Summary of environmental hazard assessment

Summary of environmental hazard assessment

Ecotoxicity data for sodium cyanide and other cyanogenic compounds show that cyanide has very high acute (e.g. single dose) toxicity to aquatic and terrestrial animals and is also toxic to plants and certain micro-organisms. It is also toxic via chronic (e.g. long term or repeat dose) exposure, such as adverse impacts on egg production and spawning in fish.

Once in the bloodstream of an animal, cyanide rapidly forms a stable complex with enzymes involved in cellular respiration, resulting in cytotoxic hypoxia or cellular asphyxiation. The lack of available oxygen causes a shift from aerobic to anaerobic metabolism, leading to the accumulation of lactate in the blood. These effects lead to depression of the central nervous system (CNS) that can result in respiratory arrest and death. A range of other enzymes and systems are also affected by cyanide. In general, effects from non lethal doses tend to be reversible over time due to metabolic cyanide degradation processes; however, fitness is likely to be impaired during recovery. There is a range of debilitating signs of cyanosis.

Toxicity of different forms of cyanide

WAD CN is generally considered the most appropriate measure of ‘biologically available’ cyanide because it includes free cyanide and various forms of cyanide which may release free cyanide once consumed by an animal, but not forms of cyanide that are unlikely to release free cyanide to an animal. From arguments which have been presented regarding the availability of weakly bound metal complexes of copper, nickel and zinc at the pH of a bird’s stomach, it appears reasonable to conclude that in many cases the actual composition of the WAD CN will result in somewhat lower toxicity than an equivalent concentration of free cyanide. This is because formation and absorption of free CN from the dissolved metal complexes occur comparatively slowly, and because complexes may partially dissociate to free CN together with an insoluble neutral metal cyanide complex which precipitates and is unavailable. However, the extent of these effects is dependent on the conditions at individual sites, which are also likely to change over time. WAD CN determinations may also underestimate bioavailable cyanide in species such as raptors, which have a stomach pH lower than that used to determine WAD CN.

Laboratory studies have been conducted where birds were exposed to cyanide in drinking water, which is expected to be the most significant exposure route at mines. Drinking water studies based on standard test guidelines indicated avian LC50 values for bobwhite quail and mallard ducks of 374 mg CN/L and 180 mg CN/L, respectively. However, these studies were considered as unreliable due to uncertain actual concentrations and exposure. The toxicity of cyanide in mine effluent and tap water with single or repeated exposure of mallard ducks has also been investigated, with LC50 values of 181-212 mg WAD CN/L and 136-158 mg WAD CN/L respectively. The results were interpreted as indicating an overall LC01 (1% mortality) of 50 mg/L for repeat exposure, which appears to be a further basis for selection of 50 mg WAD CN/L as a protective value. However, the original reports have not been seen, very limited information on the studies was available and the results are considered to be unreliable.

Other brief exposure (2-4 h) studies with mallards indicate a short exposure LC50 of ~115 mg WAD CN/L, which is consistent with field observations on acute mortality. An assessment factor of 10 could be applied to these, suggesting a concentration of ~12 mg WAD CN/L would be safe to protect mallards from any lethal effects with short term exposure. However, in extending these results to other species with different drinking behaviours and bodyweights, the relative size of a single dose would need to be considered (e.g. a dose of ~8-10 mL used for the ~1 kg mallards is relative to a total day’s consumption of ~60 mL. Mallards would be expected to take six or more drinks per day, whereas a bird weighing ~50 g would consume around 10 mL water per day, and depending on the species, may only arrive to drink once or twice per day).

The most reliable data available for toxicity for birds were from acute oral toxicity tests with seven bird species, with the acute LD50 to mallard ducks of 1.4 mg CN/kg bw the most sensitive value. Modelling based on these limited results estimated a Predicted No Effect Concentration (PNEC) of ~1 mg/L. The use of acute toxicity data for assessment of toxicity from drinking water consumption requires interpolation of the results using estimated daily water consumption. As birds (and animals) may be able to detoxify cyanide if sufficient time elapses between the intake of sublethal doses, assumptions also need to be made regarding the proportion of daily water consumption that birds would ingest in each dose. As a worst case, ingestion of the entire day’s consumption in a single dose has been considered. This is appropriate for species that arrive at water sources only once or twice per day, but is clearly conservative for species such as waterbirds (e.g. mallards) which take several drinks over the day. Such differences in drinking behaviour between species make it difficult to extrapolate toxicity results from one species to another.

There are also studies of biochemical effects and effects on pigeon flight time from cyanide exposure which indicate effects at relatively low doses. Expressed as the concentration given in a single dose of 10 mL (compared to an expected approximate daily water consumption of ~50-60 mL), significant biochemical effects occurred at concentrations as low as 20 mg free CN/L, and significant pigeon flight time effects at 50-80 mg free CN/L. The metabolism of the birds may recover from such doses, but while affected, birds may be more likely to succumb to predators or suffer reduced flying capacity. However, there is no conclusive evidence from observations or incident reports that these effects occur in the field, although in any case they would be very difficult to detect because they would occur at diffuse locations distant from the site where exposure occurred.

