Restoration of ponds, lakes and streams containing fish toxins: a review (2023)

5.1Introduction to fish toxins

Chemicals tested or used as toxic to fish and other aquatic organisms can be grouped into four categories based on their primary use in fisheries management:

Chemicals that have at least a documented use in this area are described in more detail on the following pages. Few studies have been carried out in detail on: 1) toxicity to fish and higher vertebrates; 2) effectiveness on target organisms in different water qualities; 3) residues in fish and other aquatic foods; 4) environmental waste. While data exist on the acute toxicity of some chemicals to fish and other aquatic organisms, information on chronic toxicity and reproductive effects in aquatic animals is often lacking. Furthermore, only a few chemicals are registered with regulatory authorities for use as fishing gear.*Lennon (1967), in his discussion of licensing and registration requirements for fishing chemicals in the United States, noted that some pesticide and public health authorities in the United States and Canadian provinces adopted strict standards to regulate the use of chemicals in the water. For example, the US Secretary of the Interior announced a new policy on June 18, 1970, banning the use of endrin and toxaphene on federal lands. He further stated that the following chemicals are on the list and should only be used in minor applications if other systems do not work: hexachlorinated benzene, cyanide, ethyl parathion, yellow thion, methyl parathion, phosphorus and endosulfan.

All toxic substances mentioned in this report should be considered general hazards and pollutants in the environment. All uses must be as specific as possible to the target organism and must be subject to detailed initial and follow-up studies. Lennon and Berger (1970) presented a list of preliminary observations for recovery from standing and flowing water. Furthermore, mention or discussion of fish poisons in this report should not be construed as an endorsement or recommendation of their safety or effectiveness.

5.2Fish toxicology technical data

Technical data were obtained mainly from three sources: The Merck Index, edited by Stecher, Windholz and Leahy (1968); Handbook of Pesticide Toxicity to Wildlife, Tucker and Crabtree (1970); and Water Quality Standards, J.E. McKee and H.W. eds Wolf (1963). Toxicity classification based on Annex 9.2Toxicity category combination table.

*The US Food and Drug Administration requires that all chemical tools be released and registered under clearly defined conditions for specific uses against specific species. Unregistered chemicals are illegal for use in the United States.

Ramachandran (1960; 1962) injected 12 to 18 milligrams per liter (ppm) of anhydrous ammonia into fish ponds in India to kill submerged noxious weeds, repel or kill fish, and fertilize ponds. He added that the dead fish were safe for human consumption, that the shrimp and frogs in the immediate treatment area were killed, that the ammonia was not persistent in the water, and that the treated water was not toxic to mammals. Application of 13 to 40 mg/L (ppm) of the compound to Texas lakes selectively kills fish completely, drastically reduces phytoplankton and zooplankton, causes profound changes in water chemistry, but produces no permanent waste (Klussmann, Champ, and Lock, 1969).

Antimycin is an antibiotic that is produced in culture.Streptomyces. Strong (1956) and Van Tamelen describe its chemical properties and structureand others.(1961). Strong and Derse (1964) patented it as a fish poison. The first formulation of Fintrol, an antimycin coating on sand grains, was registered in the United States and Canada in 1966.

Walker, Lennon and Berger (1964) and Berger, Lennon and Hogan (1969) reported the effects of antimycin on fish and other aquatic animals in the laboratory. Loeb (1964), Powers and Bowes (1967), Gilderhus, Berger and Lennon (1969), Callaham (1969) and Lennon and Berger (1970) conducted experiments with the application of toxicants to ponds, lakes and streams. Finucane (1969) studied the effect of antimycin on 49 species of marine fish in a salt water reservoir in Florida. Toxicity studies of this compound in birds and mammals confirmed its relative safety as a fishicide (Herr, Greselin, & Chappel, 1967; Vezina, 1967).

Radonski (1967) investigated the potential of antimycin as a selective poison against yellow perch, Avault and Radonski (1967) and Burress and Luhning (1969a) used antimycin as a selective poison against scales in catfish ponds, Stinauer (1968) developed it to stomach. Shad, carp, snook, white bass and bluegill in a largemouth bass pond. Burress and Luhning (1969b) and Moe (1970) described selective thinning of sunfish populations in ponds using antimycins and observed that repeated exposure of fish to sublethal doses of antimycins did not affect reproduction.

Antimycin is not fish repellent and is effective in controlling target fish in coastal areas or in the surface layers of thermostratified lakes without harming non-target fish in open water or deeper formations (Gilderhus, Berger and Lennon, 1969 and Lennon and Berger, 1970). Oregon also took advantage of its non-repudiation by eliminating problem fish in interconnected underground gold mines (Sayre, 1969).

