In addition, no significant arrhythmias, no increase in ventricular 

irritability, and no apparent conduction problems were seen with barium exposure. 

Brenniman et al. (1981, 1979) (portions of these studies were later published as 

conference proceedings [Brenniman and Levy, 1984]) reported the results of retrospective 

mortality and morbidity studies conducted in Illinois communities.  In the first study, 1971-1975 

cardiovascular mortality rates for Northern Illinois communities with elevated levels of barium 

in their municipal drinking water (2-10 mg/L) were compared to matched communities with low 

levels of barium in their drinking water (

#

0.2 mg/L).  Barium was the only drinking water 

contaminant that exceeded drinking water regulations in any of the public drinking water 

supplies at the time of the study.  The communities were matched for demographic 

characteristics and socioeconomic status.  Communities that were industrialized or 

geographically different were excluded.  Although the study attempted to exclude communities 

with high rates of population change, two of the four high-barium communities had about 75% 

change in population between 1960 and 1970 and were retained in the study. 

Mortality rates for cardiovascular diseases (combined), heart diseases (arteriosclerosis), 

and “all causes” for both males and females were significantly higher (p

#

0.05) in the elevated 

barium communities compared with the low-barium communities.  These differences were 

largely confined to the population 65 years old or older.  The study authors advised caution when 

interpreting these results because they did not control for several important variables, such as 

population mobility, use of water softeners that would increase barium and reduce sodium 

concentrations, use of medication by study subjects, and other risk factors, such as smoking, diet, 

and exercise. 

The morbidity study examined two communities, McHenry (n=1197) and West Dundee 

(n=1203), which had similar demographic and socioeconomic characteristics but a 70-fold 

difference in barium concentrations in drinking water.  The mean concentration of barium in 

McHenry drinking water was 0.1 mg/L, whereas the mean concentration in West Dundee 

drinking water was 7.3 mg/L.  EPA estimated the barium dose for these populations using the 

standard exposure values of 2 L/day and 70 kg body weight.  The estimated doses were 0.0029 

and 0.21 mg/kg-day for McHenry and West Dundee, respectively.  The levels of other minerals 

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