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Hazard for aquatic organisms


Hazard assessment conclusion:
PNEC aqua (freshwater)
PNEC value:
7.8 µg/L
Assessment factor:
Extrapolation method:
sensitivity distribution

Marine water

Hazard assessment conclusion:
PNEC aqua (marine water)
PNEC value:
5.2 µg/L
Assessment factor:
Extrapolation method:
assessment factor


Hazard assessment conclusion:
PNEC value:
230 µg/L
Assessment factor:
Extrapolation method:
sensitivity distribution

Sediment (freshwater)

Hazard assessment conclusion:
PNEC sediment (freshwater)
PNEC value:
87 mg/kg sediment dw
Assessment factor:

Sediment (marine water)

Hazard assessment conclusion:
PNEC sediment (marine water)
PNEC value:
676 mg/kg sediment dw
Assessment factor:
Extrapolation method:
equilibrium partitioning method

Hazard for air


Hazard assessment conclusion:
no hazard identified

Hazard for terrestrial organisms


Hazard assessment conclusion:
PNEC soil
PNEC value:
65 mg/kg soil dw
Assessment factor:

Hazard for predators

Secondary poisoning

Hazard assessment conclusion:
no potential for bioaccumulation

Additional information


Copper iodide is an inorganic compound with low water solubility at environmentally relevant pH. Upon dissociating in aqueous media, copper iodide gives rise to cuprous copper ions (Cu+) and iodide ions (I-) that may then be subject to further transformation. The resulting ionic species will be more bioavailable than the parent compound and will therefore be independently responsible for any effects seen in the event that copper iodide enters the environment as a result of its production and/or use.

In view of this fact, please refer to the separate Chemical Safety Reports (CSR) previously produced in support of the REACH registrations of copper and iodine for detailed assessments of their hazard to organisms in the following environmental compartments:

  • Aquatic compartment (including sediment) (Section 7.1).
  • Terrestrial compartment (Section 7.2).
  • Atmospheric compartment (Section 7.3).
  • Microbiological activity in sewage treatment systems (Section 7.4).
  • Non-compartment specific effects relevant for the food chain (secondary poisoning) (Section 7.5).

These documents are attached in their entirety to Section 13 (Assessment Reports) of the copper iodide IUCLID dossier.

Summary information on the ecotoxicology of copper is presented below and in IUCLID Sections 6.1 - 6.6.


The copper Risk Assessment Report (2008) and REACH Chemical Safety Report (2010) have provided detailed information on (1) the essentiality of copper; (2) the homeostatic control of copper; (3) the mechanisms of action of copper-ions; (4) the comparison between copper toxicity from dietary versus waterborne exposures.

The data clearly demonstrate that:

  • Copper is an essential nutrient for all living organisms
  • Copper ions are homeostatically controlled in all organisms and the control efficiencies increase with trophic chain. As a consequence, - Copper BCF/BAF values decrease with increasing exposure concentrations (water and food), vary depending on nutritional needs (seasonal, life stage, species dependent) and vary pending on “internal detoxification” mechanisms - Copper BMF values are <1.
  • Water-borne exposure (not diet borne exposure) is the exposure route critical to copper toxicity.

Essential Trace Element

Copper is an essential micronutrient, needed for optimal growth and development of micro-organisms, plants, animals and humans. It plays a vital role in the physiology of animals: for foetal growth and early post-natal development, for haemoglobin synthesis, connective tissue maturation especially in the cardiovascular system and in bones, for proper nerve function and bone development, and inflammatory processes. Copper acts as an active cofactor in over 20 enzymes and proteins, notably the respiratory enzymes haemocyanin and cytochrome oxidase and the anti-oxidant superoxide dismutase (WHO, 1998).  

Copper deficiency has been observed in intensive cultures of fish, crops and farm animals. The most striking examples of copper deficiency come from farming practices. Insufficient bioavailable copper in soils has been shown to reduce agricultural yields and to produce metabolic copper deficiencies in animals. Copper deficiency was first recognised in Europe in the 1930s and its incidence increased with the intensification of arable farming over the last 50 years. Copper deficiency has also been noted in a wide variety of soils world-wide (IPCS 1998). 

Depending on the organism’s metabolic need, different copper levels are found in tissues from different strains, species and life stages. 

Differences among species and strains:Aquatic invertebrates such as gastropods, some crustacea and bivalves, relying on haemoocyanin as respiratory pigment, have typically higher copper levels than invertebrates relying on haemoglobin as respiratory pigment (e.g. Timmermans et al, 1989). 

