Pesticides
In recent years, the number of pesticides available and the quantity used has considerably increased. The term “pesticide” is used to include insecticides, acaricides, herbicides, fungicides and algicides, indeed any chemical which is used to control an unwanted organism (except bacteria), even rotenone which is used to kill unwanted fish. Pesticides are chemicals which have a specific toxic action to which the pest species is particularly sensitive. The chemical is then applied at a concentration which kills the pest but does not affect a wide range of non-target organisms. The ideal pesticide is a chemical which is extremely pest-specific; for the pesticide user it should also be persistent in order to avoid the need for repeated applications. However, on environmental grounds, pesticides should be non-persistent to avoid concentrations building up in environmental compartments and causing unsuspected side-effects. For example, the insecticide DDT is very persistent and thus can build up in food chains to ultimately affect the egg-shell thickness of birds of prey.
Because pesticides are designed and used to kill living organisms, and because of the possibility of unsuspected side effects, it is tempting to implicate them in any incident of fish poisoning where there is no other obvious cause of the damage. There are many cases, therefore, where pesticides have been assumed to be the cause of damage but where the real cause was some other factor.
Some cases of pesticide poisoning of fish are obvious; accidental discharges from road accidents, factory disasters, overspraying of water, or careless disposal of unwanted spray and pesticide containers, can be clearly identified as causes of mortality, especially if the concentrations measured or calculated in the water exceed the 96 hour LC50 by a significant margin. Less easily identified are cases of long-term leaching of persistent pesticides from fields and forests. Besides these acute and chronic direct effects, an indirect action may be important. Inexpert application of aquatic herbicides or algicides to the water, or the accidental contamination of surface waters with these chemicals, may kill excessive quantities of aquatic plants and algae. The rapid decomposition of this organic matter forms a considerable dissolved oxygen demand on the water. This will lead to an oxygen deficit and the fish may die of suffocation.
Another potentially serious indirect consequence of pesticide contamination of the aquatic biota is the reduction or complete destruction of the natural food supply of the fish. Many of the organisms on which the fish feed are much more sensitive, particularly to insecticides, than the fish themselves. For example, the LC50 for the organo-phosphorus insecticide formulation “Soldep” (active ingredient 25% trichlorphon) for common carp is 545 mg per litre of water whereas for Daphnia magna it is 0.0002 to 0.001 mg per litre.
Besides the active ingredient, pesticide formulations contain a number of other chemicals which may sometimes be much more toxic to fish than the active ingredient itself.
When a pesticide enters the aquatic environment, the active ingredient may undergo chemical and biological degradation. In some cases the degradation products may be more toxic to fish than the original active ingredient. For example, parathion is biodegraded to form paraoxon, which is a more toxic compond; similarly, trichlorphon is degraded to form the more toxic compound dichlorvos. It follows that the absence of a specific active ingredient in water cannot guarantee that harmful degradation products are not present.
Some herbicides are used in fish culture and water management to kill unwanted aquatic plants (e.g. Gramoxone S, Reglone). Trichlorphon based organo-phosphorus insecticides, e.g. Soldep, Masoten, Neguvon, etc. are used to reduce the larger Daphnia in the zooplankton to prevent an oxygen deficit in the pond, to kill predatory cyclopids before stocking the pond with fish at the sac fry stage, to control parasites that infest cyprinids, and for other management purposes. Pesticides based on copper oxychloride may be used to control fish parasites, including the control of gastropod intermediate hosts, and to kill excessive growths of algae.
However, in the majority of cases pesticides have the potential to cause damage to fish. The most toxic pesticides are those based on chlorohydrocarbons (e.g. DDT, dieldrin), organo-phosphorus compounds, carbamates and thiocarbamates, carboxylic acid derivatives, substituted urea, triazines and diazines, synthetic pyrethroids, and metallic compounds.
Chlorohydrocarbon (i.e. organochlorine) pesticides
These pesticides act as nerve poisons. They are highly to extremely toxic to fish (48-hour LC50 < 1.0 mg per litre). Because of their chemical structure and their persistance, their use is now strictly controlled or banned.
The clinical signs of fish poisoning by organochlorine pesticides on the basis of chlorohydrocarbons include increased activity, followed by a long stage of reduced activity. There is no specific patho-anatomic picture in these cases of intoxication; dystrophic alterations have been recorded in the liver and kidneys.
