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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

Description of key information

There are no acute toxicity data for the potassium salts of DTPMP. Therefore data from the sodium salts have been read across. 
In a well conducted acute oral toxicity study (Safepharm Laboratories, 1982) carried out using a protocol comparable to the now deleted OECD 401, and to GLP, the LD50 for the sodium salt of DTPMP was >10 ml/kg bw in rats (>5838 mg active salt/kg bw, equivalent to >4602 mg parent acid).
In an acute dermal toxicity study (Safepharm Laboratories, 1982) conducted using a protocol comparable to OECD 402, and to GLP, the LD50 for the sodium salt of DTPMP was >10 ml/kg bw (>5838 mg active salt/kg bw, equivalent to >4602 mg parent acid) in rats.
There are no data for the inhalation route.

Key value for chemical safety assessment

Additional information

The most reliable studies for read-across substance sodium salt of DTPMP were selected as the key studies as the effects of the potassium and sodium counterions are not expected to differ significantly. In addition supporting studies also showed sodium salts of DTPMP and DTPMP (acid) to be of low acute toxicity. The key read across study for acute oral toxicity reports an LD50 of >10 ml/kg, which is presumed to be equivalent to >5838 mg/kg active salt, which in turn calculates to >4602 mg/kg parent acid. The same calculation stands true for the acute dermal toxicity LD50 final reading.

Data is also available for the calcium sodium salt of DTPMP which has been used as supplementary evidence for lack of toxicity. An acute oral and dermal LD50 of >2000 mg/kg were reported in reliable literature (Safepharm 2001). In both studies, the test substance comprised of 18% active acid, which would equate to an LD50 of >360 mg/kg. While the LD50 expressed as an acid is not a definitive demonstration of lack of toxicity seeing that the amount tested falls below classification threshold, the result supports key data which is of low acute toxicity.

In in vivo toxicity studies the local pH and ionic conditions within the stomach, GI tract etc. dominate the speciation of the phosphonate, irrespective of the form originally dosed. At a defined pH, a salt will behave no differently to the parent acid, at identical concentration of the particular speciated form present, and will be fully dissociatedto yield DTPMP acid and potassium. Hence some properties for a salt (in contact with water or in aqueous media) can be directly read across (with suitable mass correction) to the parent acid and vice versa (see CSR for mass correction values). In the present context the effect of the alkaline metal counter-ion (sodium/potassium/calcium) will not be significant and has been extensively discussed in the public literature. In biological systems and the environment, polyvalent metal ions will be present, and the phosphonate ions show very strong affinity to them.

Justification for classification or non-classification

The available read across data do not suggest that potassium salts of DTPMP should be classified for acute toxicity by any route.