Chemicals in water as a result of man's activities - دپارتمان شیلات فرد

Cyanides

Cyanides do not occur naturally in waters; they can be discharged in various industrial effluents, particularly from metal plating works and from the thermal processing of coal (e.g. for town gas production). Cyanides may be present in water either as simple compounds (nondissociated HCN, simple CN ions) or as complex compounds (e.g. complexes with iron, cobalt, nickel and other metals). Simple cyanides are very toxic or extremely toxic to fish species; lethal concentrations for the majority of species are in the range of 0.03 to 0.5 mg per litre. Cyanide toxicity is affected by the pH of the water; if the pH is low the proportion of nondissociated HCN increases and so does the toxicity (Table 2). Cyanide toxicity is also markedly enhanced by an increase in water temperature and a decrease in the concentration of dissolved oxygen in the water.

With complex cyanides, the toxicity varies according to their ability to dissociate into metal and HCN. For example, the complex iron cyanides which do not dissociate are of low to very low toxicity to fish but the complex cyanides of zinc, cadmium, copper and mercury which do are highly toxic.

The mechanism of the toxic action of cyanides is based on their inhibition of respiratory enzymes (i.e. cytochromoxidases). This blocks the transfer of oxygen from the blood to the tissues, reduces tissue respiration and leads to tissue asphyxia. The clinical symptoms of the cyanide poisoning of fish include increased depth of respiration, nervous disorders, and loss of equilibrium. If the fish are transferred to clean water while they are in the early stages of overturning, they will recover in 1 to 2 hours. The characteristic features of the patho-anatomic examination in cases of cyanide poisoning include a cherry-red colour of the gills and sometimes also leakage of tissue fluid mixed with blood into the body cavity.

Table 2: The dependence of HCN content (% of simple cyanide content) on water Ph

Cyanides

Divalent metals and their salts

Trace quantities of metals present in waters may be of natural origin. If waters are polluted with metals at greater concentrations, the source may be traced back to ore mining and processing, to smelting plants, rolling mills plants for the surface treatment of metals, film, textile and leather industries and other sources. Atmospheric precipitation can wash out metals in dust and aerosols generated by the burning of fossil fuels, by the exhaust gases of motor vehicles, and from other sources.

The mechanism of the toxic action of metals on fish is varied. Most of the metals have a great affinity for amino acids and the SH groups of proteins: as such, they act as enzyme poisons. The toxicity of metals to fish is significantly affected by the form in which they occur in water. The ionic forms of metals or simple inorganic compounds are more toxic than complex inorganic or organic compounds. The toxic action of metals is particularly pronounced in the early stages of development of the fish.

Another potentially harmful property of many metals is their ability to accumulate in the sediments and in the aquatic flora and fauna (bioaccumulation). This property is quantitatively described by the accumulation coefficient (concentration in substrate/ concentration in water) and such values can range from several hundred to many thousands; mercury, selenium and cadmium have a particularly high bioaccumulation capacity. Hence, the concentration of these metals in water does not provide a true indication of the total pollution of the aquatic medium; it is better to use the content of metals in the sediments, and especially also in the bodies of predatory fish which are the final link in the food chain, as an indicator.

The metals found to be of highest importance to fisheries in practice include aluminium, chromium, iron, nickel, copper, zinc, arsenic, cadmium, mercury and lead.

Chromium

In surface waters, the most stable forms of chromium are the oxidation states III and VI. Of these two forms, chromium III is poorly soluble and is readily adsorbed onto surfaces, so that the much more soluble chromium VI is the most common form in fresh

water. For this reason, maximum admissible concentrations for chromium are generally based on toxicity data for the hexavalent form.

