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EC number: 205-250-6
CAS number: 136-52-7
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.
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.
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.
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. 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.
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