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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

Link to relevant study record(s)

Description of key information

Short description of key information on bioaccumulation potential result: 
There were no studies about metabolism and toxicokinetic of the test substance performed. But the available acute and repeated dose toxicity studies on the test substance and structural analogues as well as the physico chemical properties of the test item indicate that the substance is not absorbed after oral or dermal application; there is also no evidence for systemic distribution.

Key value for chemical safety assessment

Bioaccumulation potential:
no bioaccumulation potential

Additional information

Read across justification

The toxicokinetic behaviour of the test item was not determined. Thus, information on kinetics, absorption and excretion are derived from physico chemical properties, experimental data of the subacute repeated dose study and from acute toxicity studies of analogue substances (calcium and di-ammonium salt) since all are salts with similar structures (a detailed read across justification is given in CSR, Annex I).

Statement on toxicokinetics

The available acute oral toxicity study (BASF AG 1981a) indicates that the test substance is not absorbed after oral application. After single application a yellow discoloration of the faeces on day 2 was observed. The time course of this observation suggests that the substance does not enter the enterohepatic cycle. The molecular weight of the test item is higher than 500 g/mol indicating limited gastrointestinal absorption. A 28 day oral toxicity study performed with the di-sodium salt revealed no clinical symptoms or abnormalities (BASF AG 2002a).

Metabolites of the substance were not examined but due to the absence of effects after subacute exposure of a well soluble analogue it is expected that the substance is either not metabolized or reduction by gastrointestinal bacterial or hepatic enzymes leads to formation of non-toxic metabolites. Discoloration of the faeces is a hint for a lack of metabolism, because cleavage of the substance into metabolites would not lead to yellow stained faeces. For the second scenario, release of amino-chloro-toluenesulfonic acid (metabolite 1) and amino-sulfonphenyl-pyrazol (metabolite 2) is possible. Substitution of chlorine from metabolite 1 by glutathione and, thereafter renal and biliary excretion is feasible. Formation of phenylhydroxylamin, leading to met-hemoglobin or acetylation of metabolite 1 is not expected. Regarding metabolite 2, limited information is available for the non-sulfonated, non-amine analogue methyl-phenyl-pyrazolone / Norantipyrin. This analogue substance is metabolized by glucoronidation, methylation or oxidation and was without pathological findings in performed studies. However, the amino group or the hydroxyl group of metabolite 2 might be conjugated, whereby toxic effects can not be excluded. On the other hand, sulfonic acid at phenyl of metabolite 2 enhances elimination without release of toxic metabolites.