Chromium compounds in the trivalent state (III) are more toxic to fish and other aquatic organisms than are those in the hexavalent state VI. From the LC50 data obtained for different fish species, chromium III compounds are among those substances with a high toxicity to fish (LC50s of 2.0 to 7.5 mg per litre) whereas chromium VI compounds are among those substances of medium toxicity (LC50s of 35 to 75 mg per litre). The toxicity of chromium compounds to fish is also considerably affected by the physico-chemical properties of water, especially the pH value and the concentrations of calcium and magnesium. At a high pH and a high concentration of calcium, the toxicity of chromium to aquatic organisms is reduced, compared to that in soft acid water. With acute poisoning by chromium compounds, the body surface of the fish is covered with mucus, the respiratory epithelium of the gills is damaged and the fish die with symptoms of suffocation. Fish suffering from chronic chromium intoxication accumulate an orange yellow liquid in their body cavity.

Aluminium

The toxicity of aluminium to fish depends to a large extent on the physico-chemical properties of the water and particularly on its pH. Aluminium is soluble at pH values below 6.0; a number of chemical species can be formed, the most toxic occurring in the pH range of 5.2 to 5.8. At higher pH values, aluminium is precipitated as the hydroxide, which can flocculate in the water. It is possible that freshly precipated aluminium (as a colloid) may be toxic; the fully flocculated hydroxide has a low toxicity similar to that of suspended solids in general.

In toxicity tests, rainbow trout fry were exposed to different aluminium concentrations at a pH of 7.0. A concentration as low as 0.52 mg aluminium per litre was found to markedly reduce the growth of these fish. When an even lower concentration, 0.05 mg per litre, was tested no such adverse effect was found, so this concentration can be regarded as safe at this pH. A mass kill of maraena and peled fry, reared in a public supply water clarified by flocculated aluminium sulphate, is a practical example. The aluminium concentration of the water was up to 0.3 mg per litre and the pH value was between 7.0 and 7.5. All the fry of maraena and peled died within 10–14 days of hatching. It is not known whether this was due to ionic aluminium or to micro flocs affecting fish respiration.

Iron

In surface waters, iron occurs in ferrous state II (soluble compounds) or ferric state III (mostly insoluble compounds). The ratio of these two forms of iron depends on the oxygen concentration in the water, the pH and on other chemical properties of the water. Fish may be harmed by iron compounds in poorly oxygenated waters with a low pH where the iron is present mainly in the form of soluble compounds. Because the gill surface of the fish tends to be alkaline, soluble ferrous iron can be oxidized to insoluble ferric compounds which then cover the gill lamellae and inhibit respiration. At a low water temperature and in the presence of iron, iron-depositing bacteria will multiply rapidly on the gills and further contribute to the oxidation of ferrous iron compounds. Their filamentous colonies cover the gills; at first they are colourless but later the precipitated iron gives them a brown colour. The precipitated iron compounds and tufts of the iron bacteria reduce the gill area available for respiration, damage the respiratory epithelium and may thus suffocate the fish. In a similar toxic action, iron compounds can precipitate on the surface of fish eggs which then die due to a lack of oxygen.

The lethal concentration of iron for fish is not easy to measure because it depends to a large extent on the physico-chemical properties of the water. In cyprinid culture, it is generally accepted that the concentration of the soluble ionized forms of iron should not exceed 0.2 mg per litre; for salmonids this limit is 0.1 mg per litre.

Nickel

Nickel can be discharged into surface waters in effluents from metal plating plants. Nickel compounds are of medium toxicity to fish. With short periods of exposure, the lethal concentration is between 30 and 75 mg per litre. As with the toxicity of other metals, the toxicity of nickel compounds to aquatic organisms is markedly influenced by the physico-chemical properties of water. For example, in soft waters with low calcium concentrations, the lethal concentrations of nickel compounds for the stickleback were less than 10 mg per litre. In such cases nickel can be regarded as highly toxic to fish. After toxic exposure to nickel compounds, the gill chambers of the fish are filled with mucus and the lamellae are dark red in colour.