Organo-phosphorus pesticides
The mechanism of the toxic action of organo-phosphorus pesticides on fish follows the same pattern as their action on homoiothermic animals, in that some hydrolytic enzymes, particularly acetylcholine hydrolase, are inhibited. The degree of inhibition of cerebral acetylcholine hydrolase in fish varies with the specific organo-phosphorus compound causing the effect. Phenitrothion-based pesticides reduce the enzyme activity to 60%, dichlorvos- and imidane-based pesticides cause a greater reduction which leaves only 22% of the physiological activity remaining. The toxicity of these pesticide formulations to fish also varies; from the 48h LC50s obtained they are ranked among those substances of very high to medium toxicity to fish (0.1–100 mg per litre). Also, salmonids are very sensitive to organo-phosphorus pesticides. The typical sign of fish poisoning with these pesticides is a darkening of the body surface at the onset of uncoordinated activity. The patho-anatomic picture of such poisoning is characterized by a considerable mucus production on the body surface and in the gills, a heavy congestion of the gills, and small isolated (“spotted”) haemorrhages in the gills when the pesticide concentration is high.
The water flea (Daphnia magna) is very sensitive to organo-phosphorus pesticides; from the 48h LC50s obtained for these substances, they can be classified as extremely toxic. It is interesting to note that the water flea was found to be sensitive to trichlorphon and dichlorvos at concentrations close to the level of detection by gas-liquid chromatography. Daphnia magna can be regarded, therefore as a sensitive indicator of organophosphorus pesticide pollution.
Carbamate and thiocarbamate pesticides
Carbamate and thiocarbamate compounds also inhibit the activity of acetylcholine hydrolase. However, unlike the toxic action of organo-phosphorus compounds, the inhibition of enzyme activity is readily reversed after carbamate and thiocarbamate poisoning. The toxicity levels of these substances to fish vary from very high to low toxicity (48h LC50s in the range of 1 to 1000 mg per litre). The clinical and patho-anatomic pictures of fish poisoning by these pesticides are not specific.
Pesticides based on carboxylic acid derivatives
A number of these pesticides are based on phenoxyacetic acid; the main representative of this group is 2-methyl-4-chlorphenoxyacetic acid (MCPA). Most of the MCPA-based products are of medium to low toxicity to fish (48h LC50s in the range of 10 to 1000 mg per litre). The clinical signs of poisoning are mostly characterized by increasing narcosis. There is no marked patho-anatomic picture in fish poisoned by these herbicides.
Pesticides based on substituted urea
Herbicides formulated from substituted ureas are of high to low toxicity to fish (48h LC50s are in the range of 1 to 1000 mg per litre). The clinical symptoms of poisoning are not specific and include increased activity, irregular respiration, uncoordinated movement and a long period of “distress”. The patho-anatomic picture is characterized by an increased amount of mucus on the darkened body surface, hyperaemia of the gills and the presence of a small amount of exuded fluid in the body cavity of the fish.
Diazine and triazine pesticides
Triazine-based pesticides are of high to medium toxicity to fish (48h LC50s range from 1 to 100 mg per litre). The clinical signs of fish poisoning by these chemicals are largely characterized by progressive narcosis. The presence of exuded fluid into the body cavity and into the digestive tract is an especially characteristic patho-anatomic sign, particularly in rainbow trout. The presence of exudates causes a marked swelling of the body cavity; in rainbow trout it has even led to a rupture of the body wall in some cases.
Diazine-based herbicidal preparations are less toxic to fish than are triazine-based preparations. Most of the former are of low to very low toxicity to fish (48h LC50 ranging from 100 to 10 000 mg per litre). The clinical course of intoxication is characterized by stages of immobility. The patho-anatomic picture is not specific to these compounds.
Synthetic pyrethroid pesticides
The 48h LC50s of these pesticides show that they rank among those substances of high toxicity (up to 10 mg per litre) to extreme toxicity (less than 0.1 mg per litre) to fish. The clinical signs of poisoning are not specific and include respiratory disorders. The most conspicuous patho-anatomic change is the presence of a small amount of exuded fluid in the body cavity.
Pesticides based on metal compounds
These include primarily the fungicides formulated from compounds containing copper, mercury and aluminium. In the majority of cases, their toxicity to fish and the clinical and patho-anatomic symptoms correspond to those found in fish poisoned by the respective metals.