Revisions to the derivation of the Australian and New Zealand guidelines for toxicants in fresh and marine waters

The Australian and New Zealand Guidelines for Fresh and Marine Water Quality are a key document in the Australian National Water Quality Management Strategy. These guidelines released in 2000 are currently being reviewed and updated. The revision is being co-ordinated by the Australian Department of Sustainability, Environment, Water, Population and Communities, while technical matters are dealt with by a series of Working Groups. The revision will be evolutionary in nature reflecting the latest scientific developments and a range of stakeholder desires. Key changes will be: increasing the types and sources of data that can be used; working collaboratively with industry to permit the use of commercial-in-confidence data; increasing the minimum data requirements; including a measure of the uncertainty of the trigger value; improving the software used to calculate trigger values; increasing the rigour of site-specific trigger values; improving the method for assessing the reliability of the trigger values; and providing guidance of measures of toxicity and toxicological endpoints that may, in the near future, be appropriate for trigger value derivation. These changes will markedly improve the number and quality of the trigger values that can be derived and will increase end-users’ ability to understand and implement the guidelines in a scientifically rigorous manner.     

Hardness corrections for copper are inappropriate for protecting sensitive freshwater biota

Toxicity testing using a freshwater alga (Chlorella sp.), a bacterium (Erwinnia sp.) and a cladoceran (Ceriodaphnia cf. dubia) exposed to copper in synthetic and natural freshwaters of varying hardness (44-375 mg CaCO3/l), with constant alkalinity, pH and dissolved organic carbon concentration, demonstrated negligible hardness effects in the pH range 6.1-7.8. Therefore, the use of a generic hardness-correction algorithm, developed as part of national water quality guidelines for protecting freshwater biota, is not recommended for assessing the toxicity of copper to these, and other, sensitive freshwater species. Use of the algorithm for these sensitive species will be underprotective because the calculated concentrations of copper in water that cause a toxic effect will be higher.     

Mechanism of toxicity of zinc to the marine diatomNitzschia closterium

The effect of zinc on cell division, photosynthesis, ultrastructure, respiration, ATP levels, mitochondrial electron-transport chain (ETC)-activity, total thiols and glutathione in the marine diatomNitzschia closterium (Ehrenberg) W. Smith was investigated. Although 65µg Zn 1^–1 halved the cell division rate, photosynthesis and respiration were unaffected by zinc concentrations up to 500µg Zn 1^–1. Most of the zinc associated with the cells was bound at the cell surface, with only 3 to 4% of this extracellular zinc penetrating the cell membrane. Once inside the cell, zinc exerted its toxicity at a number of sites. Increased ATP production and ETC activity were observed in zinc-treated cells. Zinc also enhanced cellular thiols (SH) and total glutathione, and zinc toxicity was reversible by the addition of thiol compounds such as cysteine. Zinc-thiol binding may be a detoxification mechanism for the cell. It is suggested that increased ATP production may provide the energy required for increased glutathione synthesis at the expense of other energy-requiring processes including cell division. The mechanisms of toxicity of ionic zinc and copper toN. closterium were compared.     

Sensitivities of Australian and New Zealand amphipods to copper and zinc in waters and metal-spiked sediments

The sensitivities of eight benthic amphipods, Chaetocorophium cf. lucasi, Corophium colo, Grandidierella japonica, Hyale crassicornis, Hyale longicornis, Melita awa, Melita matilda and Melita plumulosa, to copper and zinc in water-only and whole-sediment toxicity tests were compared. Whole-sediment tests used copper- (1300 mg/kg) and zinc- (4000 mg/kg) spiked sediments after equilibration for sufficient time to produce pore water and overlying water concentrations below the lowest observable effect concentrations of water-only exposures. Survival of adults (after 10 d) and juveniles (after 96 h), and the metal concentrations in the body tissues of adults, were determined at the end of the tests. Two epibenthic amphipods from the genus Melita were the most sensitive species to aqueous copper and zinc, with a 96-h LC50 value of 120 microg Cu/l for both M. awa and M. plumulosa juveniles, and a 96-h LC50 value of 640 microg Zn/l for juveniles of M. plumulosa. Juvenile amphipods (7-d old) were more sensitive than adult amphipods (>30-d old) in both water-only and whole-sediment tests, with adult-LC50/juvenile-LC50 ratios in water-only tests ranging from 1.2 to l.5 for copper and 1 to 1.4 for zinc. All species except C. colo, C. cf. lucasi and M. matilda were sensitive to the copper-spiked sediment, with survival between 14% and 74% of controls. Similarly, all species except C. colo and G. japonica, showed a response to the zinc-spiked sediment (26-81% of control survival). The epibenthic amphipods were more sensitive than the infaunal tube-dwelling amphipods and are recommended as test species.     

Mechanism of toxicity of ionic copper and copper complexes to algae

The mechanism of toxicity of ionic copper and copper complexes to growth, photosynthesis, respiration, ATP levels and mitochondrial electron-transport chain-activity in two marine diatoms, Nitzschia closterium (Ehrenberg) W. Smith (Hasle, 1964) and Asterionella glacialis Castracane, and one freshwater green alga, Chlorella pyrenoidosa Chick was investigated. Copper ions depressed both cell division and photosynthesis in A. glacialis and C. pyrenoidosa, whereas ionic copper concentrations which were inhibitory to cell division in N. closterium had no effect on photosynthesis, respiration, ATP production, electron transport or membrane ultrastructure. This suggests that in N. closterium, copper does not act on the chloroplast, the mitochondrion, or the cell membrane, since if it did, the above parameters should be affected. Copper-ethylxanthogenate was exceptional amongst the copper complexes in that it stimulated respiration, mitochondrial electrontransport and ATP formation in N. closterium under conditions of strongly inhibited cell division and slightly stimulated photosynthesis. Ionic copper toxicity may result from an intracellular reaction between copper and reduced glutathione (GSH), leading to a lowering of the GSH:GSSG ratio and suppression of mitosis. In addition, copper inhibits the enzyme catalase and reduces cell defence mechanisms against H₂O₂ and oxygen-free radicals. Lipid-soluble copper complexes are more toxic than ionic copper because both the metal and the ligand are introduced into the cell. Toxicity of ionic copper is ameliorated by trivalent metal ions in the growth medium, including those of Mn, Co, Al, Fe and Cr which form a layer of metal (III) hydroxide around the algal cell, adsorb copper and reduce its penetration into the cell. The degree of insolubility of the metal (III) hydroxide is related to its ability to protect against copper toxicity. In addition, manganese and cobalt catalytically scavenge damaging H₂O₂ and superoxide radicals, respectively, produced by the cell.