Toxicity Profiles
Condensed Toxicity Summary for BARIUM
NOTE: Although the toxicity values presented in these toxicity profiles were correct at the time they were produced, these values are subject to change. Users should always refer to the Toxicity Value Database for the current toxicity values.
Prepared by A. A. Francis, M.S., D.A.B.T., and Carol S. Forsyth, Ph.D., Chemical Hazard Evaluation Group in the Biomedical and Environmental Information Analysis Section, Health Sciences Research Division, *.
Prepared for OAK RIDGE RESERVATION ENVIRONMENTAL RESTORATION PROGRAM
*Managed by Martin Marietta Energy Systems, Inc., for the U.S. Department of Energy under Contract No. DE-AC05-84OR21400
The soluble salts of barium, an alkaline earth metal, are toxic in mammalian systems. They are absorbed rapidly from the gastrointestinal tract and are deposited in the muscles, lungs, and bone. Barium is excreted primarily in the feces.
At low doses, barium acts as a muscle stimulant and at higher doses affects the nervous system eventually leading to paralysis. Acute and subchronic oral doses of barium cause vomiting and diarrhea, followed by decreased heart rate and elevated blood pressure. Higher doses result in cardiac irregularities, weakness, tremors, anxiety, and dyspnea. A drop in serum potassium may account for some of the symptoms. Death can occur from cardiac and respiratory failure. Acute doses around 0.8 grams can be fatal to humans.
Subchronic and chronic oral or inhalation exposure primarily affects the cardiovascular system resulting in elevated blood pressure. A lowest-observed-adverse-effect level (LOAEL) of 0.51 mg barium/kg/day based on increased blood pressure was observed in chronic oral rat studies (Perry et al. 1983), whereas human studies identified a no-observed-adverse-effect level (NOAEL) of 0.21 mg barium/kg/day (Wones et al. 1990, Brenniman and Levy 1984). The human data were used by the EPA to calculate a chronic and subchronic oral reference dose (RfD) of 0.07 mg/kg/day (EPA 1995a,b). In the Wones et al. study, human volunteers were given barium up to 10 mg/L in drinking water for 10 weeks. No clinically significant effects were observed. An epidemiological study was conducted by Brenniman and Levy in which human populations ingesting 2 to 10 mg/L of barium in drinking water were compared to a population ingesting 0 to 0.2 mg/L. No significant individual differences were seen; however, a significantly higher mortality rate from all combined cardiovascular diseases was observed with the higher barium level in the 65+ age group. The average barium concentration was 7.3 mg/L, which corresponds to a dose of 0.20 mg/kg/day. Confidence in the oral RfD is rated medium by the EPA.
Subchronic and chronic inhalation exposure of human populations to barium-containing dust can result in a benign pneumoconiosis called "baritosis." This condition is often accompanied by an elevated blood pressure but does not result in a change in pulmonary function. Exposure to an air concentration of 5.2 mg barium carbonate/m3 for 4 hours/day for 6 months has been reported to result in elevated blood pressure and decreased body weight gain in rats (Tarasenko et al. 1977). Reproduction and developmental effects were also observed. Increased fetal mortality was seen after untreated females were mated with males exposed to 5.2 mg/m3 of barium carbonate. Similar results were obtained with female rats treated with 13.4 mg barium carbonate/m3. The NOAEL for developmental effects was 1.15 mg/m3 (equivalent to 0.8 mg barium/m3). An inhalation reference concentration (RfC) of 0.005 mg/m3 for subchronic and 0.0005 mg/m3 for chronic exposure was calculated by the EPA based on the NOAEL for developmental effects (EPA 1995a). These effects have not been substantiated in humans or other animal systems.
Barium has not been evaluated by the EPA for evidence of human carcinogenic potential
(EPA 1995b).
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Last Updated 10/07/97