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C uJ< ^ SfrlKijlx- sAl i'l i KOiOjl c d Sjpe*/^ \fi- ea ; proved a useful toxicity of heavy vith chromium iny of the metal to ibed as follows: ite = 3.9 ` $i 0.63 1 t ntration in mg of water and y is exfor 50-percent hill j ons,. potassium bi- ; than chromic acid, light-hour TLm for per liter; for potasrg per liter. e of the relation of gical effect is apsted iu the earlier ieology, the rectanto describe a wide gent, biological re: would be well to >is relationship for h, mixohalinc, and number of aquatic lia squinado, if exvater, accumulates esophagus, proveny glands in much than in blood. In hn of mercury inthe-medium. Some :akes place.11 j removed from the ?cl in clean water, are lost from most : exception to this Metals . 63 was the blood, which retained a relatively high and fairly constant concentration of mercury throughout the experimental pe riod (4 weeks)."11 The mercury in blood is apparently attached rather firmly to pro tein. It is possible that mercury, in Maia, exerts its poisoning effect by interfering with mechanisms for copper metabolism. Copper Copper is naturally present in sea water in various amounts depending on location, proximity to industrial effluents, currents, and unknown factors. Table 5-II summar izes the sources of the available data.8-7 TABLE 5-II AMOUNT OF COPPER IN SEA WATER Location Copper Concentration (in mg/Uier) Reference No. Kiktcoff, France 1 W infritli, England 2.9 - 1.0 mg/cu m Woods Hole, Mass. 8 - 35 Lmg Island Sound 0-95 ISaluimas 1-8 of Mexico X - 25 Friday Harbor, Wash. 1-2 Japan 0.8- 2.5 Plymouth, England 1.5-25 7 35 IS IS 18 38 8,9 29, 30 2 Under conditions listed in Table 5-II, marine organisms tln-ive and cany on the usual life processes. It is evident that small amounts of copper are nontoxic to marine animals. In fact, small amounts of copper are essential for the production of certain respiratory pigments in animals. There is a tlireshold of toxicity for cop per. Experiments using Nereis virem as the test organism suggest that such a thres hold for copper toxicity is about 0.1 mg copper per liter. Even at very high con centrations and for long exposure periods, a few individual animals resist the lethal action of the metal. Nereis abstracts copper from the water MGrounding it and concentrates the metal in the body wall and in the gut wall (Fig. 5.1). The rate of uptake is reported to be directly proportional to the concentration of copper in the water. For example, if Nereis is exposed to a 0.2-ppm solution of copper in sea water for four days, there is a steady increase in the copper content of body wall and gut; control worms kept in fresh sea water show no change in cop per content of the gut but may lose copper from the body wall.88 Copper in higher concentrations is lethal for Nereis (Fig. 5.2). The shore crab, Carcinus, has a copper toxicity threshold of 1 or 2 ppm (11- to 12-day exposure time). It is known that 3 ppm of copper is a lethal concentration for oysters. Lower concentrations have been reported to facilitate the settling of larvae. The work has not been con firmed.38- 8-7 The niuety-six-hour TLt o for Japanese oysters exposed to copper is reported to be 1.9 ppm.1 The American oyster is ap parently more sensitive to copper.38 More over, if oysters are exposed to a copper concentration as low as 0.13 ppm, they turn green in about twenty-one days.17 Such oysters are unmarketable, although nontoxic to man. They represent a total economic loss to those depending on their sale for a livelihood. Lead Lead poisoning in experimental animals is known to be associated with cellular alterations of erythrocytes: swollen mito chondria, simple and compound vacuoles, clusters of ferritin in the cells. Alterations of the mitochondria have been ascribed to a blockage of heme synthesis.34 Detailed examination of the blood in fishes suspected of being exposed to lead poisoning may be of value. Hematological changes could very well be the first bio logical responses of fishes to threshold DUP050312914 Ml*. iki 64 The Biological Aspects of Water Pollution levels of lead. Greatly lacking is detailed rosis, muscular dystrophy, and related phe. background information on blood changes nomena. in fishes as a result of stress from physical or chemical agents. Vigorous research to Mercury clarify these matters should be productive Mercury in poisonous amounts can enter of much valuable information. natural bodies of water from industrial In higher animals and man, exposure to effluents originating in factories which pro very small amounts of lead is accompanied duce mercury-containing compounds or by changes in blood enzymes.50 For ex which use mercury in their processes. In ample, blood serum aldolase activity in hu addition, runoff from areas where mer man beings exposed to amounts of lead, curial formulations may have been used as so small as to elicit no signs or symptoms fungicides is a source of pollution. of