Antimycin is pH sensitive and degrades within hours at a pH of 8.5 or higher. In waters where the pH varies significantly from day to night, recovery should be planned for early morning to ensure lethal exposure of the target fish before the pH rises and the poison becomes ineffective. In soft, acidic water, antimycins usually break down to harmless components within 7 to 10 days. However, this compound can be quickly and easily inactivated with potassium permanganate (Gilderhus, Berger and Lennon, 1969; Loeb and Engstrom-Heg, 1970).

Antimycin preparations are spread on the water by planes, ships or people on foot. Manual or motorized seed spreaders can be used to easily and evenly discharge a wide variety of toxins (Lennon, Berger, & Gilderhus, 1967), or they can be used to discharge toxins into the washing fluid of a motorized boat. The Fintrol-5 formula releases antimycin into the first 1.5 m (5 ft) of water as the sand sinks. The Fintrol-15 formulation released antimycin in the first 4.6 m (15 ft) of depth (Lennon and Berger, 1970). These sand formulations are particularly suitable for treating wetlands and water bodies blocked by new and non-emerging aquatic plants. Sand particles bounce off vegetation and penetrate weed-clogged water, and circulation is severely impeded. Liquid poisons are generally not very effective in this situation because they stick to or dry to emerging vegetation and cannot penetrate water with weeds.

Fintrol concentrate is a liquid formulation of an antimycin that can be applied to streams through a drip irrigation system or applied as other liquid poisons to ponds and lakes. However, like other liquid toxins, it should not be sprayed from aircraft, as volatile solvents are often lost in the air, leaving insoluble toxins in surface films of water.

A formulation of antimycin cakes for use in streams is under development (Lennon, 1970a). Preliminary tests showed that the cake could be suspended in a stream, dissolving and releasing its antimycin at a consistent rate over a period of time. This cake will eliminate many of the problems encountered in the long-term operation of drip irrigation equipment and save labor.

Regarding the increasing use of antimycins in streams, Marking (1969b) demonstrated that the venom was compatible with the fluorescent dyes rhodamine B and sodium fluorescein and could be used to trace the movement of venoms in streams or downstream. Furthermore, since fisheries managers in some cases wish to treat the tributaries with antimycin and the receiving lake with rotenone, Howland (1969) studied the interaction between the two toxins. He concluded from experiments with rainbow trout and sunfish that the poisons were compatible and would not neutralize each other when mixed.

St. Amant, Johnson and Whalls (1964) reviewed the toxicity of Aqualin to fish. After successful laboratory tests on goldfish, the compound was applied to several small lakes in California, including a frozen lake, at concentrations of 1 to 3 mg/liter (ppm). Goldfish and other fish species were eliminated, and the researchers recommended further research on Aqualin. However, they point out that the compound is tear-producing and toxic and must be stored in airtight containers and injected underwater through a closed pump system.

Howell reported the highly toxic activity of Bayluscide against lamprey and rainbow trout larvaeand others.(1964). Furthermore, they found that the compound acts synergistically with 3-trifluoromethyl-4-nitrophenol as a selective poison for lamprey larvae. Marking and Hogan (1967) reviewed the literature on the toxicity of belucid to plankton, fish and mammals when used as a molluscicide and showed that laboratory bioassays showed the compound to be toxic to 17 species of game and raw fish. High and general toxicity. Small scale tests in ponds have shown that Bayluscide is rapidly toxic to bulls, but the poison itself breaks down rapidly in high pH water where bulls are abundant and undesirable. Formulation problems, residues in water and fish and product costs must be addressed before the poison can be registered and accepted for use in fisheries. At the same time, heavy particulate formulations of Bayluscide were increasingly used to sample lamprey larvae in deep or turbid streams in Canada and to eradicate populations of lamprey larvae in estuaries or lakes in the Great Lakes (Tibbles, Lamsa, & Johnson, 1969).

Huston (1955 and 1956) conducted experiments with calcium carbide as a selective carp control. Granules of this compound are coated with tallow, paraffin, liquid plastic or placed in gelatin capsules to make them waterproof and attract carp. After the fish has ingested the pellets, the coating material is digested and the carbides react with the liquid in the gut to form large amounts of acetylene gas. Intestinal distension leads to the death of the fish. During field trials with tallow-coated pellets, some carp, bullheads and dead carp were found, but evidence of carbide was inconclusive.

Chlorine in liquid, gaseous, or powder form has been used to disinfect fish hatcheries since at least the mid-1930s (Connell, 1939). Initial large-scale use included disinfection and disinfection of a series of earthen ponds, connecting ditches, and a natural stream section to control bacterial disease problems in trout hatcheries in New Hampshire (Davis, 1938). Panikkar (1960) suggested the use of calcium hypochlorite to kill fish and tadpoles in partially drained fish ponds. A more comprehensive study of chlorine as a fish poison was carried out by Jackson (1962), both in the laboratory and in the field. He pointed out that the amount of chlorine added must be sufficient to cover the water's chlorine needs, in addition to a lethal dose for the species to be controlled; Reclamation of water supply reservoirs with toxic substances.

