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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

No data available on mammalian Adsorption, Distribution, Metabolism, Excretion (OECD TG 417). From its toxicological profile the substance is characterised by local irritation or corrosion depending on the concentration applied. General systemic effects are considered to be secondary and caused by repeated (primary) local toxicity. Bioavailability of parent compound is unlikely because of its direct chemical reactivity. Bioaccumulation of this ionic compound is not expected because of the low log Pow.

Key value for chemical safety assessment

Bioaccumulation potential:
no bioaccumulation potential

Additional information

ADME testing is considered not necessary because of the existing comprehensive toxicity data package for the oral and the dermal route. It could be demonstrated that primary toxicity of THPC causes local effects at the site of first contact and no metabolism is necessary.

ADME is considered not necessary because of limited exposure with THPC during its life cycle: Formulation and application includes three chemical reactions of the THPC molecule (Urea, Ammonia, Hydrogenperoxide) resulting in polymeric coating on cotton fabris. Further, there is low migration from fabrics treated with tetrakis(hydroxymethyl) phosphonium chloride (THPC)-urea (CPSC, 1999, 2001; Environmental Health Criteria 218, 2000).

ADME is considered not necessary because of the reactive nature of THPC. Systemic bioavailability of THPC is therefore unlikely.

Degration of THPC is spontaneous at basic pH (Paulus, 2005, part I-chapter The abstaction of the ß-proton of 1-hydroxyalkyl phoshphonium ion results in the release of formaldehyde and the in situ formation of Tri hydroxymethyl phosphine (THP), a strong reducing agent. It is able to reduce disulphide aminoacid (cystine) residues of microbial cell entities to SH amino (cysteine) components. The phosphine is converted (inactivated) to phosphine oxide. It should be noted that the chemistry of the Tetrakis hydroxymethyl phosphonium ion is driven by the electrochemistry of the phosphine species. Phosphines exist in the +3 oxidation state and most phosphine chemistry results in a phosphorus +5 species.

Its reactivity as well as the hydrophilic nature makes bioaccumulation of THPC unlikely. An estimation of the BCF by means of EPIWIN supports negative bioaccumulation potential. THPC has been shown to react electrophilically with guanosine at the 2-amino position to give N-(bis (hydroxymethyl) phosphino) methyl guanosine (Loewengart, van Duuren, 1976). In vitro, THPC is genotoxic. In vivo, no mutagenicity has been found.

Bioaccumulation of this ionic compound is not expected because of the low log Pow.