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Ecotoxicological information

Toxicity to aquatic algae and cyanobacteria

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Administrative data

Link to relevant study record(s)

Description of key information

Six publications are included in the dossier report on the potential adverse effects on iron.


Reported long-term no-effect levels were well above the solubility limit of ferrous/ferric ions. None of the studies provide a full characterization of the Fe-speciation during the test period. Due to the complexity and reactivity/solubility of Fe as a function of parameters like pH, redox-potential, dissolved organic carbon content, it is virtually impossible to properly qualify and quantify the time-dependent Fe-speciation profile during a chronic exposure testing period. Adverse effects could not be related to a specific Fe-species or to precipitates (intrinsic toxicity vs physical toxicity).


The research data that were recently published by Arbildua et al (2017) agree with the literature in that the effect of Fe(III) on aquatic organisms is associated with indirect nocive effects of Fe oxyhydroxides (e.g., blocking access to nutrients, impairment of respiration, interference with movement). In the particular case of the Fe(III) effects on algae in laboratory standard assays, the study showed that the mechanism of action is mediated by phosphorus depletion, through coprecipitation with the hydrolysis products of Fe(III).

Arbildua et al (2017) this concluded that the effect of Fe on P. subcapitata in reconstituted laboratory waters depends largely on the level of phosphorus in the assay media as well as the presence of DOC. The P-related effects do not represent the intrinsic toxicity or iron.

Key value for chemical safety assessment

Additional information

Intrinsic toxicity and bioavailability of metals in general is related to the free ion form. Due to the limited solubility of iron, the free ion concentration in test media will be within the range concentrations that are found in the environment at background/ambient concentration levels. It is thus reasonable to assume that organisms are adapted to the maximum concentrations of free iron that can be achieved in an aqueous solution. Therefore, adverse effects that may be noted at high exposure concentrations are not due to the intrinsic toxicity of iron.


Mechanisms that are related to precipitation processes are most likely causing the observed toxicity, but only effects caused by the intrinsic toxicity of a chemical should be considered for derivation of a PNEC.