In higher organisms (vertebrates), homeostatic control of copper supply is achieved mainly by storage in the liver and biliary secretion (Underwood and Suttle, 1999). Copper is bound to proteins such as ceruloplasmin and metallothionenin, functioning as copper storage and mobilised as needed.

Differences within species: Of all factors that affect the physiology of animals, body size exerts the major effect and provides an integrated value of all physiological processes (Marsden and Rainbow, 2004). In aquatic environments, several investigators demonstrated an inverse relation between copper tissue levels and the length or weight of the organisms (e.g. Timmermans et al, 1989). 

Different copper needs are of relevance to both agricultural and medical practices:

Copper supplements are provided to piglets and pigs to enhance growth. Considering the high needs during the fast growth stages, copper levels given to piglets are much higher than those given to adult pigs.

The copper concentration in the liver of a mammalian and human foetus is much higher during the last term of pregnancy than in an adult. This is because of the high copper need during this period, as well as during the first months after birth, and because breast milk contains little copper. Consequently, the milk formulae for premature babies contain higher copper levels than those for newborns.

In summary, as an essential element, all organisms will naturally accumulate copper without deleterious effects. Different levels of accumulation in tissue reflect differences in nutritional needs.

Homeostatic control, uptake and depuration of copper ions

The natural copper levels, available for plants, micro-organisms and animals, living in a specific environment, depend on the natural geological and physico-chemical characteristics of the water, sediments and soils. Homeostatic regulation of copper allows organisms, within certain limits, to maintain the physiologically required levels of copper in their various tissues, both at low and high copper intakes. 

The molecular mechanism of copper homeostasis is related to 2 key elements: P-type ATPases that can pump copper across biological membranes in either direction or copper chaperones, important for intracellular copper homeostasis (Odermatt et al, 1992). The latter is considered to be universal as the sequences of copper chaperones are highly conserved between species (Wunderli et al. 1999).

Besides these active cellular regulation mechanisms, some groups of organisms have developed additional mechanisms (molecular binding to e.g. metallo-thioneins and sequestration in granules) to prevent copper excess (Borgmann, 1993 and Rainbow, 1980, 1985, 1989; Marsden and Rainbow, 2004).

Vertebrate dietary copper exposure studies (fish, mammals, birds and humans) demonstrate additional organ-related homeostasis. Intestinal adsorption/biliary excretion of copper is regulated with varying dietary intakes (WHO, 1998). 

Due to the homeostatic regulation of copper (and other metals), BCF/BAFs are not independent of exposure concentration (e.g. Mc Geer et al., 2003). Increased/decreased copper intakes/eliminations, lead to BCFs and BAFs that are inversely related to exposure concentration (i. e. decreasing BCF/BAFs with increasing exposure concentration (water and diet). For copper, this inverse relationship was clearly demonstrated for BCFs, BAFs and biota-sediment accumulation factors (BSAFs) (Adams et al., 2003). 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 concentrations, organisms are able to excrete excess metals or limit uptake.

Additionally, different BCFs for different species, life stages and seasons have been observed, depending on the organism’s metabolic need (in e.g. Cu-enzymes). Further complicating the application of BCF and BAF to metals is that many aquatic organisms store metals in detoxified forms, such as in inorganic granules or bound to metallothionein-like proteins. The use of granules is of particular note in the context of BCFs, because high body burdens are often associated with this storage mechanism, but there is a lack of adverse effects.

Using BCF and BAF for essential metals and their compounds to assess ecotoxicity therefore ignores fundamental physicochemical and toxicological properties associated with these substances.

Compared with the diffusional uptake of neutral organics, metal uptake is complex. It includes a diversity of mechanisms, accumulation of both essential and non-essential elements from the natural background, homeostatic control of accumulation, as well as internal detoxification, storage and elimination.

Mechanism of action of copper toxicity/deficiency


From the copper risk assessment, it was clearly concluded that the most sensitive uptake route for acute and chronic copper toxicity is directly from the water with free Cu-ions as most potent Cu-species. The key indicator of copper toxicity is disturbance of the sodium homeostasis (e.g. Paquin et al., 2002; De Schamphelaere and Janssen, 2003; Kamunde et al., 2001 & 2005). The key target tissue for copper toxicity is therefore the water/organism interface, with cell wall and gill-like surfaces acting as target biotic ligands in all species investigated.

The importance of water-borne exposure was confirmed from the freshwater chronic ecotoxicity database, demonstrating:

·       The influence of water chemistry on chronic copper toxicities (influence of DOC, pH,... on chronic NOECs)

·       The small inter-species variability in observed NOECs (after BLM normalisation) (max/min NOEC ratio of 23 for 27 species),

·       Small acute to chronic ratios (typically a factor of 1 to 3)

·       Higher sensitivity of smaller compared to larger organisms (Grosel et al., 2007).

