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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.

The new ECHA CHEM database has been released by ECHA, and it now contains all REACH registration data. There are more details on the transition of ECHA's published data to ECHA CHEM here.

Diss Factsheets

Administrative data

Key value for chemical safety assessment

Additional information

Only one study rated as reliable (with restriction) is available for selenous acid.

Itoh (1996) described the induction of micronuclei in the bone marrow of mice following i.p. exposure towards selenous acid (H2SeO3). A significant increase in micronucleated cells was observed, with a clear positive finding in the maximum dose of 5 mg/kg. All lower dose levels were in the range of the control (0.0-0.3% MNPCE). However, the dose selection was not clearly justified and a description of the toxic effects is lacking. As stated below one might speculate that the maximum dose already showed signs of near-lethal toxicity, making this positive finding of questionable biological significance. Due to reporting deficiencies this reference will only be used as supportive information.

The findings in the in vivo test for selenites (Itoh, 1996) indicate that positive findings are only obtained at very high, near lethal doses.

Furthermore, an overwhelming database of positive findings for other selenium compounds in in vitro tests was identified during the literature search and in the ATSDR (2003). However, especially for metal compounds false positive findings have repeatedly been published which, can be attributed to osmolality or pH instead of genotoxic effects exerted by the metal ion itself and are therefore of limited biological relevance.

Furthermore, the risk assessment document published by the European Food Safety Authority (EFSA, 2006) summarise the genotoxic effects of selenium compounds as follows: “In vivo, only toxic amounts were shown to be active, keeping in mind the central role of hydrogen selenide in the metabolism of most selenium compound it is likely that overproduction of this and other auto-oxidisable selenium metabolites could promote the formation of DNA reactive oxygen radicals. [...] Genotoxicity has been seen in a number of in vitro systems and also in vivo at toxic doses. It is likely, however, that these effects may be related to the generation of reactive oxygen radicals, being dose dependent and showing a threshold in vivo and not occurring at nutritionally adequate intakes.

Based on the above given information it can be concluded that in vivo clastogenic effects may occur at high, nearly lethal doses which are not attributable to exposure conditions for workers, consumers and humans exposed via the environment. Thus, this effect is considered of no biological relevance for humans.


ATSDR (2003). Agency for toxic substances and disease registry. Toxicological profile for selenium. U.S. Department of Health and Human Services, Public Health Services, Atlanta, Georgia.

Selenium, In: European Food Safety Authority (EFSA) (2006) Tolerable upper intake levels for vitamins and minerals, page 65f.

Endpoint Conclusion:

Justification for classification or non-classification

Only one reliable study is available for selenous acid and these data should only be used as supportive information. The effect observed in this study is considered of no biological relevance for humans. The classification criteria according to regulation (EC) 1272/2008 are not

met, and no classification is required for selenous acid.