Systolic blood pressures and body weights were measured at 1, 2, 4, 8, 12, and 16
months, and organs (heart, liver, kidney, and aorta) were collected, weighed, and assayed for
barium at 1, 4, and 16 months. No change in mean systolic blood pressure was seen in groups
exposed to 1 ppm barium in the drinking water. However, after groups were exposed for 8
months to 10 ppm, mean systolic blood pressure increased by 6 mm Hg (p<0.01) and continued
to be significantly elevated through 16 months (+4 mm Hg, p<0.01). Significant increases
(p<0.01) in mean systolic blood pressure were evident at 100 ppm starting at 1 month (+12 mm
Hg) and continuing through 16 months (+16 mm Hg) of exposure. An additional 12 rats exposed
for 16 months to 100 ppm had reduced ATP and phosphocreatinine content of the myocardium,
depressed rates of cardiac contraction, and depressed electrical excitability of the heart as
compared with an additional control group of 18 rats. No mortality was reported. Growth rates
were unaffected by barium, as were tissue weights. Both 10 and 100 ppm barium resulted in
significant increases in tissue barium. This study identifies a NOAEL of 1 ppm (0.17 mg Ba/kg-
day) and a LOAEL of 10 ppm (0.82 mg Ba/kg-day) for hypertension in rats maintained on low-
mineral-content diets.
4.2.1.8. Schroeder and Mitchener (1975a, b)
Schroeder and Mitchener (1975a) exposed Long-Evans rats (52/sex/group) to 0 or 5 ppm
barium (as barium acetate) in drinking water from weaning to their natural death. Dosages from
drinking water were estimated to be 0.61 mg Ba/kg-day for males and 0.67 mg Ba/kg-day for
females, using reference body weights and water intakes from U.S. EPA (1988). The diet was
characterized as a “low metal” diet, and it included 60% rye flour, 30% dried skim milk, 9%
corn oil, 1% iodized table salt, and assorted vitamins; the barium content was not reported.
Barium administration had no significant effect on the growth of males but increased the growth
of older females. The lifespan of the rats was not significantly affected. The incidence of
proteinuria in males exposed to barium for approximately 152 days (at 173 days of age) was
significantly higher (p<0.05) than in controls; proteinuria was assessed by a dipstick method.
Female rats at 532 and 773 days of age had higher (p<0.001) serum cholesterol concentrations
than did controls tested at 516 and 769 days of age. Serum glucose levels for males at these ages
were also different from controls but did not follow an age-related pattern. The authors attached
no biological or toxicological significance to these serum chemistry results. Histopathology of
heart, lung, kidney, liver, and spleen did not reveal alterations. No significant increases in the
gross number of tumors were observed in the barium-exposed male (8/30) or female (15/33) rats
as compared with the controls (4/26 and 17/24, respectively). This study identifies a LOAEL of
0.61 mg Ba/kg-day for renal glomerular damage evidenced as proteinuria in male rats
maintained on low-mineral diets.
26
Schroeder and Mitchener (1975b) exposed white mice of the Charles River CD strain
(36-54/sex) to 0 or 5 ppm barium (as barium acetate) in drinking water for their lifetimes. Doses
from drinking water were 1.18 mg Ba/kg-day for males and 1.20 mg Ba/kg-day for females (U.S.
EPA, 1988). The diet was characterized as a “low-metal” diet, and it included 60% rye flour,
30% dried skim milk, 9% corn oil, 1% iodized table salt, and assorted vitamins; the barium
content of the diet was not reported. Growth and body weights were not affected by the barium
treatment. Histology of the heart, lung, liver, kidney, and spleen was normal. In males,
longevity (defined as the mean lifespan of the last surviving five animals of each sex in each
treatment group) was significantly reduced (p
#
0.025); longevity of the barium-treated males was
815 days compared with 920 days for the controls. The mean lifespan, however, was not
affected. The incidences of lymphoma plus leukemia, and lung tumors in the male (7/37 and
4/37, respectively) and female (5/21 and 3/21, respectively) mice exposed to barium were not
significantly different from the incidences in the control mice (3/38 and 3/47 for lymphoma and
leukemia in males and females, respectively, and 5/38 and 9/47 for lung tumors).
4.2.2. Inhalation Exposure
Data on the toxicity of barium compounds in animals following inhalation exposure are
limited to a subchronic study conducted by Tarasenko et al. (1977). In this study, male albino
rats (strain and number of animals per group were not reported) were exposed to 0, 1.15, or 5.2
mg/m
3
barium carbonate (0, 0.8, or 3.6 mg Ba/m
3
) for 4 hours/day, 6 days/week for 4 months.
No information on aerosol generation or the size distribution of the particles was reported. In the
introduction section of the paper, the authors stated, “We have demonstrated by electron
microscopy that the size of almost 80% of the dust particles is less than 2
:
m”; however, it is not
known if this statement refers to the aerosols generated for this study. The following endpoints
were used to assess toxicity: body weight gain, arterial pressure, hematology (hemoglobin,
leukocytes, and thrombocytes) and serum chemistry (glucose, phosphorus, total protein, alkaline
phosphatase, and cholinesterase) parameters, urine calcium levels, bromosulfophthalein test of
liver function, EKG measurement, and histologic examination (tissues examined were not
listed).
The authors noted that no alterations were observed in the rats exposed to 1.15 mg/m
3
barium carbonate. In the 5.2 mg/m
3
group, a number of alterations were reported; however, it
does not appear that the data were statistically analyzed. The alterations included a 21%
decrease in body weight gain, a 32% increase in arterial pressure, altered hematology parameters
(decreases in hemoglobin and thrombocyte levels and increases in leukocyte levels), altered
serum chemistry parameters (decreased sugar and total protein levels, increased phosphorus
levels, decreased alkaline phosphatase activity, and increased cholinesterase activity), increased
27