poisoning, is increased. A number of studies indicate that salts Information on blood enzymes of fishes of mercury alter markedly the epithelium is scanty. It seems probable that the esti of skin and gills in fishes.30 Fishes immersed mation of serum aldolase and of other en in solutions of mercuric chloride and of zymes in blood of fishes exposed acciden phenyl-mercuric acetate accumulate mer tally and experimentally to lead could yield cury in the body. useful information. Such tests might be Curves of concentration and survival particularly revealing in circumstances time of mercuric chloride for several spe involving low concentration of lead for cies of fishes show that the relationship is prolonged periods of exposure. linear on double logarithmic paper and In man, it is known that chronic lead that there is a break point for each species. poisoning shows a clinical picture much Above the break point (higher concentra like that of multiple sclerosis.15 Further, it tion), the slope of the line is significantly has been suggested that there is a com less than below (lower concentration). mon pattern of causal mechanisms involved The equations for the lines above ant! in multiple sclerosis and in the central below the break point all are of the follow nervous system damage due to lead poison ing general form ing.13 Reports of muscular dystrophy occur log T = a log C + log K ring naturally in fishes and amphibians are where T is survival time in minutes, a the not uncommon.40 Such reports lead one to slope of the line, C the concentration of speculate whether "naturally occurring" mercury in mg per liter, and K a constant. cases of multiple sclerosis and so forth in In direct terms, the relationship has the fishes and amphibians may be quite un form natural and are perhaps associated with some metal poisons (e.g., lead) in the en T=K O vironment. When cases of neuromuscular The exponent a will be different above diseases are reported in fishes or amphib and below the break point for each spe ians, it would be well to examine the en cies. Below the break point (lower concen vironment thoroughly for lead and other trations), a is remarkably constant for at metals which in small amounts over long species studied (Table 5-III). exposure periods might cause signs of dis Above the break point, it is also qu!tt ease aping the pattern of multiple scle constant except for Tilapia. The brent- ^ f.,r -! !! <;< - f iInput y , ;H|HUtltS s.r'f'io Mo:iu__ jxiiitt fails liter. Klevatcd u ity of Ug \ ivc longo JIgCh that logarithmic !`.;.iinst sur Aitli poxitiv describes t. whereT is : ami K is a The folic ;irt the vis `ction of II Hid the gi rinly weigh .o 1 hi- value i ite of dv;i > 'M-iilooiic ' ` wilt tula UMHIipt in s. reuses a: !i is C ll .ll v`-v.il time ! DUP050312915 v elated pilo ts can enter i industrial which prolpounds or ocesses. In vhere mereen.used as ion. e that salts epithelium s immersed ide and of mlate mer- nd survival ;everal spcationship is paper and aeh species. concentru ignificantly tration). above and the follow- K mites, a the nitration of a constant, aip has the .nvnt above r each spc>vor conccnitant for all also quite The break Metals 65 TABLE 5-iri Values for slopes and break points for fishes exposed to HgCla. General equation is Jog T=a log C-f-log KA Sp e c ie s Tilapia Eupomolis Ambloplites Sahno hebistes Gasterosteus Mean Sl o p e Below Break Above Break - .90 - .94 -1.29 -1.1S -1.09 -1.11 -.20 -.43 -.42 -.38 -.38 -.40 -1.08 -.37 Br e a*: Po ix t (mg Hg/litei) 18 30 30 10 14 10 19 point falls between 10 and 30 mg Hg per liter. Elevated temperature increases tlie tox icity of HgCI2 to fishes. Larger fishes sur vive longer in a given concentration of HgCl2 than do smaller ones. On double logarithmic paper, a plot of body weight against survival'time gives a straight line with positive slope. The following equation describes the relationship T = K W0-27 where T is survival time, W is body weight, and K is a constant. The following argument is used to sup port the view that the primary site of toxic action of HgCl2 is tire surface of the body and the gills in fishes.5 The equation for body weight and survival time is rewritten as . i w-- 27 The value of 1 divided by T is then the "rate of death " Respiratory metabolism in cold-blooded animals varies with the body weight taken to the 0.73 power.20 Oxygen consumption per unit weight, therefore, decreases as Oa = K-W0-37 It is clear that both the reciprocal of sur vival time (i.e. the rate of death) and the intensity of respiration decrease according to 0.27 power of the body weight. Both phenomena are consequently proportional to relative body surface W- 73/W. In sea water, mercuric chloride is not so toxic to fishes as in fresh water. The addition of 10 fig per liter of HgCi2 to water containing developing eggs of Paracentrotus lividis brings about a severe disturbance of development; a concentra tion of 5 p.g per liter retards development markedly. The threshold for harmful ef fects of HgCl2 on developing eggs of Para centrotus is between 2 and 3 gg per liter.41 Minamata Disease A large-scale poisoning occurred in Ja pan as a result of water polluted with mer cury. An industrial plant on the shores of Minamata Bay, Kyushu, Japan, used mer cury chloride as a catalyzer in the produc tion of vinyl chloride. Effluent from the factory loaded with waste mercury salt was poured into Minamata Bay.