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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

Ecotoxicological information

Long-term toxicity to fish

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Administrative data

Link to relevant study record(s)

Description of key information

Five publications on freshwater chronic toxicity are included in this dossier, as well as one publication on the chronic toxicity of iron to a marine fish species.  Similar to the findings reported on acute iron toxicity studies to fish, the inherent physicochemical properties of iron make it virtually impossible to interpret the data in a way such that a meaningful PNEC could be identified.


Reported long-term no-effect levels were situated well above the solubility limit of ferrous/ferric ions: precipitation of iron in test media was reported by several authors (Birge et al, 1985 ; Sykora et al, 1972), and it was indicated that this process could have affected the outcome of the test. 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 due to gill smothering).

Key value for chemical safety assessment

Additional information

Intrinsic toxicity and bioavailability of metals are in general 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.

Precipitation processes are most likely causing the toxicity, but only effects caused by the intrinsic toxicity of a chemical should be considered for derivation of a PNEC.