Personal communication related to this report indicates that chlorine is the fish poison and disinfectant of choice in some hatcheries and fish farms where rapid containment and rapid return to production is required. The ease of neutralizing chlorine with sodium thiosulfate is considered another advantage.

Titcomb (1914) was probably the first to use copper sulfate to kill entire populations of fish. The use of the compound as a fish poison continued, but it did not always kill the fish completely and often produced side effects, including large numbers of phytoplankton, zooplankton, insect larvae and molluscs (Smith, 1935 and 1940). These deficiencies, along with the introduction of rotenone and the presence of other fish poisons, have led to a decline in the use of copper sulfate in fish control.

Allison (1964) controlled the reproduction of sunfish in Ohio agricultural lakes by placing copper sulfate crystals in nests containing eggs or fry, but Beyerle and Williams (1967) used the same technique in eight Michigan lakes with almost no success. The compound was successful in selectively controlling shad, shad, and bullhead in 10 Texas lakes with total alkalinity below 100 mg/L (ppm) (Toole, 1968). In recent years, Virginia may have used more copper sulfate than any other state in fisheries management (Stroud and Martin, 1968). Based on 10 years of laboratory and field trials, the agent has been used in ponds from 0.4 to 60.7 ha (1 to 150 a) for selective control of raw fish.

Croton seed powder is the residual product after croton seeds are pressed from croton oil (crotonI.). This powder is one of the fish poisons that have been used in China for many years to eliminate predators in carp ponds (Hora and Pillay, 1962).

some South American Indians usecloveas fish poison. In laboratory tests, simple aqueous extracts of the leaves had rapid and highly toxic effects on guppies and goldfish (Quilliam and Stables, 1968). The typical response of the fish is strenuous activity followed by loss of coordination, paralysis and death.

Srivastava and Konar (1966) conducted laboratory bioassays of dichlorvos on fish and insects and concluded that the compound is a potent inhibitor of predatory fish and insects and competing fish species in Indian fish farms. A promising selective poison. The lethal dose for fish is much higher than the lethal dose for aquatic insects. Sreenivasan and Swaminathan (1967) recommended this compound as a selective fish poison and as an effective tadpole poison in fish ponds. Comparative tests conducted by Konar (1969) showed that dichlorvos is better than phosphoramide because it is more effective for fish, is not adversely affected by turbidity, and breaks down faster.

Hoff and Westman (1965) tested a 0.1 mg/liter (ppm) 3:2 mixture of dibromide and malathion (active ingredient) in freshwater ponds in New Jersey and reported that white bass, pike, sunfish, pumpkinseed, and possibly other sunfish also has been selectively controlled without causing undue harm to largemouth bass. Meyer (1966) reported an experimental treatment in California that resulted in the death of 30% of large populations of green sunfish and bluegills. Limited testing elsewhere in hard water has not shown selective toxicity of the chemical mixture.

Henderson, Pickering, and Tarzwell (1959) reported that endrin was by far the most toxic insecticide to all fish species and the most toxic chemical tested in their laboratory. The most widespread use of endrin as a fish poison appears to be in Malaysia, where Soong and Merican (1958) removed all fish from 108 ponds and fishponds before reintroduction. Yatomiand others.(1958) tested three endrin formulations on fish in Japanese rice fields and found that toxicity could last for more than a month. A small lake in Michigan has been treated with only partial success at 0.008 mg/l(ppm) and further use of endrin is not recommended (Hooperand others., 1964).

More recently, Bhimachar and Tripathi (1967) reported that endrin at 0.1 mg/L (ppm) was used to kill predatory fish and weeds in Indian carp ponds. A generous dose of charcoal works well to detoxify treated water.

Some commercial fish farmers have anecdotally reported that Guthion is very effective in selectively removing nuciferous fish from baited minnow tanks, but is generally considered unsuitable for use in catfish tanks. Meyer (1965) successfully killed green sunfish and other undesirable species in ponds in Arkansas without harming channel catfish. He noted that temperature and water quality had little effect on Guzion's performance; the compound had more potential to control fish than malathion, parathion, or trithion; but the fish killed by Guzion were not edible.

Indigenous peoples of the lower Amazon in Brazil used the leaves of this small herb.last fish, has long been used as fish poison (Casconand others., 1965). The leaves are incorporated into bait made from grasshopper or tapioca flour, which is then thrown into the water for the fish to swallow. This application is different from rotenone = plants containing rotenone, where the toxic substance is applied directly to the water.

The active ingredients in the herb's leaves are fish alcohol and fish alcohol acetate. Casconand others.(1965), who reported the isolation and identification of these compounds, indicated that guppies reacted rapidly to traces of poison during extreme agitation and died after a few minutes.

