TOXICOLOGICAL PROFILE FOR BARIUM AND COMPOUNDS ...

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2. HEALTH EFFECTS
plasma fibrinogen; serum protein, albumin, globulin, bilirubin. creatine,
calcium, phosphorus, chloride, 5'-nucleotidase, glutamic pyruvic transaminase,
glutamic oxaloacetic transaminase, and alkaline phosphatase) (Borzelleca et
al. 1988). Intermediate and chronic oral exposure of rats to barium acetate
and barium chloride in drinking water has not been associated with any
significant or treatment-related changes in a variety,of hematological
parameters (Schroeder and Mitchener 1975a; Tardiff et al. 1980). Elemental
barium doses in these intermediate and chronic drinking water studies ranged
from 0.7 mg/kg/day to 35 mg/kg/day.
Musculoskeletal Effects. The predominant musculoskeletal effect
observed in cases of barium toxicity in humans is progressive muscle weakness,
often leading to partial or total paralysis (Das and Singh 1970; Diengott et
al. 1964; Gould et al. 1973; Lewi and Bar-Khayim 1964; McNally 1925; Morton
1945; Ogen et al. 1967; Phelan et al. 1984; Wetherill et al. 1981). In severe
cases, the paralysis affects the respiratory system (Das and Singh 1970; Gould
et al. 1973; Lewi and Bar-Khayim 1964; Morton 1945; Ogen et al. 1967; Phelan
et al. 1984; Wetherill et al. 1981).
Very limited animal data are available regarding the musculoskeletal
effects of barium following oral exposure. No changes in femur weight and no
gross or microscopic lesions of the femur were observed in rats following
intermediate exposure to doses of 35 mg barium/kg/day as barium chloride in
drinking water (Tardiff et al. 1980). Gross and microscopic lesions of the
sternebrae and femur were not observed in several intermediate and chronic
experiments in which rats were exposed to an unspecified barium compound in
drinking water (McCauley et al. 1985). However, these experiments were flawed
in that barium was detected as a contaminant in the rat chow of both control
and treated animals; consequently, no true "untreated" controls were available
for comparison. Thus, the results should be interpreted with caution.
Hepatic Effects. In one case study involving accidental acute ingestion
of barium carbonate in an adult female, some degeneration of the liver was
noted post-mortem .(McNally 1925). Adverse hepatic effects in animals
following oral barium exposure have been minor or have not been observed.
Decreased liver/brain weight ratio and darkened liver were observed in rats
exposed acutely by gavage to 198 mg barium/kg/day as barium chloride; however,
these changes were not associated with any microscopic hepatic lesions
(Borzelleca et al. 1988). Acute gavage exposure of rats to four doses ranging
from 66 to 198 mg barium/kg/day as barium chloride was not associated with any
significant changes in the activities of serum glutamic pyruvic transaminase
(SGPT), serum glutamic oxaloacetic transaminase (SGOT), or alkaline
phosphatase (ALP) (Borzelleca et al. 1988). Changes in these enzyme levels in
blood can be indicative of liver damage. Significantly reduced blood urea
nitrogen was noted at all exposure doses. A reduction in this particular
blood chemistry parameter is a potential sign of altered liver function.
However, insufficient information was presented in the published study to