concentration. Wobeser (1975) fed graded concentrations of methyl mercury chloride to rainbow trout and found that dietary concentrations of mercury up to 24 mg/kg did not cause mortalities, but that fish fed 16 mg/kg or more showed hyperplasia of the gill epithelium and reduced hematocrits. Coho salmon fed dogfishmeal with 2.3 mg total mercury/kg to replace 50 percent of the herring meal in an Oregon moist diet grew as large as control fish and did not accumulate total body mercury concentrations above the U.S. Food and Drug Administration (FDA) tolerance level of 0.5 mg/kg (Spinelli and Mahnken, 1976).

Fish accumulate mercury in muscle tissue and the rate is influenced by dietary form and concentration (Pennacchioni et al., 1976) and fish size (Scott and Armstrong, 1972). The bioaccumulation of mercury is directly correlated with fish size (Friedman and Shibko, 1972). Feedstuffs fed to fish grown for human consumption should be scrutinized for mercury concentration because mercury could possibly accumulate in the fish and exceed the FDA tolerance level. Selenium was found to reduce the toxicity of methyl mercury (Ganther et al., 1972; Friedman et al., 1978) and decrease the rate of mercury bioaccumulation in fish, crayfish, and lake sediment biota (Rudd et al., 1980).

Water-borne cadmium has been shown to be toxic to many fish species (Sangalang and O'Halloran, 1972; Kumada et al., 1973; Clearley and Coleman, 1974; Benoit et al., 1976; Smith et al., 1976). Cadmium absorbed through the gastrointestinal tract (by gastric intubation) was shown to cause liver necrosis and mortality at doses as low as 5 µg/g body weight.

The main source of arsenic in ingredients used in fish feeds comes from marine fishmeal. Reinke et al. (1975) reported arsenic concentrations in tissues of a number of commercial fish species from the North Atlantic ranging from 1.8 to 40 mg/kg; however, most of the arsenic was in the form of an organic complex rather than the highly toxic arsenite. The potential toxicity to fish of feeding diets containing organic arsenic compounds is not known.

The polychlorinated biphenyls (PCBs) are widely used industrially as plasticizers and as heat-transfer, dielectric, and hydraulic fluids. They are poorly biodegraded and accumulate in lipids, and have been found in marine and freshwater organisms from almost all areas of the United States (Addison, 1976; Ito and Konishi, 1980; Peneva, 1980; Brunn et al., 1981; Falandysz and Ganowiak, 1981; Veith et al., 1981). Fish oil and meal represent the primary sources for PCB contamination of fish diets (Hansen et al., 1976). A PCB dosage of 14.5 mg/kg body weight resulted in 100 percent mortality of coho salmon after 260 days (Mayer et al., 1977). Sublethal effects of PCB exposure in fish include liver enlargement, lesions in the liver ultrastructure, inhibition of hepatic aryl hydrocarbon hydroxylase and other hepatic microsomal enzymes (Lidman et al., 1976; Addison et al., 1977, 1978, 1979; Gruger et al., 1977; Shelton et al., 1984), and decreased thyroid activity (Leatherland and Sonstegard, 1978, 1980). These compounds accumulate in fish tissues (Guiney and Peterson, 1980); therefore, prolonged feeding of dietary concentrations below the toxicity level may result in tissue accumulation that would be toxic to the fish or that are above FDA-approved levels (0.2 mg/kg) for human food.

The FDA restrictions on the use and concentration of pesticides in agricultural products used for human or animal consumption make it unlikely that fish feeds will be sufficiently contaminated to cause acute toxicities. Fish are most likely to be exposed to pesticides through accidental contamination of feedstuffs with hazardous quantities of insecticides or rodenticides, or use of water that has been contaminated by these chemicals, such as through aerial spraying. Most pesticides bioaccumulate in fish, therefore, prolonged exposure to small amounts, from the water or the diet, may result in accumulations in the tissue that will affect the health of the fish or the marketability of the product for human food. Ashley (1972) evaluated the toxic effects of chlorinated hydrocarbons in several fishes. Toxicity was greatest in young fish, characterized by dysplasia and sterility of gonads, lethargy, nervous disorders, anorexia, and death. The toxicity to DDT decreased among fish species in the following order: rainbow trout, brown trout, guppy, bluegill, and channel catfish. The insecticide DDT caused inhibition of gill and kidney Na⁺- and K⁺-ATPase (Campbell et al., 1974), liver tumors (Halver, 1967), nervous disorders (Bahr and Ball, 1971), and acute toxicity (Buhler et al.,1 969) in various fishes.

Front Matter (R1-R12)

Overview (1-2)

1. Dietary Requirements (3-32)

2. Other Dietary Components (33-37)

3. Antinutrients and Adventitious Toxins (38-42)

4. Digestibility and Absorption (43-48)

5. Diet Formulation and Processing (49-54)

6. Feeding Practices (55-61)

7. Nutrient Requirements Table (62-63)

8. Composition of Feed Ingredients (64-71)

References (72-94)

Appendix (95-102)

Authors (103-104)

Index (105-116)