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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

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Ecotoxicological information

Toxicity to other above-ground organisms

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Description of key information

As concluded in chapter 4.4, based on the available information (BCF values lower than 100 and BCF and BAF values decreasing with increasing soil or water concentrations) there is no indication of a bioaccumulation potential, hence, secondary poisoning is not considered relevant.

Key value for chemical safety assessment

Additional information

As previously discussed, cobalt has a low bioaccumulation potential in both aquatic and terrestrial pathways (see section 4.4) and as an essential element for plants and animals (Gal et al 2008) homeostatic mechanisms maintain cobalt concentrations in tissues and body fluids within ideal levels by actively accumulating or depurating cobalt depending on metabolic requirements. Therefore there is no indication of a bioaccumulation potential, hence secondary poisoning is not considered relevant.


The PNECoral values represent dietary predicted no effect concentrations, below which food concentrations are not expected to pose a risk to birds or mammals. Although a PNECoral value is not relevant for cobalt, an approximate no effect dietary concentration was estimated for both bird and mammal pathways using a Tier 1 approach according to ECHA TGD R.7.13. In this approach, a default assessment factor was applied to the lowest available NOEC identified for both the bird (7.5.1) and mammal (7.5.2) ingestion pathways. The Tier 1 results reinforce the low risk of secondary poisoning of cobalt to birds and mammals.


A complete review of data on the toxicological effects of cobalt compounds to humans and mammals can be found in chapter 5 of this report. An additional study was identified from the terrestrial toxicity database that examined the toxicity of cobalt to growing pigs (Huck & Clawson, 1976). This long-term dietary study (16 weeks) evaluating effects of cobalt on growth meets the requirements for calculating a predicted no-effect concentration in the food (PNECoral) as indicated in section R.10.8 (ECHA 2008). The Huck & Clawson study reported no adverse effects at 200 mg Co/kg feed, with significant behavioural effects and weight loss at 400 mg Co/kg in feed. Relying on the available data, a NOEC of 200 mg Co / kg dietary tissue is estimated. An assessment factor (AF) of 30 was applied (as suggested in the ECHA guidance Section R.10, Table R.10-13 (ECHA 2008)) to account for both interspecies variation and lab-to-field extrapolation, resulting in an estimated dietary PNEC of 6.67 mg Co / kg diet.

A soil-worm-bird pathway is designated as the terrestrial food chain as described by Romijn et al. (1994), ECHA TGD R.10.8. Worm internal body concentrations of cobalt, after gut content depuration, ranged from 1.7 to 7.0 mg Co/kg ww. This concentration suggests a substantial safety factor for exposure, further evidence that indirect toxicity for secondary poisoning through the terrestrial food chain is unlikely.


The risk to fish-eating predators is related to the water-fish-animal or water-invertebrate-animal aquatic food chain pathways. Internal body concentrations of cobalt in aquatic organisms have been measured in freshwater and marine fish and marine mussels. The concentrations ranged from 0.02 to 2.24 mg/kg ww (Edrogrul and Ebrilir 2007, Turkey; Lwanga et al 2003, Ghana) in freshwater fish, from 0.006 to 1.12 (Turkmen et al 2005, Mediterranean) in marine fish and from 0.012 to 2.4 mg/kg ww (Unlu et al 2008, Mamara Sea; Lafabrie et al 2007, Mediterranean coast) for mussels. These low cobalt tissue concentrations are less than or equal to the estimated PNEC for birds and mammals.

The National Academy of Sciences (NAS) Mineral Tolerances of Domestic Animals (2005) reported cobalt deficiency is a much more common occurrence than toxicosis. Cobalt is an essential component of vitamin B12 (cobalamin). Non-ruminant mammals do not synthesise vitamin B12 but consume it through diet. Ruminants synthesise their own vitamin B12 through ruminal bacteria provided an adequate dietary dose from 0.1 to 0.15 mg Co/kg diet is available (NAS 2005).The food chain exposures to terrestrial and aquatic organisms seem less critical compared to direct toxicity of cobalt towards wildlife birds and mammals and safe thresholds for direct toxicity will therefore also be protective for secondary poisoning through the terrestrial and aquatic food chains.