Lime in various forms has been used for many years to fight pests in aquariums. Schäperclaus (1933) suggested the use of caustic lime to control parasites and disease-causing organisms in drained ponds, and Markevich (1951) suggested the use of milk of lime at 2500 kg/ha (2230 lb/yr) to disinfect dehydrated ponds containing sick fish. Pratherand others.(1953) stated that the use of slaked lime as a disinfectant in ponds would kill unwanted fish, and Hora and Pillay (1962) reported that quicklime was often used in Chinese carp ponds to eliminate toxic organisms, including fish. Recently, Sidthimunka and Choapaknam (1968) showed that predators in shrimp ponds can be controlled by liming.

There is an extensive literature on the biological activity of malathion, including its effects on fish and aquatic invertebrates (Walker, 1969). Toxicity among fish can vary from a few parts per billion to a few parts per million, with a 1000-fold range, depending on exposure, temperature, pH and water hardness. Some private pond farmers use this differential toxicity to control predatory or competitive fish in production ponds. For example, Al-Hamed (1967) found that it was possible to eliminate wild fish from lakes in Iraq without harming farmed carp. Undesirable sunfish can be selectively removed from walleye ponds by applying 0.5 mg/L (ppm) malathion when water temperatures are between 4.4 and 26.7°C (U.S. Sport Fisheries and Wildlife Bureau, 1970b).

Malathion may have some registrable uses in fish farming if residue tolerances are established in water and fish products.

Srivastava and Konar (1965) conducted phosphoramidite bioassays on rohu and predatory fishes such as silver carp, kolawai perch, nandus, kalisa, alpinist and tengla. They concluded that predatory fish and predatory insects could be eliminated without harming the carp.

Research into fish poisons in Russia led to the development of polychloropine (Burmakin, 1965). The compound is a chlorinated turpentine that is similar in some ways to toxaphene. By 1963, 118 ponds in Russia had been treated with 0.05 to 0.20 milligrams per liters (ppm) of the compound to control raw fish, and some trials had begun in small ponds in Germany (Schäperclaus, 1963). By 1965, 241 lakes in Russia, totaling 17,000 ha (42,000 a), had been restored with polychloropinenes (Burmakin, 1967). The poison remains in lakes in northern Russia for up to 1.5 years, and its degradation in water depends on water concentration, water temperature, alkalinity, depth and degree of mixing. Small shallow ponds are the preferred treatment method, and intensive management of food fish production is often followed by recovery.

Bizyaev, Antimov and Moskalev (1965) noted that Russia continues to look for toxic substances for fish. The polychloropine has some drawbacks, such as non-specificity for fish, greater persistence in water and safety concerns when used around humans, they added. Unlike the polychloropine, the researchers were looking for a poison that was highly toxic to fish, harmless to warm-blooded animals and would break down quickly.

For centuries, hominids around the world used the rotenone-containing roots of many plants in the legume family to stun and kill fish (Leonard, 1939). Rotenone root powder, which contains approximately 4% rotenone, was first used as a fish poison in Michigan in 1934 and quickly became popular for pond and lake recovery. Soon, different uses, different application techniques and new formulations appeared. Davis (1940) and Greenbank (1941) demonstrated that warm water fish could be controlled by treating the trout pond water layer with little harm to the trout. Wales (1942) Control carp by poisoning spawning bays in lakes. Surber (1948) found that emulsified rotenone was superior to the powdered form. By 1949, 34 states and several Canadian provinces were routinely using rotenone in restoration projects (Solman, 1950).

When starting to use rotenone in fisheries management, the recommended concentration is around 0.5 mg/l (ppm), which is sufficient under ideal conditions. However, errors often occur under less than ideal conditions, with the result that application rates gradually increase to empirically prescribed levels. Generally, people tend to calculate the required quantity and add some surplus to provide a margin of safety. Depending on the amount of water being treated and other conditions involved, the excess can be as much as two to three times the "normal" dose.

Product instability and inconsistent results were the first problems with rotenone. Moorman and Ruhr (1951) noted that a decrease in the strength of stored rotenone could lead to recovery failure. Almquist (1959) stated that the toxicity of rotenone can be reduced by exposure to light, heat, oxygen, alkalinity and turbidity. Pintler and Johnson (1958) found that cubed powder contained between 2% and 5% rotenone. However, in the 1950s, preparations with a guaranteed rotenone content were produced.

Rotenone formulations were continuously developed, and Shannon (1969) tested nine commercially available formulations for toxicity and detoxification. They include a wettable powder and eight emulsions. Some formulations of the latter contain 5% or more orothinone; others contain 2.5% rotenone and synergists; some are homogenized to improve performance in specific cases. These toxins are effective on both freshwater and marine fish. However, liquid formulations are malodorous due to the solvent or vehicle and are significantly repulsive to fish. Therefore, great care must be taken during the recovery to not allow any sort of escape for the target fish.

