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Polyphosphoric acid is a mixture of the corresponding acids to phosphate anion and its condensed phosphates as follows:

- orthophosphoric acid or phosphoric acid (17 -76%),

- pyrophosphoric acid (23 -50%),

- triphosphoric acid (1.5 -25%),

- tetraphosphoric acid (0 -12%)

- and pentaphosphoric acid (0 -7%).


A condensed phosphate anion M(n+2)PnO(3n+1)has one or several P-O-P bonds and has been obtained by heating (dehydration). When the substance polyphosphoric acid is in contact of excess of water, a rapid hydrolysis is observed with the longer chains (tri, tetra or penta) while a very slow hydrolysis is observed for the dimer form to ortho phosphate. The pyrophosphate ion is the simplest form of a condensed phosphate group. As the group contains only two phosphate groups, both of the phosphorus ions are classified as “terminal phosphorus”. The pyrophosphate can undergo ionisation with loss of H+ from each of the two –OH groups on each P and therefore can occur in the -1, -2 -3 or -4 state. The degree of ionisation is dependant upon the associated cations (if there are) and the ambient pH (if in solution).

No partition coefficient value was determined for these substances as they are inorganic phosphates that are highly ionic (depending on ambient pH). Because of this ionic nature the passive passage across biological membranes will be negligible. Pyrophosphate is an anion that occurs in all living cells and is formed mainly by the synthesis of DNA from Nucleotide triphosphates (DNAn + Deoxyribonucleotide triphosphate → DNAn+1 + pyrophosphate). Usually it is cleaved rapidly into two orthophosphate molecules by one of the different members of the alkaline phosphatase family which are present in all tissues. Pyrophosphate nevertheless is generally relatively stable against uncatalyzed hydrolysis (half life = 10 d in autoclaved Flat branch sediment (Blanchar RW and, 1976, Tripolyphosphate and pyrophosphate hydrolysis in sediments, Soil sci. soc.Am. J 40: 225-229)).


Genetic toxicity in vitro with phosphoric acid

Bacterial reverse mutation assay (Ames test)

Harlan Laboratories Ltd (2010) performed a bacterial reverse mutation assay (Ames test, the method conforms to the guidelines for bacterial mutagenicity testing published by the major Japanese Regulatory Authorities including METI, MHLW and MAFF. It also meets the requirements of the OECD Guidelines for Testing of Chemicals No.471 "Bacterial Reverse Mutation Test", Method B13/14 of Commission Regulation (EC) Number 440/2008 of 30 May 2008 and the USA, EPA (TSCA) OPPTS harmonised guidelines) inSalmonella typhimuriumstrains TA1535, TA1537, TA98, TA100 andEscherichia colistrain WP2uvrA- with and without metabolic activation (rat liver homogenate metabolising system: 10% liver S9 in standard co-factors). The dose range was determined in a preliminary toxicity assay and was 50 to 5000 µg/plate in the first experiment. The experiment was repeated on a separate day (pre-incubation method) using the same dose range as experiment 1, fresh cultures of the bacterial strains and fresh test material formulations. Vehicle and positive controls without metabolic activation (N-ethyl-N'-nitro-N-nitrosoguanidine: 2 µg/plate for WP2uvrA-, 3 µg/plate for TA100 and 5 µg/plate for TA1535; 9 -aminoacridine (9AA): 80 µg/plate for TA1537 and 4 -Nitroquinoline-1 -oxide (4NQO): 0.2 µg/plate for TA98) and with metabolic activation (2 -Aminoanthracene (2AA) and Benzo(a)pyrene (BP)) were tested simultaneously and were observed to be valid. Phosphoric acid tested negative with and without metabolic activation.

In vitro mammalian chromosome aberration test from The National Institute of Environmental Research (2005) performed a chromosome aberration test with phosphoric acid in Chinese Hamster Lung (CHL/IU) cell line with and without metabolic activation (according to OECD Guideline 473). As data access could not be obtained a new study was launched in Harlan Laboratories (LTD). Results are expected in August 2013.

Mammalian cell gene mutation assay (Mouse Lymphoma Assay):

Harlan Laboratories Ltd (2010) performed a mouse lymphoma assay according to the UK Environmental Mutagen Society guidance which is equivalent/similar to OECD Guidance 476 and EU method B.17. Concentrations of 0, 61.25, 112.5, 245, 490, 735 and 980 µg/mL were tested on the L5178Y TK+/- 3.7.2 c mouse lymphoma cell line. Solvent control and positive control (ethylmethanesulphonate without metabolic activation and cyclophosphamide with metabolic activation) were tested simultaneously. Phosphoric acid was found to be negative with (4 hours of exposure) and without metabolic activation (4 and 24 hours of exposure). Cytotoxicity was very modest: no evidence of any reductions in viability was observed. Therefore, no residual toxicity occured.

Genetic toxicity in vivo with phosphoric acid

No reliable data were available on the genetic toxicity in vivo endpoint. Phosphoric acid tested negative in vitro toxicity tests (Ames test, mammalian chromosome aberration test, mouse lymphoma assay) and therefore no in vivo mutagenicity tests should be performed with this substance.

Endpoint Conclusion: No adverse effect observed (negative)

Justification for classification or non-classification