·       No concern of secondary poisoning from copper mesocosm studies:

·       Roussel (2007) reported for a lentic mesosocm study a low sensitivity of the predating fish compared to the invertebrates and algae.

·       The freshwater pond mesocosms (Schaefers et al, 2002 and Rousel (2007) and the marine pond mesocosm (Foekema et al 2010) did not show a concern from copper secondary poisoning.


Freshwater and marine organisms face very different ion- and osmo-regulatory problems related to living in either a very dilute or concentrated salt environment. These differences in ion- and osmo-regulatory physiology may also lead to differences in metal accumulation and metal toxicity (Prosser, 1991; Wright 1995; Rainbow, 2002). Marine organisms are, as freshwater organisms, also exposed via the gills. But in addition, they take in water via the gut exposing an additional series of epithelial structures to the metals (Wang and Fisher 1998; Glover et al 2003; Mouneyrac et al 2003). Both the epithelia of gills and gut are thus important and potentially sensitive targets because they provide a variety of essential physiological functions such as the energy dependent transport of nutrients across the interface and the maintenance of homeostatic balance. Despite these apparent physiological differences, it has been shown that marine fish also suffer from osmo-regulatory disturbances under metal exposure. 

The importance of waterborne exposure was confirmed from marine ecotoxicity databases, demonstrating:

·       The mitigating effect of DOC on the marine NOECs/EC10s.

·       The absence of a higher copper sensitivity with increasing trophic chain level.

·       For the bivalve Mytilus edulis, the short term (48 hrs) early life stage NOEC was similar to the 10 days growth inhibition NOEC.

The 83 days marine mesocosm study (Foekema et al., 2010), furthermore showed that the safe level in the mesocosm could be predicted from the single-species SSD and DOC correction, developed for water-only exposure.

The interaction between free copper-ions and “gill-like structures” induce osmo-regulatory stress. Osmo-regulatory disturbance from waterborne exposure is recognised as the primary symptom of copper toxicity to aquatic organisms.  

Copper toxicity from dietary versus waterborne exposures 

Invertebrates:A few key studies are available:

- De Schamphelaere and Janssen (2003) demonstrated the influence of water characteristics on the chronic toxicity of D. magna and showed that, for D. magna, waterborne copper and not dietary copper uptake is responsible for copper toxicity (De Schamphelaere and Janssen, 2004).

Similarly, Allinson (2002) investigated 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. destructor does not appear to be sensitive to dietary copper.


- Kamunde, 2001 observed that dietary copper pre-exposure decreased the uptake of copper across the gills, providing further evidence of homeostatic interaction between the two routes of uptake. Rainbow trout regulated dietary copper at the level of the gut by increasing clearance to other tissues, at the liver by increasing biliary copper excretion, and at the gill by reducing waterborne copper uptake in response to dietary exposure. The modest morphological changes in the intestinal tract suggested high cell and organelle turnover and local regulation of copper. In spite of possible increased energy demand for regulation and tissue repair, there was no significant growth inhibitory effect following dietary exposure.

- Blust et al., 2007, reviewed the literature on copper toxicity after dietary copper exposures of fish and compared waterborne versus diet borne toxicity of copper to fish. After detailed evaluation of the Clearwater et al., 2002 review paper, Blust derived critical diet borne toxicity effects value for Atlantic salmon and Rainbow trout of respectively 15.5 and 44 mg Cu/kg fresh weight/day. Blust et al, 2007 further assessed if the waterborne exposures, PNEC of 7.8 µg Cu//l, as derived in the copper risk assessment, would result in a dietary copper dose or copper food concentration exceeding a critical level. The concentrations in food were calculated from the regressions presented in McGeer et al. (2003) which allow the estimation of the whole body copper concentration, for different types of aquatic organisms, as a function of the copper waterborne concentration. The results of the simulations show that aquatic invertebrates exposed to 8µg Cu/l waterborne copper reach mean Cu body levels of 53-84 mg Cu/kg dry weight (depending on the diet). The resulting daily uptake by fish at 7.8 µg Cu/L was < 4.20 mg Cu/kg fresh weight/day. These results lead to the conclusion that the copper concentrations in food items and daily dietary copper dose in fish are unlikely to cause negative effects at the threshold waterborne copper concentration of 7.8 µg/l.