Commercially available rotenone preparations can be fully or partially detoxified with potassium or chlorine permanganate. In addition, experimental work has shown that water treatment plants with sufficient activated carbon capacity can produce safe and palatable drinking water (Cohenand others., 1961 and Bonn and Holbert, 1961).

Hooper (1955) gives a review of techniques and equipment for water recovery using rotenone. He points out that it is difficult to distribute toxic substances in water deeper than 4.7 to 6.3 m (15 to 20 feet) unless the chemicals are pumped into the water through heavy hoses or the chemical is dispersed throughout the water body. deep. Bassett (1956) made an economic evaluation of several rotenone formulations and showed that some spread more readily at depth than others. Turner (1959) analyzed the results of treating ponds on 56 farms in Kentucky with four preparations of rotenone. The liquid formulation is sprayed onto the surface of the pond with a motorized pump, and 1 mg/liter (ppm) is enough to kill the fish. He noted that the formulation has an effective penetration depth of 1.5 to 2.4 m (5 to 8 ft) during both summer and fall treatments. Total mortality occurred in 97 percent of the 24 ponds treated during summer when water depth exceeded 2.4 m (8 ft), stagnant water, and insufficient dissolved oxygen. However, only 72% of the 32 lakes were completely destroyed by the fall, and Turner (1959) hypothesized that the fish escaped the cerostenone in deep water, which was now thermostated and well oxygenated. He concluded that treatment of agricultural lakes in Kentucky deeper than 2.1 m (7 ft) should be limited to the summer months of June through mid-September.

In a review of the use of fish poisons in Quebec, Canada, Prévost (1960) noted that lake restoration through fish poisoning was the best tool available to fish managers. He lists rotenone as the main poison, but advises managers to consider thermoclines, weed beds, floating islands, springs, water temperature, turbidity and alkalinity, and to consider beaver dams, swamps, isolated ponds when dealing with lakes and upstream and downstream. sources of reinfection during flux treatment. He cited the example of some lakes that have been cleared of rough fish 10 years after restoration, resulting in a significant trout catch. Stroud and Martin (1968) reviewed the treatment of lakes and streams in the United States and Canada and noted that rotenone was the most commonly used poison in the United States. Kinney (1968) suggested the use of rotenone to completely, partially or selectively kill target fish. Howland (1969) showed that rotenone and antimycin are compatible when both are used together for restoration of lake systems.

Many researchers have studied how rotenone works in fish. Hamilton (1941) reported that rotenone is a respiratory toxin in fish that acts by vasoconstriction of the gill capillaries. Oberg (1967) found that rotenone is a potent inhibitor of the respiratory chain in fish, and its site of action is located in the flavoprotein region of the respiratory chain. The special structure of the gills facilitates the penetration of rotenone into the blood, where it is transported to vital organs to inhibit respiration. This effect was reversible, and Bouck and Ball (1965) showed that methylene blue could be used to rescue warm-water fish from rotenone poisoning.

The effects of rotenone on aquatic invertebrates have been reviewed by Taube, Fukano and Hooper (1954), Almquist (1959), Wollitz (1962) and Binns (1967). Oral LD50s for ducks and pheasants exceed 1000 mg/kg (Tucker and Crabtree, 1970), while oral LD50s for some mammals are: 60 mg/kg for guinea pigs, 1.5 g/kg for rabbits, 3 g/kg for dogs ( Cohen)and others., 1960). Tilemans and Dormal (1952) reported an oral LD50 of 2850 mg/kg for human rotenone.

Saponins are water-soluble glycosides found in 75 or more plant families. They are foaming agents that have historically been used to wash silk, wool and cotton fabrics; to make sparkling wine and sparkling water; and for washing silk, wool and cotton fabrics. and as an ingredient in expectorant medicines. 300 to 400 species of saponin-containing plants, including rhododendron, camellia, rhododendron and heather, have since ancient times been known in Asia as "fish plants" for gathering fish in ponds, rivers and estuaries (Tang, 1961 and Knoller, 1965). Tea seed cake, a common form of fish poison, is the saponin-containing residue left after pressing oil from camellia seeds. The cake contains 10% to 13% saponin.

Soong and Merican (1958) cite the use of tea seed cakes in Malaysia and China to remove fish from ponds. Tang (1961) noted that Chinese fish farmers often used tea seed cakes to control unwanted fish in ponds before stocking them. He also conducted successful experiments in Taiwan using powdered saponin and crushed tea seed cake to control predatory fish in shrimp ponds. . Ryther (1968) noted that tea seed cake is commonly used for this purpose in the Singapore region.

In the USA, Lunz and Bearden (1963) tested low concentrations of saponins in a small shrimp pond in South Carolina and killed most of the fish. But they concluded that tea seed cake was too expensive here to be economically viable as a fish poison.

