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EC number: 215-572-9
CAS number: 1332-65-6
There is a considerable amount of copper accumulation data available. The data have been reviewed by two authors in view of assessing the relation between the CuBCF/BAF values and the copper concentrations in the water and sediment. Additionally some researchers have assessed the influence of water chemistry (dissolved organic matter), and the physiology of the organisms (species, age, seasons...) on the observedBCF/BAF values.The information demonstrates that copper is well regulated in all living organisms and thatBCFand BAF values have no meaning for a hazard assessment.The data also demonstrate that waterborne exposure is most the critical exposure route and that copper is not biomagnified in aquatic ecosystems.The section further includes critical data related to (1) the accumulation of copper on critical target tissues (eg gills in aquatic organisms); (2) the influence of environmental parameters (eg Organic Carbon, pH, Cationic Exchange Capacity) as well as food intake on the accumulation of copper. This information is relevant to the understanding of the accumulation as well as the mechanism of actions, described in the section "ecotoxicological information".Information relevant to assessing copper toxicity from dietary exposure - of relevance to a secondary poisoning assessment is included in the section "ecotoxicological information".
Bioconcentration factors (BCF)
and bioaccumulation factors (BAF)
There is a considerable amount of copper
accumulation data available, that could potentially be used to calculate
bioconcentration factors (BCF)
and bioaccumulation factors (BAF) and assess the corresponding potential
risks in aquatic food chains. However due to the homeostatic regulation
of copper (and other metals), theBCF/BAF are not independent of exposure
concentration (Review papers of Adams et al., 2003; Mc Geer et al.,
2003; supported by many papers from many authors (see IUCLID supportive
record-summaries). Increase/decreased copper intake/eliminations, lead
to BCFs, BAFs that are inversely related to exposure concentration (i.
with increasing exposure concentration (water and diet). Particular to
copper, this inverse relationship was clearly demonstrated for BCFs,
BAFs and biota-sediment accumulation factors (BSAFs). The observed
inverse relationship has been explained by homeostatic regulations of
internal tissue concentrations: at low metal concentrations organisms
are actively accumulating metals in order to meet their metabolic
requirements while at high ambient metal concentration, organisms are
able to excrete excess metals or limit uptake.
A more mechanistic understanding of copper
regulations of accumulations as well as internal copper binding
mechanisms and sequestrations are provided by eg Borgmann, 1993 and
Rainbow (1980, 1985, 1989).
Additionally, different BCFs for different
species, life stages and seasons have been observed, depending
on the organism’s metabolic need (in eg Cu-enzymes). Resulting
different copper levels are found in tissues from different strains,
species, life stages and species. Moreover,
aquatic invertebrates such as gastropods, crustacea and bivalves,
relying on phaetocyanin as respiratory pigment have typically higher
copper levels (and thus higher BCFs) than invertebrates relying on
haemoglobin as respiratory pigment (eg Timmermans, 1989; Amiard et al.,
Field data further show that copper
concentrations in tissues of marine mammals and coastal seabirds,
regardless of species, except brain, tend to decrease with increasing
age (Eisler 1984, Lock et al., 1992). Neonatal marine mammals have
higher copper levels compared to the mothers (Law et al., 1992).
As a result, use of a simple ratio
Cbiota/Cwater or Cbiota/Csediments as an overall approach for estimating
copper bioconcentration factors or copper body burdens is not
to mention that the non-applicability of BCFs for metal and especially
for essential metals was already recognized in the regulatory framework
of aquatic hazard classification (OECD,2001).
The section further includes critical data
related to the accumulation of copper to the critical target tissue for
copper (eg gills in aquatic organisms) and on the influence of dissolved
organic matter, calcium and sodium on the accumulation of copper.
- Benoit, 1975, Perez, 1991 and Kaland 1993,
described the importance of copper target accumulation to the gills
- Playle,1993a demonstrated that copper
concentrations in the target organ (gills) correlates to the free copper
concentration, not to the total copper concentration in the test water.
The study provides a mechanistic understanding of the biotic ligand
model by determining the Metal- Gill stability constant and thereby
predicting metal accumulation on gills and therefore toxicity to fish.
-McGeer et al, 2002, demonstrated that the
addition of dissolved organic matter (administered as humic acids)
decreased Cu accumulation in gills and liver.
-Playle 2003b provides a mechanistic
understanding of the protective effect of dissolved organic matter for
copper toxicity to fish because: copper
levels in gills decreased with increasingDOC.Lakeof
origin or molecular size fraction ofDOCdid
not influence Cu binding to gills, while DO concentration did.