Comparison of the dietary copper levels and “normal” background Cu levels in live food items

Cu is a naturally occurring element and is essential to all living organisms. Naturally, a background Cu burden is present in all organisms to fulfil their biochemical requirements. Table 1 presents a summary of a few ‘background’ Cu concentrations in freshwater biota that may serve as food items for fish.


Table66: Background Cu burdens of selected freshwater biota that may be considered food items for fish.



(mg/kg dry wt)


Daphnia magna(adults)


10.2 - 22.1

Bossuyt et al. (2005a,b)a

Daphnia magna(juveniles)


20 - 120

Bossuyt et al. (2005a,b)a

Hyalella azteca



Borgmann et al. (1993)

aFifth or 6thgeneration daphnids taken from a multi-generation exposure; 1µg/L was sufficient to avoid deficiency


Bossuyt et al. (2005a, b) reported background body burdens of 40d-old D. magna at 1 µg Cu/L between 10.2 and 22.1 mg Cu/kg-1 dry wt. Juvenile daphnids of up to 2 days old seemed to have higher copper body burdens between 20 and 120 mg Cu/kg-1 dry wt. Borgmann et al. (1993) report a Cu burden inHyalella. aztecaof 79 mg Cu/kg-1 dry wt in organisms exposed to control conditions, i.e. 3.5 µg Cu/L.

The background copper burdens (10 - 120 mg Cu/kg dry weight) as determined above, furthermore encompass the simulated Cu body levels of 53 - 84 mg Cu/kg dry weight calculated for aquatic invertebrates exposed to 8 µg Cu/l waterborne copper and therefore provide additional evidence that the Cu concentrations in food items and daily dietary Cu dose in fish are unlikely to cause negative effects at the threshold waterborne Cu concentration of 8 µg/l. 

Waterborne Cu is therefore recognised as the critical copper exposure route for invertebrates and fish.

Critical papers of relevance to bio-magnification

The absence of copper bio-magnification, 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 detail 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 bio-magnification in this estuarine system. Copper concentrations ranged between 0.27 µg Cu/g dw (Omnivore: Monacanthus and 88 µg Cu/g dw (Herbivore: Bembicum auratum (gastropod with haemocyanin)). The higher levels (e.g.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 bio-magnification from the sediment to herbivores, omnivores, detrivores and carnivores.

- Wang (2002) noted the bio-diminution 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 mine 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 positions, determined from15N radio isotope determination, indicated that the trophic chain had no effect on copper levels in the insects.

Copper is therefore not bio-magnified across the trophic chain.


There is a substantial amount of information available on copper.

The data clearly demonstrate that:

·       Copper is an essential nutrient for all living organisms.

·       Copper ions are homeostatically controlled in all organisms and the control efficiencies increase with trophic chain. As a consequence,

·       copper BCF/BAF values decrease with increasing exposure concentrations (water and food).

·       vary depending on the nutritional needs (seasonal, life stage, species dependent).

·       vary pending on “internal detoxification” mechanisms.

·       Copper BMFs values are < 1.

·       Copper waterborne exposure (and not diet borne exposure) is the exposure route critical to copper toxicity.


Conclusion on classification

Special guidance is available for the environmental classification of metals and metal compounds. For metals, classification is based on comparing the soluble metal concentration, measured after Transformation/Dissolution (T/D) with the Ecotoxicity Reference Values (ERVs) of the corresponding metal ion. 

Accordingly, for the environmental classification of copper iodide, ERVs based on ecotoxicity data for soluble copper compounds are compared to the results of T/D testing on this compound (Section 1.3, Physicochemical properties).

Acute and chronic ERVs developed in the copper CSR are summarised in the following Table:

Summary of the acute and chronic ERVs used for the classification of coppercompounds

pH range

Acute ERV L(E)C50 (mg Cu/l)

Chronic ERV NOEC (mg Cu/l)

pH 5.5-6.5



pH >6.5-7.5



pH >7.5-8.5



Across pHs




The average dissolved copper concentrations measured in a 24 hour T/D screening test with a copper iodide loading of 100 mg/L were as follows:

  • At pH 6 an average dissolved copper concentration of 3643 ± 49 µg Cu/L was found.
  • At pH 8 an average dissolved copper concentration of 2201 ± 34 µg Cu/L was measured.

Comparing these values with the ERVs set out above, it is clear that the water solubility of copper iodide is too high to affect the environmental classification applied to soluble copper compounds. It is therefore assigned the same classification as copper sulphate as a worst case.

Conclusions on Acute classification for the environment:

Copper iodide is classified Acute Category 1. An M factor of 10 is applied.

Conclusions on Chronic classification for the environment:

Copper iodide is classified Chronic Category 2. An M factor of 1 is applied.