Copper

Although copper is highly toxic to fish, its compounds are used in fish culture and fisheries as algicides and in the prevention and therapy of some fish diseases. The physical and chemical properties of the water exert a strong influence on the toxicity of copper to fish. In water containing high concentrations of organic substances copper can become bound into soluble and insoluble complexes. In very alkaline water it forms hydroxides of low solubility, and in waters with a high bicarbonate/carbonate concentration copper precipitates as poorly soluble or insoluble cupric carbonate. Compounds that are slow to dissolve or are insoluble are unlikely to be taken up to any extent into the fish body, so their toxicity to fish is low. A good example of this effect of solubility is a comparison between the different LC50s for carp recorded during 48 hours exposure to CuSO₄.5H₂O in a pond water [pH 7.6; acid capacity to a pH of 4.5 (a measure of bicarbonate alkalinity), 2.2 mmol per litre; COD_Mn32 mg O₂per litre] and in a well water [pH 6.2; acid capacity to a pH of 4.5, 0.6 mmol per litre; COD_Mn2.2 mg O₂per litre]: in the hard pond water the LC50 was 8.1 mg per litre and in the softer well water it was 1.5 mg per litre.

The maximum admissible copper concentration in water for the protection of fish is in the range of 0.001 to 0.01 mg per litre, depending on the physical and chemical properties of water and on the species of the fish. The characteristic clinical symptoms of fish poisoned by copper ions and copper compounds include laboured breathing and, in cyprinids, gasping for air at the water surface. The typical patho-anatomic appearance includes a large amount of mucus on body surface, under the gill covers and in the gills. Acute copper intoxication can be diagnosed on the basis of a chemical analysis of the gills in which the concentration of copper is much greater than in other parts of the body of the fish. The gills of fish caught in waters free of copper contamination contain up to 10 mg of copper per 1 kg of dry matter.

Zinc

Zinc poisoning of fish is most frequently encountered in trout culture. Rainbow trout and brown trout, and especially their fry, are extremely sensitive to zinc and its compounds. The lethal concentrations are around 0.1 mg per litre for salmonids (some authors even suggest a level of 0.01 mg per litre) and 0.5 to 1.0 mg per litre for cyprinids. Resistance to zinc compounds increases with age. The toxicity of zinc to fish is influenced by the chemical characteristics of water; in particular, increasing calcium concentrations reduce the toxicity of zinc. The clinical symptoms and patho-anatomic picture of zinc poisoning in fish are similar to those found for copper. The best remedy to avoid frequent occurrences of zinc toxicity in trout culture is to avoid using galvanized pipes for the supply of water and to avoid using galvanized containers and equipment, especially in areas where the water is soft and acid.

Cadmium

Cadmium in surface waters is usually found together with zinc but at much lower concentrations. The cadmium present in surface waters may be either dissolved or insoluble. Of the dissolved forms, those which may be poisonous to fish include the simple ion and various inorganic and organic complex ions. Apart from an acute toxic action which is similar to that of other toxic metals (damage to the central nervous system and parenchymatous organs), very small concentrations of cadmium may produce specific effects after a long exposure period. Chief among these specific effects are those exerted on the reproductive organs. An adverse influence of long exposure to cadmium upon the maturation, hatchability and development of larvae in rainbow trout was recorded at concentrations as low as 0.002 mg l¹. The acute lethal concentration of cadmium for different species of fish is from 2 to 20 mg l¹. Cadmium toxicity is reduced with increasing levels of calcium and magnesium in the water. For salmonids, the maximum admissible cadmium concentration in water is 0.0002 mg per litre, and for cyprinids 0.001 mg per litre (Schreckenbach, 1982).

Arsenic

As a rule arsenic occurs in water in the oxidation state V but some of it may also be present in non-stable forms, i.e. in the oxidation state III. As with mercury (see later) biological (particularly bacterial) activity may lead to the formation of organic methyl derivatives of arsenic. The main sources of arsenic pollution in surface waters include industrial effluents e.g. from tanneries, ore processing plants and dyestuff production plants. Arsenic is able to accumulate in large quantities in the sediments on the bed of water courses and reservoirs, and in aquatic organisms. Arsenic compounds in the third oxidation state (arsenites) are absorbed fairly rapidly into fish and are more toxic than

arsenic compounds in the oxidation state V (arsenates). From concentrations found to be lethal to different species of fish during 48 hours of exposure, diarsenic trioxide, for example, can be included among those substances which have a medium to high toxicity to fish; lethal concentrations are between 3 and 30 mg per litre.