- Consump tion of fishes caught in the bay was fol lowed by severe illness and even death. (The fatal outcome of this so-called Mina mata disease is very high.) The mercury content of organs from man and animals killed by eating fishes and shellfishes from the bay was extremely high. The mercury was especially concentrated in the brain. Fishes and shellfishes caught in the bay had very large amounts of mercury in their tissues.47 The effects on man of eating seafood from. Minamata Bay were identical with the effects of mercury poisoning. Cats and rats that had been administered organic mercury compounds experimentally ex hibited identical clinical signs and patho logical responses as did animals that were fed on seafood from Minamata Bay. It is interesting to note that an inorganic mer cury salt, originating in an industrial effiu- DUP050312916 toe fit*' 66 The Biological Aspects of Water Pollution ent, was in all probability transformed into an organic mercury compound during its passage through the marine food net. When seafood from the poisoned bay was eaten by man, signs and symptoms (as well as pathological findings) of organic mercury intoxication resulted. The process by which tire inorganic form of mercury was changed to an organic form is unknown. This serious epidemic indicates dra matically the havoc which can be wrought through poisoned waters. It also suggests that poisons, as they pass through the bio logical food net in a body of water, may be modified in such a way as to confuse invesigators who are attempting to iden tify the source and nature of the poison. It is important to realize that natural bodies of water are living dynamic systems--not dead or lifeless "sinks" into which any sort of waste may be discarded with impunity. Metal wastes are particularly insidious because they can persist in solution for long periods of time.61 Moreover, if pre cipitated from solution, through the action of organic sewage, heavy metals can form a poisonous blanket on the bottom of the body of water. Finally inorganic forms of metals may, in passing through the aquatic food web, be converted into organometal compounds or complexes with altered bio logical effects. Silver Silver is well known to be poisonous to aquatic animals. For example, a concentra tion of 400 p.g per liter will kill 90 percent of tested adult Balanus balanoides in fortyeight horns.10 Concentrations of AgN03 from 10 to 100 p.g per liter cause abnormal or inhibited development of eggs of Paracentrotus. Even at a concentration of 2 pg of AgN03 per liter of water, there is a delay in development and deformation of the resulting plutei.'1 The threshold for effect is slightly below 0.25 pg of A.\o per liter. The adverse effects of short posure to silver in water persist for xcvru' days after the toxicant is removed from tb medium. The developing eggs of Arbacia ar. somewhat more resistant to silver in so!.,, tion than are those of Paracentmtus. 'll, threshold concentration for effect of Ag\'f > on development in Arbacia is in the vicin' ity of 0.5 pg per liter. Copper also exerts an adverse effect t,n development of Paracentmtus eggs. With silver, copper acts additively on development, not synergistically. Silver on a comparative basis is about eighty times as toxic as zinc, twenty tinu-v copper, and ten times mercury as evalu ated with respect to effect on developing echinoderm eggs.41 Because of its gn-.u toxicity, silver may play an important rob in the ecology of plankton. The fact that silver and mercury, in sub lethal concentrations, exert profound ef fects on developing eggs is additional c\ sdence of die importance of assessing suc-h subletiial responses in water pollution studies. The direct killing action of a water contaminant is, of course, important. I low ever, it is not all-important. Subletiial ef fects which involve disruption of normal embryology or of nutrition, for example, may be of even greater importance since the future of an aquatic species depend* on its capacity to reproduce, to feed, to grow, to establish itself in a location. A toxicant which interferes with any of lliej' processes is deleterious and not desival'U' in a body of water. As knowledge of water pollution icomes more complete, it may develop thn die subletiial effects of pollutants arc in1'1'' critical in die long view than are the acut* lethal effects. This possibility should ^ kept in mind in the planning of future n- v; .- i- \ v* .XX i , ? d. 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