Barium oxide, obtained by calcining witherite

Carcinogenicity

Description of key information

No increased tumor incidence in mice (NTP, 1994, NOAEL 160 mg/kg bw/day)
No increased tumor incidence in rats (NTP, 1994, NOAEL 60 mg/kg bw/day)

Key value for chemical safety assessment

Carcinogenicity: via oral route

Endpoint conclusion

Endpoint conclusion:

no adverse effect observed

Dose descriptor:

NOAEL

60 mg/kg bw/day

Study duration:

chronic

Species:

rat

Quality of whole database:

BaO rapidly hydrolyzes to Ba(OH)2, a strongly alkaline substance, upon contact with water. Barium chloride dihydrate as well soluble barium salt was used to assess the potential of BaO to cause barium toxicity. The study was performed similar to OECD TG 451, is well documented and both rats and mice were tested.

Carcinogenicity: via inhalation route

Endpoint conclusion

Endpoint conclusion:

no study available

Carcinogenicity: via dermal route

Endpoint conclusion

Endpoint conclusion:

no study available

Justification for classification or non-classification

No increased incidence of tumors was observed. Therefore, the present data on carcinogenicity do not fulfill the criteria laid down in regulation (EU) 1272/2008, and a non-classification is warrented.

Additional information

BaO rapidly hydrolyzes to Ba(OH)₂, a strongly alkaline substance, upon contact with water. Barium chlorid dihydrate and barium oxide share the barium ion as cation which may be the toxophore of the registered compound barium oxide. For details on comparability of the two compunds, please refer to the weight-of-evidence justification.

Only one study addressing barium compound carcinogenicity exists (NTP, 1994). The study was conducted similar to OECD TG 451 (no information on GLP compliance) and investigated the effects of barium chloride dihydrate on F344/N rats and B6C3F1 mice. The animals were exposed to 0, 500, 1250, or 2500 ppm barium chloride dihydrate via drinking water continuously for two years.

Compound uptake was determined experimentally and allowed calculation of the absolute compound uptake, which was 0, 15, 30, and 60 mg/kg bw/day for male rats in the different dose level groups and 0, 15, 45, or 75 mg/kg bw/day for female rats. At the end of the 2-year study, the animals in the high dose, but not the 1250 ppm group, showed decreased body weight. There were no chemical-related clinical or pathological findings in any of the dose groups. Further, the tumor incidence was not increased in treated animals compared to controls. Male rats showed decreased incidences of adrenal medullar pheochromocytoma and mononuclear cell leukemia.

The compound uptake of mice was higher than that of rats, corresponding to average daily doses of 0, 30, 75, and 160 mg/kg bw/day for males and 0, 40, 90, and 200 mg/kg bw/day for females. This situation might explain why in mice, but not rats, the high dose level group exhibited signs of toxicity, manifested in increased mortality, decreased body weight, and increased incidence of non-neoplastic kidney lesions. In the 1250 ppm dose level group, these effects were not observed. There was no increase in the incidence of neoplasms in any dose level group. In contrast, the incidence of hepatocellular adenoma was decreased in male mice.