The acutely toxic effects of Ba are similar in monogastrics and ruminants. This argues that 1) Ba is a valid water quality concern for livestock and wildlife, and 2) subacute and chronic effects are probably similar, if not identical, between these species. The putative toxic mechanism(s) of the Ba2+ ion in rodents and humans involve physiologic mechanisms that are highly conserved (i.e. very similar) throughout terrestrial mammals; therefore, any species-specific differences in toxicity logically derive from species-specific differences in the toxicokinetics of Ba. In monogastric mammals, the oral toxicity of Ba compounds correlates with their water solubility. Less soluble forms of Ba (notably BaSO4) are poorly absorbed and are thus considerably less toxic than more soluble salts such as BaCl2, barium nitrate (Ba(NO3)2), or barium hydroxide (Ba(OH)2).105 There is no equivalent data in ruminants. Theoretically, reduction of the SO4 salt to sulfide by rumen microflora might result in increased bioavailability of the Ba2+ ion. There is some precedent for differences in metabolism of Ba between monogastrics and ruminants144, but much more needs to be done. As a practical matter, however, this theoretical effect would be significant only in solid feedstuffs as insoluble forms of Ba (i.e. BaSO4) will presumably not be present in drinking water in any significant concentration.
The long-term effects of Ba, especially on reproduction, have been incompletely investigated in any species. A single Russian report of Ba inhalation toxicity describes reproductive lesions in both male and female rats145 whereas more recent rodent studies did not note alterations in reproductive tissues or reproductive function following acute-, intermediate- or chronic-duration exposure to Ba.129,131,132 Kidney damage was observed in laboratory rodents following two-year exposure to 200 mg Ba/kg BW and in long-term (91-day) oral exposure to 450 mg Ba/kg BW, but it was not seen after administration of 250 mg Ba/kg BW for 36-46 weeks.131,132
The only quantitative data available in cattle indicates 138 mg Ba/kg BW, as BaCO3 in dry feedstuffs was acutely toxic to steers, whereas 69 mg Ba/kg BW was not.117 Assuming water consumption of 20% BW, this translates to 690 mg Ba2+/L in drinking water as being acutely toxic or 345 mg Ba2+/L as the NOAEL. This contrasts with the report of Richards et al.116 that 2 mg soluble Ba2+/L water, plus some undetermined amount of Ba from sediment, was immediately toxic to cows and calves. It is also much higher than the toxic dose reported in goats, where 7 mg/kg BW BaCl2(4.6 mg Ba/kg BW) was lethal.115 It is likely that BaCO3 in feed is not as bioavailable as the Ba2+ ion in water. The acutely lethal dose in the goat study translates to 23 mg Ba2+/L under the assumptions outlined in the Introduction.
Obviously, much more research needs to be done with Ba in ruminants, but, given the current state of knowledge, soluble Ba2+ concentrations should be held to well below 23 mg/L to avoid acute toxicity. There is absolutely no data on chronic Ba2+ ion toxicity in any of our species of interest. This, plus the limited and conflicting data from chronic studies in other animals, makes it impossible to postulate a long-term "safe" level of the Ba2+ ion in drinking water for domestic livestock and/or wildlife species with any degree of certainty.
We do not recommend using water containing more than 10 mg Ba2+/L even for short periods. Until there is better data, it is impossible to make any recommendations regarding chronic exposure.Back to Index