On the other hand, Russian research on piscicides, which are highly toxic to fish, harmless to warm-blooded animals and humans, and rapidly degradable, has focused on saponins (Bizyaev, Antimov, and Moskalev, 1965). They confirmed the toxicity of rhododendron glycosides to fish and other aquatic organisms, but concluded that the main source of saponins in Russia appears to be sugar beets. Saponins are mainly found in the surface layer, in the fine root and in the tail of sugar beet. The saponin concentrate is obtained by centrifuging the foam in the beet juice produced by pressing the beets into briquettes. The liquid concentrate is toxic to fish at a concentration of 0.2 mL/L (ppm), while the dry saponin is toxic at a concentration of 2 mg/L (ppm). Toxic effects on fish occur within 20 to 24 hours, and saponins are completely degraded within 7 to 10 days. The authors demonstrate that sugar beet saponins are the most effective and acceptable means of removing harmful fish species from inland waters.

Bridges (1958) introduced the use of sodium cyanide as a fish poison after experiments in laboratory aquariums and farm ponds in Illinois. He reports that 1 mg/L (ppm) sodium cyanide is readily available in the form of 28 grams of cyano eggs, which will kill a wide variety of warm water fish at various temperatures and pHs at a cost of $0.55/1,000. m3. Within minutes, fish begin to emerge and the desired species can be transferred to fresh water for full recovery. The water in the small farm lakes remained toxic for about four days.

Lewis and Tarrant (1960) continued experiments in Illinois demonstrating the effectiveness of sodium cyanide as a collection tool and general poison. They recommend this compost for preparing breeding and hatching tanks. Related to these experiments, Leland (1964) investigated the loss of cyanide in water, soil, and fish. He determined that cyanide residues in the sediments were not a problem; the toxic substance disappeared from the water in 4 to 20 days and disappeared more slowly in cold water or under ice; cyanide residues in live fish decreased to 0.1 mg after 24 hours in fresh water/kg or less.

Miller and Madsen (1964) in Nebraska demonstrated the various uses of sodium cyanide, including live removal of northern pike from ponds, rescue of fish from irrigation canals, and monitoring of fish populations in lakes and streams. water. lake. In South Dakota, the agent has been used with varying degrees of success to remove live spoteye from culture tanks and restore the tanks for restocking the following year (Hanten, 1966). Whitley (1967) reviewed the effects of sodium cyanide on fish in Missouri and noted that the compound was toxic at all temperatures but was more rapid in warm water. Currently, the largest use of cyanide is concentrated in the lower Mississippi River basin, where fish farmers use thousands of kilograms of cyanide in aquariums to destroy competing fish and invertebrate predators (Prewitt, 1970). Snakes and birds that eat fish sometimes die from fish treated with high levels (10 mg/liter [ppm] or more) of cyanide.

Sodium hydroxide pellets were placed in the nests of troublesome sunfish to kill eggs and fry (Jackson, 1956). However, this control is limited to waters where nests can be easily located and removed with reasonable time and effort.

The LC50 for sodium pentachlorophenate for channel catfish species is 0.46 mg/l (ppm) (Clemens and Sneed, 1959). Walker (1969) showed that concentrations as low as 0.06 mg/l (ppm) were lethal to fish under laboratory conditions and that piscicidal activity varied with temperature, pH and other factors. A private pond owner told us that sodium pentachlorophenate effectively removed fish from his pond but did not kill tadpoles or snails. He found that the residues of the compound were harmful to the early stages of development of the fish, causing excessive mortality and deformities, especially in goldfish, and discontinued the use of the compound.

Westman and Hunter (1956) experimentally used 168 milligrams per liter (ppm) of sodium sulfite in a small lake in New Jersey to save some fish and reduce others. They concluded that salvage operations were possible on a small scale, but the complex was too expensive for large bodies of water. Sodium sulfite will quickly reduce the concentration of dissolved oxygen in the water, causing the fish to suffocate. Water is non-toxic and dissolved oxygen is quickly recovered. Rescue by transferring affected fish to fresh water. Species with poor mouths have difficulty swallowing air at the surface, making them more likely to suffocate.

Grice (1961) reported that 100 mg/L (ppm) sodium sulfite followed by 50 mg/L (ppm) sodium sulfite approximately 22 hours later in a Massachusetts lake was effective for white-eyed fry. pond in Massachusetts. More recently, Vanderhorst and Lewis (1969) used cobalt chloride to catalyze sodium sulfite and concluded that this combination holds promise for the selective removal of fish, especially channel catfish.

Squoxin was patented in 1968 as a result of research at the University of Idaho into a selective poison for blobfish, a troublesome predator of salmonids (MacPhee and Ruelle, 1968). In a subsequent report, MacPhee and Ruelle (1969) demonstrated a 10- to 17-fold difference between the minimum LC100 of two shortnose fish and the maximum LCO of the least tolerant salmon. Markering (1969a) listed 96-hour LC50 at 12°C for nine fish species ranging from 0.182 to 0.779 mg/l (ppm).

summarized inCommercial fishing review(Anon., 1970) classified Squoxin as a poison with particular selectivity for puffer fish. The main advantages of Squoxin are: trout lethal concentrations have no effect on aquatic invertebrates, mammals or humans; poison is short-lived in water; and has no repellent effect on catfish.

