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Ecotoxicological information

Short-term toxicity to fish

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Description of key information

All available studies show that mortality is caused by low pH values. When adjusted to environmentally relevant pH values, phosphoric acid as pyrophosphate salt do not cause acute adverse effects on fish.

Key value for chemical safety assessment

Additional information

In accordance with Annex XI, section 1.5 of Regulation (EC) No 1907/2006 (REACH) a read across approach may be used when substances have similarities based on the likelihood of common breakdown products via physical and biological processes, which result in structurally similar chemicals. As mentioned in the hydrolysis summary, polyphosphoric acid is hydrolysed to orthophosphate in environmental conditions. Thus a read across from orthophosphoric acid to pyrophosphoric acid is justified. In addition, studies performed with pyrophosphate salts can also be used. Pyrophosphate salts are ionic in nature and therefore dissociate readily into cations and anions in water. Cations as potassium and sodium are essential micronutrients that are ubiquitous in the environment. As such, their uptake is tightly regulated and is therefore not considered to pose a risk for ecotoxicity. In environmental conditions, the pyrophosphate anion is unstable and a number of different processes result to an ultimate breakdown product of orthophosphate.

The study from Ellgaard and Gilmore (1982) focuses on the pH effects caused by phosphoric acid. Different pH levels have been tested in bluegill sunfish. The pH induced by phosphoric acid which caused 50% mortality was between 3.0 and 3.25, while no mortality was observed at pH 3.5 or above after 96h exposure. At neutral pH 7.5 no fish died.

Similar results were obtained for Aphanius dispar (Alkahem, 1989) with a median lethal pH of 3.58. Another study showed that a 96h-LC50 of phosphoric acid of 75.1 mg/L was obtained in Oryzias latipes (Korean study, 2005) when the pH was not adjusted to relevant environmental values. No mortality was observed at 100 mg/L when the pH was adjusted.

The studies show that a pH caused by adding phosphoric acid roughly between pH 3 (or lower) and 4 is critical for fish.

A study showed that survival times increased with increasing pH, and that this increase was more rapid at pH values above 3.5 (Gueylard and Duval, 1922). It can thus be concluded that it is the low pH which is causing the toxic effects. Wallen et al. cited by Von Burg as well described a study in which fish (Gambusia affinis) were exposed to both phosphoric acid and turbidity (600 ppm of clay particles), and in which phosphoric acid precipitated turbidity to levels below 25 ppm. The median tolerance limit after 24, 48 and 96h exposure was 138 ppm (i.e. about 138 mg/L). Townsend and Cheyne (1944) showed that exposure of Oncorhynchus kisutch fingerlings to 20 ppm of phosphoric acid (i.e. pH 6.75) induced no mortality at relatively normal dissolved oxygen concentrations (4.95 -8.15 ppm). However, when the dissolved oxygen concentration was lowered to 1.50 ppm, phosphoric acid at 12.0 and 20.0 ppm induced 100% mortality, which is obviously caused by the combination of the low dissolved oxygen concentration and the presence of increased hydrogen ion concentrations.

As regulatory ecotoxicity tests need to be conducted at pH 6-9, it can be expected that phosphoric acid will not cause adverse effects to fish when in this pH range.

To confirm this observation, a fish toxicity test study performed on rainbow trout with a pyrophosphate salt (tripotassium trihydrogen diphosphate dihydrate) has been investigated and gave a 96h LC50 of greater than 100 mg/L (Priestly, 2010). Indeed, no toxic effect has been observed at the highest test concentration (i.e. 100 mg/L).