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EC number: 205-250-6
CAS number: 136-52-7
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.
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.
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.
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. An
assessment factor (AF) of 30 was applied (as suggested in the
ECHA guidance Section R.10 (ECHA 2008) guidance) to account
for both interspecies variation and lab-to-field extrapolation, resulting
in an estimated dietary PNEC of 1.67 mg Co / kg dietary tissue.
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.
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
low cobalt tissue concentrations are less than or equal to the estimated
PNEC for birds and mammals.
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.
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