Intensive research work by the US Fish and Wildlife Service led to the development of TFM as a selective agent for sea lamprey larvae (Applegate)and others., 1961). The compound has proven to be a practical and safe control agent for sea lampreys in the upper Great Lakes. Its toxicity is greatly affected by water hardness and pH, and it is most effective for lamprey larvae in slightly acidic water in late fall, winter and early spring.

Since TFM is relatively expensive, research into more cost-effective methods of controlling sea lampreys continues. howelland others.(1964) found that the addition of 2% Bayluscide synergized with TFM, maintained selectivity for lampreys, and reduced processing costs by about 50% Accurate dosing of a liquid mixture of TFM and Bayluscide in streams kills lamprey larvae in bottom mud, with little effect on other aquatic life and game fish. Baldwin (1968) reviewed the status of control efforts and improvements in sport and commercial fisheries in the upper Great Lakes region.

Tanite was tested at 0.7 to 1.5 mg/L (ppm) in Illinois ponds to determine its potential for live fish removal and selective and complete fish kill (Lewis, 1968). The compound first has a numbing effect on the fish, at this stage the desired species can be easily collected on the surface. Its recovery in fresh water is rapid and complete. Live harvesting of adult largemouth bass from ponds has been very successful. Lewis (1968) also observed that tanite could act as a selective poison against carp in the presence of carp and carp. Leland (1964), working with Lewis, showed that cyanide was present in the blood of fish killed by tanite, but this cyanide was rapidly lost from the blood of fish exposed to fresh water.

Additional research on tanite as a fishing gear is being conducted at the US Fish and Wildlife Service's Fish Control Laboratories in La Crosse, Wisconsin and WarmSprings, Georgia.

Schoettger (1970) investigated the toxicology of endosulfan in fish and aquatic invertebrates to determine the potential of this compound as a fish poison. He also reviewed the literature from the early 1960s on the properties of endosulfan and its performance as a fish poison in limited trials. He found that fish were at least seven times more sensitive to endosulfan than invertebrates; exposure to 50 mg/l (ppm) for 2 hours was not toxic to fertilized rainbow trout eggs; Of little value as a selective fish poison; the compound may be a good general fish poison under some conditions; toxic residues remain in the skin and muscles of fish exposed to acute concentrations and various subacute concentrations.

The future of endosulfan as a fishing gear is still in doubt. It is a chlorinated hydrocarbon insecticide; and may not be able to compete with non-sustainable and more selective fishing regulations in the registration process.

In Southeast Asia, tobacco residues are added as fertilizer to dairy fish ponds with the advantage that nicotine kills aquatic insects (Bardach, 1968). Personal communication indicates that Taiwan's lakes use approximately one ton of tobacco waste per year. The nicotine in the tobacco combined with lack of oxygen from rotting plants can poison and suffocate unwanted fish, fish parasites and possibly bacteria. . Tobacco dust with a nicotine content of 12 to 15 kg/ha kills fish, snails and polychaete worms. Soot can also be used as a direct fertilizer and speed up the fertilization of rice straw, rice bran and other plant materials.

In India, Konar (1970) suggested that nicotine could be very useful as an aid in fish gathering and as a poison. Rohu exposed to 3.2 mg/L (ppm) nicotine and rohu exposed to 5.0 mg/L (ppm) nicotine emerged in 5 to 10 minutes and returned to fresh water in 2 to 4 minutes. Some fish left in the nicotine solution showed signs of acute poisoning and died, while others showed no signs of poisoning. The low concentrations of nicotine tested were less toxic to aquatic insects than to fish.

Toxaphene consists of a mixture of polychlorinated bicyclic terpenes, mainly chlorinated camphenes. At its highest purity, it contains 67% to 69% chlorine. It has been used extensively to control a variety of pests (Gebhards, 1960). Surber (1948), who was probably the first to test toxaphene on fish, observed that 0.04 milligrams per liter (ppm) of toxaphene killed all fish in small ponds. Tarzwell (1950) observed that toxaphene was much more toxic to fish than rotenone and suggested that this compound could be used for fish management. Hemphill (1954) conducted the first large-scale field trials of toxaphene as a fish poison in two Arizona lakes in 1951. A concentration of 0.1 milligrams per liters (ppm) eliminated rough fish, including carp, from a lake and significantly reduced your numbers. Other things. Toxaphene kills more slowly than rotenone and can last for days, he added. The insect life in the lake was severely affected but not eliminated.

