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Ecotoxicological information

Toxicity to birds

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Description of key information

Cobalt bioaccumulation in aquatic and terrestrial food chains is presented in Sections 4.3.1 and 4.3.2, respectively and is discussed in Section 4.3.3. The indication is that bioaccumulation of cobalt by both aquatic and terrestrial organisms is low with trophic transfer factors less than 1 and tissue levels are generally homeostatically controlled in organisms.  These characteristics indicate the possibility of secondary poisoning is unlikely and a detailed PNECoral assessment is waived according to ECHA TGD Guidance on information requirements and chemical safety assessment R.16. Environmental Exposure Estimation, pg. 43.  

Key value for chemical safety assessment

Long-term EC10, LC10 or NOEC for birds:
50 mg/kg food

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 PNECoralvalues represent dietary predicted no effect concentrations, below which food concentrations are not expected to pose a risk to birds or mammals. Although a PNECoralvalue is not relevant for cobalt, an approximate no effect dietary concentration was estimated for both bird and mammal pathways using aTier 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.

 

The potential to cause toxic effect to birds was estimated based on a weight-of-evidence approach. Three studies were identified from the terrestrial toxicity database that examined the toxicity of cobalt to the chick (Gallus domesticus). Although none of the studies met the requirements of a high quality study, in our best professional judgment the combined information can be used to estimate safe dietary concentrations of cobalt. Diaz et al (1994) and Ling and Leach (1979) conducted sub-chronic dietary exposure studies that examined potential effects on the survival and grow of chicks fed dietary concentrations of cobalt. The Diaz study reported effects on both mortality and body weight gain at all tested dose levels, with the lowest cobalt concentration being 125 mg Co/kg in feed. Ling and Leach (1979) on the other hand, reported no effect on exposed chicks at a dietary concentration of 50 mg Co/kg diet and effects at concentrations higher than that of Diaz, but the study suffered because cobalt diet concentrations were not analytically confirmed. Relying on the available data and using a weight-of-evidence approach, a NOEC of 50 mg Co / kg dietary tissue is estimated.Anassessment factor (AF) of 30was applied (as suggested in the ECHA guidance Section R.10 (ECHA 2008) guidance) toaccount for both interspecies variation and lab-to-field extrapolation,resulting in an estimated dietary PNEC of1.67 mg Co / kg dietary tissue.

 

A soil-worm-bird pathway is designated as the terrestrial food chain asdescribed 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.The food chain exposures toterrestrial 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.