Toxicological profile for barium and barium compounds

51 

BARIUM AND BARIUM COMPOUNDS 

3.  HEALTH EFFECTS 

dose of 198 mg barium/kg/day as barium chloride in water (Borzelleca et al. 1988).  Increases in relative 

kidney weight (kidney to brain weight ratio) were also observed in female rats receiving gavage doses of 

66, 96, or 138 mg barium/kg/day as barium chloride in water for 10 days, but not at 198 mg 

barium/kg/day (Borzelleca et al. 1988).  Significant reductions in blood urea nitrogen (BUN) were also 

observed in females exposed to 66–198 mg barium/kg/day and in males exposed to 198 mg 

barium/kg/day.  The changes in BUN levels were not considered to be biologically significant because 

BUN levels are typically increased in response to kidney damage, the magnitude of change was slight 

(less than 15%), and there were no differences between the barium-exposed groups.  The changes in 

relative kidney weights or BUN levels were not associated with gross or microscopic renal lesions.  

Studies of rats and mice did not find significant alterations in kidney weights or the incidence of renal 

lesions following a 15-day exposure to 110 or 70 mg barium/kg/day, respectively, as barium chloride in 

drinking water (NTP 1994).   

Exposure of rats to doses as high as 65 mg barium/kg/day for an intermediate duration did not result in 

any alterations in kidney weight or the occurrence of histopathological lesions (McCauley et al. 1985; 

NTP 1994; Tardiff et al. 1980).  At 115 mg barium/kg/day, significant increases in absolute and relative 

kidney weights were observed in female rats (NTP 1994).  Electron microscopy detected glomerular 

lesions consisting of fused podocyte processes and thickening of the capillary basement membrane in rats 

exposed to 150 mg barium/kg/day (McCauley et al. 1985).  At slightly higher doses (180 mg 

barium/kg/day), minimal to mild dilatation of the proximal convoluted tubules of the outer medulla and 

renal cortex was observed in male and female rats (NTP 1994).  In mice, nephropathy characterized by 

mild to moderate tubule dilatation, regeneration, and atrophy was observed in males and females exposed 

to 450 mg barium/kg/day as barium chloride, but not to 205 mg barium/kg/day (NTP 1994). 

Three chronic-duration studies assessed the renal toxicity of barium.  No adverse effects were observed in 

rats exposed via drinking water to 15 mg barium/kg/day of an unspecified barium compound for 68 weeks 

(McCauley et al. 1985), 60 mg barium/kg/day as barium chloride for 2 years (NTP 1994), or lifetime 

exposure to 0.7 mg barium/kg/day as barium acetate (Schroeder and Mitchener 1975a).  In mice, exposure 

to 160–200 mg barium/kg/day resulted in moderate to marked nephropathy, characterized by extensive 

regeneration of cortical and medullary tubule epithelium, tubule dilatation, hyaline cast formation, 

interstitial fibrosis, and glomerulosclerosis (NTP 1994); at the next lowest dose tested (75 mg 

barium/kg/day), the incidence of nephropathy did not differ from controls.  No kidney lesions were 

observed in mice following lifetime exposure to 0.95 mg barium/kg/day as barium acetate (Schroeder and 

Mitchener 1975b). 

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52 

BARIUM AND BARIUM COMPOUNDS 

3.  HEALTH EFFECTS 

Dermal Effects.    

No studies were located regarding dermal effects in humans or animals after oral 

exposure to barium.   

Ocular Effects.    

No studies were located regarding ocular effects in humans after oral exposure to 

barium.  In studies with Sprague-Dawley rats, ocular discharge following administration of a single 

gavage dose of 198 mg barium/kg/day as barium chloride (Borzelleca et al. 1988); this was not reported 

in rats dosed for 10 days (Borzelleca et al. 1988).  A nonsignificant increase in retinal dystrophy was 

observed in rats following intermediate and chronic oral exposure to 12–37.5 mg barium/kg/day as an 

unspecified barium compound (McCauley et al. 1985).  Although the retinal dystrophy was statistically 

insignificant, a dose-related trend was observed if different duration exposure groups were combined 

(McCauley et al. 1985).  Both ocular discharge and retinal dystrophy are commonly observed in Sprague-

Dawley rats; consequently, the ocular lesions noted in these animal studies cannot necessarily be 

attributed to oral barium exposure.  Ocular lesions were not observed in F344 rats or B6C3F1 mice 

exposed to barium chloride in drinking water for 90 days or 2 years to doses as high as 180 mg 

barium/kg/day in rats and 450 mg barium/kg/day in mice (NTP 1994). 

Body Weight Effects.    

Body weight has been monitored in a number of acute, intermediate, and 

chronic studies in which rats and mice were exposed orally to barium compounds (Borzelleca et al. 1988; 

McCauley et al. 1985; NTP 1994; Perry et al. 1983, 1985, 1989; Schroeder and Mitchener 1975a, 1975b; 

Tardiff et al. 1980).  In general, body weight effects have only been observed at lethal doses.  A decrease 

in body weight was observed in rats receiving a single gavage dose of 198 mg barium/kg/day as barium 

chloride (Borzelleca et al. 1988), in rats exposed to 200 mg barium/kg/day as barium chloride in drinking 

water for an intermediate duration (NTP 1994), and in mice exposed to 450 or 160 mg barium/kg/day as 

barium chloride in drinking water for intermediate and chronic durations, respectively (NTP 1994).   

Metabolic Effects. 

Hypokalemia is a common finding in cases of severe barium poisoning (Deng et 

al. 1991; Diengott et al. 1964; Downs et al. 1995; Gould et al. 1973; Jha et al. 1993; Koch et al. 2003; 

Lewi and Bar-Khayim 1964; Phelan et al. 1984; Talwar and Sharma 1979; Wetherill et al. 1981).  In a 

group of cases examined by Deng et al. (1991), serum potassium levels ranged from 0.8 to 2.7 mEq/L; 

normal values range from 3.5 to 5 mEq/L.  Alterations in serum potassium levels have not been reported 

in rats exposed to 110 or 180 mg barium/kg/day as barium chloride in drinking water for 15 or 90 days,, 

respectively (NTP 1994). 

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