Mutagenic properties of Aroclor 1221 and 4-monoch1orobi phenyl to bacteria 

 were Indicated by positive Ames tests, and Aroclor 1260 and Kanechlor 500 were 

 demonstrably carcinogenic to mice and rats (NAS 1979). Unexpectedly, Aroclor 

 1254 prevented carcinogenesis and mutagenesis in rainbow trout. Trout fed 100 

 ppm dietary Aroclor 1254 for 3 months were significantly more resistant to 

 liver carcinomas (induced by dietary aflatoxins) when PCBs were prefed prior 

 to carcinogenic insult (Shelton et al. 1983). At the time of aflatoxin 

 administration, trout contained 594 mg/kg PCBs in fat which declined rapidly 

 over the next 12 months to 3.9 mg/kg. Aflatoxin-induced mutagenesis in trout 

 liver cells was also significantly inhibited (67%) by Aroclor 1254 under 

 similar conditions (Shelton et al . 1983). 



Histopathology was reported in sensitive marine teleosts following 

 exposure for 2 weeks to PCB concentrations of 0.5 ug/1 ; similar damage effects 

 were recorded in oysters held for 24 weeks in 5 ug/1 of Aroclor 1254, but not 

 for 30 weeks in 1 ug/1 (Ernst 1984). 



A wide variety of biochemical perturbations were recorded among teleosts 

 stressed by PCBs. The primary biochemical effect of PCBs is to induce hepatic 

 mixed function oxidase systems, thus increasing the organism's capacity to 

 biotransform or to detoxify xenobiotic chemicals and endogenous steroids 

 (Melancon and Lech 1983; Shelton et al . 1983). Coho salmon injected 

 intraperitoneal ly with 50 to 100 ug Aroclor 1254/kg body weight just prior to 

 smoltification contained elevated levels of PCBs in liver (500 to 1,200 ppb) 2 

 weeks after injection when compared to controls (25 to 45 ppb), showed 

 depressed gill Na-K ATPase and plasma thyroxin levels, and experienced great 

 difficulty in adapting to seawater (Folmar et al . 1982). Biochemical 

 indicators suggested that tissue accumulations of PCBs (at concentrations that 

 clearly could be derived through a contaminated diet or from water column 

 exposure) delayed events preparatory to, and involved in, saltwater adaptation 

 in coho salmon. Mixtures of Aroclor 1242 and 1254 fed to rainbow trout and 

 coho salmon at dietary concentrations of 500 ppm PCBs for 7 to 10 weeks 

 produced inhibited growth, enlarged livers, elevated muscle water content, and 

 lowered muscle lipid content (Leatherland and Sonstegard 1981). Salmon showed 

 disrupted calcium and magnesium metabolism in blood, muscle, and skeleton. 

 After about a week on PCB diets, both trout and salmon showed signs of poor 

 muscle coordination and tetany, accompanied by lateral or ventral caudal 

 flexion (scoliosis or lordosis). Brown trout fed diets containing 10 ppm of 

 Clophen A-50 for 43 days were anemic, hyperglycemic, and showed altered 

 cholesterol metabolism (EPA 1980). Brook trout held in Aroclor 1254 solutions 

 of more than 0.43 ug/1 for 48 days had decreased concentrations of 

 hydroxyprol ine in collagen isolated from the backbone (Johnson and Finley 

 1980). However, Aroclor 1254 did not markedly affect adrenaline response in 

 gills of rainbow trout, or glycogen storage in muscle (Kiessling et al . 

 1983). 



Maximum Acceptable Toxicant Concentration (MATC) values bracket the "no 

 effect," and "measurable effect" levels, and are based on chronic exposure, 

 and variables such as growth, reproduction, and metabolic upset. MATC values 



49 



