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Environmental fate & pathways

Bioaccumulation: aquatic / sediment

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Description of key information

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".

Key value for chemical safety assessment

Additional 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. e., decreasingBCF/BAFs 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., 1985).

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 appropriate. Useful 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 Clhomeostasis and reduces accumulation and toxicity of waterborne Cu.

-Taylor(2000) 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 information”)

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 poisoning.    

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 pigment haemocyanin.

- 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 assessment.