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
9
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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