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Administrative data

Key value for chemical safety assessment

Additional information

The substance Potassium Phosphonate did not induce reverse mutation in Salmonella typhimurium or Escherichia coli (Scarcella, 2013) and not induce mutation at the TK locus of L5178Y mouse lymphoma cells (Bisini, 2013).

Statistically significant increases in the incidence of micronucleated cells were observed in Chinese hamster V79 cells after in vitro treatment in the absence of S9 metabolic activation. Since the positive result is obtained from the test without methabolic activation it is reasonable to state that an in vivo study is not to be proposed in regards of the animal welfare, because methabolism prevent to express the suspected mutagenic potential.


Further considerations need to be made based on the DAR, volume 3, Annex B, B.6, April 2005 in the framework of the assesment of the substance for PPP application.

From the DAR in fact the following considerations need to be taken into account:

The salt dissociates in water to potassium and phosphite, which is readily excreted via urine and faeces.

However, there is evidence for lacking in vivo mutagenicity of phosphite from available information on the comparable active substance Fosety 1-Al: According to the U.S. EPA Registration Eligibility Document for Fosetyl-Al, eight mutagenicity tests performed with Fosetyl-Al were negative (US EPA OPP 1990). The tests included two micronucleous test in Swiss mice and CD1 mice. Fosety I-Al did not produce a mutagenic effect in any of the test

A review is available for the micronucleus test that was conducted according to OECD Guideline 474 with CD1 mice. The study was done at doses ranging from 0.6 to 3.6 g/kg (which is 75% of its LD50 value) (FELKNER 1982). A more detailed review of the same study is available from the Netherlands RIVM, Centre for Substances and Risk Assessment (BAARS 1998):

Groups of CDI mice (5 mice/sex/dose) were given orally 1 or 2 doses of 0, 600, 1200, 2400 and 3600 mg Fosetyl-Al/kg, separated by hour interval. The vehicle was 10% aqueous acacia. No increase in the incidence of polychromatic erythrocytes with micronuclei was observed in the bone marrow of any of the treatment groups, 30 hours after the single dose or 24 hours after the second dose.

Remark: The dose levels given corresponded to 12.5, 25, 50 and 75% of the acute oral LD5o (4800 mg Fosetyl-Al /kg). All animals that received 1 or 2 doses of 3600 mg Fosetyl-Al/kg per oral and 10% of those given a single dose of 2400 mg Fosetyl-Al/kg died. At the dose level of 2400 mg Fosetyl-Al /kg at 30 and 48 hours slight cytotoxicity (a decrease in polychromatic erythrocytes and nucleated cells) was observed. Thus, only mice given the 3 lower dose levels were evaluated.

Since Fosetyl Al has been shown to release phosphite anions, the results of these studies are applicable to Potassium phosphite. It is, therefore, reasonable to conclude that potassium phosphite is not mutagenic. If it were, the effect would be reflected in the tests for Fosetyl-Al.

Severalvitroandin vivomutagenicity studies were performed with Fosetyl-Al. Some of these are briefly discussed by the U.S. EPA (US EPA OPP 1990), and some, in more depth, by BAARS et al. (1998). The tests included two Ames tests with S.typhimirium,two phage induction tests using E. coli, two micronucleus tests in Swiss mice and CD-1 mice, one DNA repair test using E.colt,and onesaccaromicae cerevisiaeassay. BAARS et al. (1998) described a chromosome aberration test on mammalian cells, in which no increase was found in the number of cells with chromosome aberrations, following three hours of exposure of the cells to doses of 3 - 100 mg Fosety I-Al/ml culture medium.

Based on consistent negative results of eight studies, the U.S. EPA concluded that Fosetyl-Al is not a mutagen. Due to the fact that Fosetyl-Al releases phosphite, this conclusion is applicable to Potassium Phosphite. Each molecule of Fosetyl-Al releases 3 molecules of phosphite. Therefore, if phosphite was a mutagen, this would be reflected in the results of the studies with Fosetyl-Al. Potassium ion is not mutagenic.


Furthermore, an oncogenicity feeding study with monosodium phosphite was conducted in rats. The study is applicable to Potassium Phosphite. According to GREGER et al. (1991) sodium and potassium salts have the same toxicokinetics effects. Ingestion of inorganic anions, increased urinary excretion of anions, whether the anions were ingested as sodium or as potassium salts. Thus, informationon studies with sodium phosphite can be used to make inferences to Potassium Phosphite


Based on all above considerations no proposal for genotoxicity is made for potassium phosphonate.

Justification for selection of genetic toxicity endpoint
No selection can be made, since the assessment is made on a Weight of evidence approach

Short description of key information:
Non mutagen

Endpoint Conclusion: No adverse effect observed (negative)

Justification for classification or non-classification

The substance is not classified genetic mutagen because it doesn't meet the classification criteria of the CLP regulation n. 1272/2008:

- Category 1 (1A; 1B): substances known to induce heritable mutations or to be regarded as if they induce heritable mutations in the germ cells of humans. Substances known to induce heritable mutations in the germ cells of humans;

- Category 2: substances which cause concern for humans owing to the possibility that they may induce heritable mutations in the germ cells of humans.