Mercury

Mercury is transported to the aquatic environment mainly in discharges of industrial effluents and by atmospheric precipitation. Unpolluted waters will contain trace amounts of mercury which do not exceed 0.1 μg per litre.

Mercury concentrations found in surface waters are not a true measure of the actual total amount of mercury present and therefore do not represent the extent of the mercury pollution there; this is because mercury is transferred from water to the sediments on the bed of water courses, lakes and reservoirs where it accumulates mainly as the sulphide. Elementary mercury and its organic and inorganic compounds can undergo methylation (a process induced by the activity of microorganisms) in the sediments. The toxic end-product of this methylation, methyl mercury, enters the food chains and bioconcentrates in increasing amounts in aquatic organisms up the food chain.

Mercury can be taken up into fish from food via the alimentary tract; the other routes are through the gills and skin. Absorption from the alimentary tract has proved to be of the greatest importance in methyl mercury accumulation; evidence for this has been provided by the results of investigation at sites in the drainage area of the Berounka River in Central Bohemia. The total mercury content in the flesh of fish from these localities is about 10 times that recorded in their food. This coefficient of bioaccumulation can be compared with the food efficiency coeficient of fish living in open waters and feeding on the aquatic invertebrates. Of the other aquatic organisms in the drainage area of the Berounka River, the greatest mercury levels were recorded in leeches and this can be ascribed to their exclusively predatory mode of feeding. With their wide distribution in different types of waters, leeches (e.g. Helobdella stagnalis) may be considered as good indicators of mercury contamination of the aquatic medium.

Carnivorous fish contain the highest amounts of mercury because they form the final link in the aquatic food chain. The problem of mercury in the aquatic medium is important not only for environmental and hygienic reasons but also from the viewpoint of

fish culture. It has been shown that mercury compounds can cause damage to some vital tissues and organs in fish and may also have a harmful effect on reproduction. At very low concentrations they reduce the viability of spermatozoa, reduce egg production and affect the survival rate of developing eggs and fry. Acute lethal concentrations of inorganic mercury compounds are in the range of 0.3 to 1.0 mg per litre for salmonids and 0.2 to 4.0 mg per litre for cyprinids, depending on the physical and chemical properties of the water. The acute lethal concentrations of commonly found organic mercury compounds are from 0.025 to 0.125 mg per litre for salmonids and from 0.20 to 0.70 mg per litre for cyprinids. For salmonids the maximum admissible concentration of inorganic forms is about 0.001 mg per litre and for cyprinids about 0.002 mg per litre. For fish in general, the maximum admissible concentration of mercury in organic compounds has been suggested to be as low as 0.0003 mg per litre.

Lead

A significant source of airborne lead contamination, and therefore of surface waters, is the exhaust fumes of motor vehicles which contain the break-down product of tetraethyl lead. In surface waters, lead largely accumulates in bottom sediments at concentrations about four orders of magnitude greater than in the water.

Lead toxicity to fish and other aquatic organisms is significantly influenced by the water quality and depends on the solubility of lead compounds and on the concentration of calcium and magnesium in water. The water solubility of lead compounds is reduced with increasing alkalinity and pH value of the water. Also, the toxicity of lead is known to be reduced with increasing calcium and magnesium concentrations in water. The acute toxic concentrations in different types of water are in the range of 1 to 10 mg per litre for salmonids and of 10 to 100 mg per litre for cyprinids.

Acute lead toxicity is characterized initially by damage to the gill epithelium; the affected fish are killed by suffocation. The characteristic symptoms of chronic lead toxicity include changes in the blood parameters with severe damage to the erythrocytes and leucocytes, and degenerative changes in the parenchymatous organs and damage to the nervous system. In trout, a characteristic symptom is a blackening of the caudal peduncle; a biochemical effect is the inhibition of amino levulinic acid dehydrase (ALA-D) in fish blood. The maximum admissible lead concentration in water is 0.004 to 0.008 mg per litre for salmonids and 0.07 mg per litre for cyprinids.

Chemicals in water as a result of man’s activities