Tanner and Hayes (1955), evaluating toxaphene as a fish poison in Colorado, indicated that a pond could be effectively treated with this compound at a cost of about $0.10/1000 m3 compared with $0.77/1000 per cubic meters of rotenone. Although they acknowledge that toxaphene is economically attractive, they warn that it is an extremely potent poison and more toxic to warm-blooded animals than rotenone, requiring more precautions in handling. They concluded that toxaphene could remain at toxic levels for at least seven months in lakes with a pH of 8.0 or higher.

In Michigan, Hooper and Grzenda (1957) demonstrated that toxaphene was more toxic to fish in hard water than in soft water and more toxic in warm water than in cold water. Although toxaphene at 0.1 mg/L (ppm) has good effects on fish, ponds are toxic to fish for 2 to 10 months. Demersal invertebrates die in large numbers, but quickly reappear in large numbers.

Toxaphene at 5 micrograms per liters (ppb) in hard water killed small fish but left large sunfish and largemouth bass unharmed, an observation that led Fukano and Hooper (1958) to suggest that the compound had selectively toxic potential. Stringer and McMynn (1958) applied 0.01 to 0.10 milligrams per liters (ppm) of the compound to eight alkaline lakes in British Columbia, killing all fish and amphipods. They noted that toxaphene was an effective and cost-effective fish poison, but nine months after treatment the lakes remained toxic to the fish. In a follow-up study, Stringer and McMynn (1960) discussed toxaphene delivery method, time of fish death, lowest lethal concentrations for many fish species, and factors affecting degradation. They note that small concentrations of toxaphene, used to control carp and common carp, can persist at toxic levels for two years in deep, clear, stratified lakes in British Columbia. On the other hand, the detoxification process in some turbid lakes is so rapid that relatively high concentrations cause only partial fish death.

Laboratory and field trials with toxaphene in fish in Iowa have been encouraging (Rose, 1958). Carp and bullfish require more than 25 micrograms per liter (ppb) to kill in cold, clear water, and 200 micrograms per liters (ppb) to kill the same species in very turbid water. The slime is suspected of having a direct detoxifying effect.

McCarraher and Dean (1959) reviewed the results of a 4-year toxaphene recovery effort in Nebraska lakes. They found that at least 0.5 milligrams per liter (ppm) of toxaphene was required to completely kill fish in sandy mountain lakes with moderate alkalinity, high turbidity, and a pH of 8.5 to 9.5. However, they documented serious problems during aerial application of toxic substances. Aerial application of toxaphene at 0.61 milligrams per liters (ppm) to a pond killed all mallards, but the carp and manatee survived. A similar application of 0.52 mg/L (ppm) toxaphene in another lake killed all but 33% of the fish. Mallards and 29% mallards were present in the treated area, but less than 10% gulls and grebes. Waterfowl losses range from 15% to 100% for each aerial application of toxaphene. Mammal deaths likely associated with these actions include raccoons, dogs, skunks, and livestock. In contrast, when toxaphene was sprayed into the water from boats, few birds died.

Gebhards (1960) documented the increasing use of toxaphene in western North American states and provinces. He also discusses the toxicity of toxaphene to humans, livestock, waterfowl, fish, and aquatic invertebrates, noting that the factors that increase the rate of toxaphene detoxification are sunlight, high concentrations of dissolved oxygen, high temperature, circulating water, and turbulence. Kallman, Cope, and Navarre (1962) demonstrated that aquatic plants in treated lakes accumulated high concentrations of toxaphene and that rainbow trout and black bulls concentrated the toxin in their bodies. Hunt and Keith (1963) discussed the biomagnification of toxaphene residues resulting in bird death. After treating Big Bear Lake, California, Johnson (1966) recommended that toxaphene not be used as a fish poison anywhere in the state. terrierand others.(1966) observed persistence of toxaphene in Oregon lakes for up to 6 years with residue accumulation of up to 14 mg/L (ppm) in rainbow trout and 17 mg/L in aquatic plants (ppm). Additional reviews of the performance and persistence of toxaphene were made by Nehring (1964), Johnson, Lee, and Spyridakis (1966), Henegar (1966), and Moyle (1968).

A 1966 study found that toxaphene was the second most common fish poison in the United States, after rotenone, but the first in Canada (Stroud and Martin, 1968). Anwand (1968b) described the limited use of fish poisons in Germany. However, use of the compound as a fish poison declined rapidly in the United States in the late 1960s, in part due to a ban in 1963 by the US Department of the Interior (Dykstra and Lennon, 1966). The reasons for this ban are the persistence of toxaphene in water, the high toxicity to invertebrates and vertebrates, especially waterfowl, and the accumulation of residues in plants and animals. Prohibit further use of toxaphene as a fish poison in federal or federally assisted programs. Walker (1969) noted that toxaphene is one of the most widely used fish poisons in the United States and Canada.