Toxicological profile for barium and barium compounds

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BARIUM AND BARIUM COMPOUNDS 

3.  HEALTH EFFECTS 

3.8.2 

Biomarkers Used to Characterize Effects Caused by Barium  

Reports of individuals exposed to high levels of barium suggest that cardiovascular, nervous, and 

gastrointestinal systems are targets of barium toxicity (Das and Singh 1970; 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; McNally 1925; Ogen et al. 1967; Phelan et al. 1984; Talwar and Sharma 1979; Wetherill et al. 

1981).  The likely cause of most of these effects is barium induced hypokalemia.  Gastrointestinal 

disturbances are usually the first symptoms of acute barium exposure.  Hypokalemia, hypertension, and 

abnormalities in heart rhythm frequently occur shortly afterwards.  General muscle weakness is a frequent 

symptom, sometimes followed by paralysis.  Nerve conduction is often affected, resulting in numbness 

and tingling of the mouth, neck and extremities.  Loss of deep tendon reflexes may also occur.  Not all 

symptoms appear in every case of acute barium poisoning.  Although the observation of hypokalemia and 

gastrointestinal upset may be indicative of exposure to high doses of barium, other toxicants and disease 

states can produce these effects.   

Animal studies also suggest that the kidney is a target of barium toxicity; the observed nephropathy is not 

specific to barium and would not be a sensitive biomarker of effect. 

3.9 

INTERACTIONS WITH OTHER CHEMICALS  

There are no data regarding the interaction between barium and various chemicals potentially found at 

hazardous waste sites.  However, there are data that suggest that barium may interact with other cations 

and certain prescription drugs.  Drug interactions are of relevance because individuals exposed to barium 

by living or working near hazardous waste sites contaminated with this substance may also be taking 

prescription drugs. 

The cations potassium, calcium, and magnesium also interact with barium.  Barium exposure, for 

example, may cause a buildup of potassium inside the cell resulting in extracellular hypokalemia, which 

is believed to mediate barium-induced paralysis.  In fact, potassium is a powerful antagonist of the 

cardiotoxic and paralyzing effects of barium in animals (Foster et al. 1977; Jaklinski et al. 1967; Roza and 

Berman 1971; Schott and McArdle 1974) and is used as an antidote in cases of acute barium poisoning.  

Calcium and magnesium suppress uptake of barium by pancreatic islets in vitro.  Conversely, barium, in 

low concentrations, stimulates calcium uptake in these cells.  Although the data are insufficient to 

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BARIUM AND BARIUM COMPOUNDS 

3.  HEALTH EFFECTS 

determine the significance of these findings to human health effects, displacement of calcium may be the 

mechanism by which barium stimulates insulin release (Berggren et al. 1983). 

Among the drugs that are known to interact with barium, the barbiturates sodium pentobarbital and 

phenobarbital, were found to have an increased depressive effect on the hearts of rats exposed to barium 

(Kopp et al. 1985; Perry et al. 1983, 1989).  This hypersensitivity of the cardiovascular system to 

anesthesia was not observed in similarly treated animals that were anesthetized with xylazine plus 

ketamine.  Results of the study indicated that the hypersensitivity was specific to the barbiturates and not 

a generalized effect of anesthesia (Kopp et al. 1985). 

Other medically prescribed drugs interact with barium.  Experiments with mice indicated that atropine 

significantly antagonized antinociception and death induced by intracerebroventricular injection of 

barium chloride (Segreti et al. 1979; Welch et al. 1983).  These same studies also found that naloxone, a 

narcotic antagonist, inhibited the lethal toxicity of barium (Segreti et al. 1979; Welch et al. 1983).  

Propranolol had no effect on barium-induced paralysis in rats (Schott and McArdle 1974).  Verapamil 

rapidly abolished cardiac dysrhythmias in rabbits injected with barium chloride (Mattila et al. 1986).  In 

the same study, pretreatment with the tricyclic antidepressant, doxepin, was found to offer some 

protection against barium-induced dysrhythmias (Mattila et al. 1986).  Ouabain, which is an inhibitor of 

Na

+

-K

+

 ATPase, while not widely prescribed, has been shown to rapidly reverse the paralyzing effects of 

barium.  It has been hypothesized that ouabain works by reducing barium-induced hypokalemia by 

allowing some intracellular potassium to escape.  However, this hypothesis has not yet been proved or 

disproved because of the complexity of the mechanism involved (Schott and McArdle 1974). 

Other substances can affect barium pharmacokinetics.  One study showed that sodium alginate could 

reduce retention of orally administered barium, possibly by inhibiting absorption in the gut (Sutton et al. 

1972).  This could be useful in treating cases of acute barium ingestion.  Lysine and lactose increase 

absorption of barium and could increase the toxic effects of oral exposure (Lengemann 1959). 

A human study involving one adult female was performed by applying barium chloride, alone and in 

combination, with dimethyl sulfoxide to the cervical epithelium.  Dimethyl sulfoxide significantly 

enhanced the ability of barium chloride to induce dysplasia with unusual cell formation in the cervical 

epithelium (Ayre 1966).  The significance of this is difficult to determine since there was only one 

subject, there were no controls, and few details of the experiment were provided. 

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