The section further includes some critical
data of relevance to secondary poisoning
- Kamunde et al, 2005 demonstrated
interaction between Cu uptake from water and diet: from
detailed copper uptake experiments, they demonstrated that elevated
dietary NaCl modulates Na+and Cl–homeostasis
and reduces accumulation and toxicity of waterborne Cu.
provided evidence on the interaction between water and food for the
homeostasis of copper: The
data suggest that the availability of food prevents growth inhibition
and initial ion (Na) losses that usually result from waterborne Cu
exposure. The data further demonstrate copper acclimation: a
2 fold increase in LC50 after pre-exposure of the fish to copper.
- Kamunde, 2001 observed that dietary copper
pre-exposure decreased the uptake of Cu across the gills providing
further evidence of homeostatic interaction between the two routes of
uptake. Rainbow trout regulated dietary Cu at the level of the gut by
increasing clearance to other tissues, at the liver by increasing
biliary Cu excretion, and at the gill by reducing waterborne Cu uptake
in response to dietary exposure. The modest morphological changes in the
intestinal tract suggested high cell and organelle turnover and local
regulation of Cu. In spite of possible increased energy demand for
regulation and tissue repair, there was no significant growth inhibitory
effect following dietary exposure.
- Hansen et al (2004), performed a metal
exposure study on growth performance in rainbow trout fed a live diet
pre-exposed to metal contaminated sediments. The study indicates the
absence of copper toxicity at high dietary copper levels.
- Allinson (2002) investigates the
bioaccumulation of copper through a simple food chain (Lemna minor –
C. destructor) and observed regulation of copper by the crayfish,C.
destructor, with the gills being the main site for absorption and
depuration of copper to and from the water column.C. destructordoes
not appear to be sensitive to dietary copper.
- Nott,1994 showed that copper, detoxified by
the snails are unavailable to the crabs and they pass straight through
the gut and appear in the faecal pellets.
Additional information of relevance to the
absence of secondary poisoning is available from a well designed study
from De Schamphelaere et al, 2004, clearly relating copper toxicity to
waterborne and not dietary exposure route (see the section “ecotoxicological
Importantly, the copper mesocosm study from
Roussel (2007) reported in the section "additional ecotoxicological
information" demonstrated a low sensitivity of the predating fish and
did not show a concern from secondary poisoning. Also the freshwater
pond mesocosm (Schaefers et al, 2002) and the marine pond mesocosm
(Foekema et al 2010) (both reported in the section "additional
ecotoxicological information" did not show a concern from secondary
Last but not least secondary poisoning of
birds and mammals via fish or mussels was investigated for metals,
including copper, by RIVM (Smit et al, 2000) (also in section additional
ecotoxicological information) who concluded that for copper it was not
necessary to integrate secondary poisoning aspects into the copper
aquatic quality criteria
Biomagnification factors (BMF)
The absence of copper biomagnification, with
consistent BMFs<1, was shown from several papers:
- Barwick and Maher (2003), compared trace
metal levels in a contaminated seagrass ecosystem in Lake Macquire, the
largest estuary in New South Wales (Australia). The structure of the
estuarine food web was studied in details and all organisms (algae,
invertebrates, fish) were categorised as autotrophs, herbivores,
planktivores, detrivores, omnivores and carnivores. The results of the
analysis showed the absence of copper biomagnification in this estuarine
systems. Copper concentrations ranged between 0.27 µg Cu/g dw (Omnovore:Monacanthusand
88 µg Cu/g dw (Herbivore:Bembicum auratum(gastropod with
haemocyanin)). The higher levels (eg. B. auratum) were associated
with species with active accumulation of copper into the respiratory
- Farag et al., 1998, studied copper
concentration in benthic invertebrates that represent various functional
groups and sizes from de Coeur d’Alene river,Idaho,
influenced by mining activities. The copper concentrations noted across
the trophic chain, demonstrated the absence of biomagnification from the
sediment to herbivores, omnivores, detrivores and carnivores
- Weis & Weis (1999) demonstrated the absence
of trophic transfer of metals in consumers associated with chromated
copper arsenate treated wood panels.
- Wang (2002) noted the biodiminution of
metals in the classical marine planktonic food chain (phytoplankton to
copepods to fish) and explained the phenomenon as the result of the
effective efflux of metals by copepods and the low assimilation of
metals by marine fish.
- Quinn et al., 2003, evaluated trophic chain
transfer of metals in insects (35 species) from a stream food web
influenced by acid main drainage with copper levels up to 100 µg Cu/L.
They demonstrated that metal concentrations were higher in water and
insects closer to the mining sites and taxa richness increased with
distance away from the site. The relation between the trophic position,
determined from15N radio isotope determination, indicated
that trophic chain had no effect on copper levels in the insects.
Considering that bioaccumulation has no ecotoxicological meaning
for copper, a summary of the relevant information on copper
essentiality, homeostasis, copper mechanism of action, biomagnification
and potential for secondary poisoning is provided as an annex to the PBT
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