Observations also indicate that birds do not avoid drinking cyanide-contaminated mine waste water and may remain in a pond and take further drinks, potentially leading to a cumulative toxicity effect. Depending on drinking behaviour (e.g. species differences) a bird may also take in a greater relative dose. However, it is also noted that birds are averse to drinking hypersaline water. Consequently, cyanide intake is reduced where the water is hypersaline and field studies show mortalities do not occur at hypersaline conditions even at WAD CN concentrations exceeding 50 mg/L.

Similarly, the most reliable toxicity data for mammals were acute oral toxicity studies, with the acute LD50 of 2.3 mg CN/kg bw the most sensitive value for rabbits. Modelling based on these results and drinking water consumption tables again estimated a Predicted No Effect Concentration (PNEC) of ~1 mg/L.

No toxicity data were available for reptiles (e.g. snakes, lizards, tortoise), but data from mammals and birds are considered indicative in the absence of reptilian data.

Toxicity to terrestrial plants

Many plant species contain organocyanide forms, (glucosides) for chemical defence, and cyanide is also produced as a by-product in the synthesis of the plant hormone ethylene. Higher plants contain enzymes that are irreversibly damaged by cyanide, but have other enzymes that can detoxify it. Experimental data with basket willows conducted to explore their use in phytoremediation found that when plants were grown in aqueous solutions doses of 8 and 20 mg CN/L in aqueous solution resulted in mortality in <1 week. When the plants were grown in sand, there were no toxic effects with irrigation by cyanide solutions at 10 mg CN/L; at 20 mg CN/L transpiration was reduced by 50%, but plants survived; while at 30, 40 and 50 mg/L transpiration was greatly reduced and the plants died. It should be noted that other components of tailings also influence phytotoxicity, including the resulting pH and salinity.

For aquatic assessment, a range of acute and chronic toxicity data are available with free cyanide for a range of fresh water and marine species, including fish, invertebrates, algae and aquatic macrophytes. The ANZECC Water Quality Guidelines trigger value for cyanide for protection of 95% of aquatic organisms is 0.007 mg free CN/L at the boundary of freshwater mixing zones, or 0.004 mg free CN/L at the boundary of mixing zones if release is to coastal waters.

Hydrogen cyanide has been used as a fumigant to treat various arthropod pests in some countries. As a fumigant, HCN has a rapid paralysing effect on most insect species. Sublethal concentrations may bring about apparent death, but if exposure is insufficient stupefied insects may recover. However, susceptibility of species varies, and insects which prefer cyanogenic food sources (e.g. lima bean foliage) may be highly tolerant of cyanide in their diet, with cyanide a feeding cue and stimulant to them.

Some species of bacteria exposed to cyanide may exhibit decreased growth, altered cell morphology or other harmful effects, but not all micro-organisms are affected by cyanide and microbial populations can become acclimatised to cyanide and can then degrade wastes with higher cyanide concentrations. Microbes can degrade cyanide by various pathways to yield a variety of products. Several species of fungi can metabolise cyanide, and cyanide compounds are formed as secondary metabolites by many species of fungi and some bacteria by decarboxylation of glycine.

There have been incidents in Australia where hundreds or thousands of birds have been killed within a relatively short period at a single gold ore processing site through exposure to cyanide residues in a TSF or associated facilities. Records indicate smaller numbers of birds have died on an intermittent, ongoing basis at gold ore processing site TSFs and heap leach facilities in Australia and the USA. Field data from the past need to be viewed with some caution due to various practical difficulties in obtaining field observation data, and it is likely that the extent of impacts has been significantly underestimated in the past.

Reliable corresponding information on WAD CN concentrations in areas to which the dead animals were exposed is not always available. However, there is now a body of evidence from scientific observations, anecdotal sources and incident reports at mine sites which indicates that where significant mortalities are observed, WAD CN concentrations are > ~50 mg WAD CN/L. Scientific studies observed relatively few or no mortalities at lower WAD CN concentrations, and the observed mortality at concentrations < 50 mg WAD CN/L in those studies may or may not have been associated with cyanide toxicity. There are some brief published reports indicating mortalities at cyanide concentrations ~20 mg/L, but there is insufficient information for these to be considered reliable – e.g. the animals may have been exposed to higher WAD CN concentrations at an earlier time or different point to where samples were obtained, or died from other causes. Thus field studies give a general indication that 50 mg WAD CN/L is protective of significant bird death incidents, while 1 mg WAD CN would be unnecessarily low, but some caution is needed because field observations to determine the extent of sublethal effects are lacking.