lowered birth rate, hyperpigmentation, skin eruptions, eye problems, and 

 negatively altered behavioral patterns. Males were less sensitive than 

 females; however, when fed diets containing 300 ppm of Aroclor 1248 for one 

 month, both sexes showed hair loss, purulent discharges from the eyes, 

 acneform skin eruptions, and hypertrophy of the liver and gastric mucosa. 

 Rhesus monkeys can efficiently absorb Aroclor 1248 from the gut; 90% of a 

 single oral dose of 1,500 or 3,000 mg/kg body weight was reported absorbed 

 from the gastrointestinal tract. This, and the fact that rhesus monkeys were 

 unable to efficiently eliminate or metabolize certain PCB congeners (i.e., 

 2,5,2' ,5'-tetrachlorobiphenyl ) when compared to other species, may partially 

 account for the sensitivity of this species. Infant rhesus monkeys, born to 

 mothers exposed to 2.5 ppm of Aroclor 1248 in the diet during pregnancy and 

 lactation, survived over 4 months; PCB levels in their fat declined over a 

 period of 8 to 23 months. 



In Japan, humans were accidentally poisoned by rice oil containing 2 to 3 

 mg of Kanechlor 400/kg (EPA 1980; Lucier and Hook 1985a, b). Symptoms included 

 increased eye discharges and swelling of upper eyelids, acneform skin 

 eruptions, skin pigmentation, hearing and vision problems, gastrointestinal 

 disturbances, and altered blood chemistry. Infants born of Japanese women 

 married to afflicted males were small for their age, had unusual pigmentation, 

 premature eruption of teeth, and exophthalmia (popeyes). Three years after 

 exposure, 50% of the patients were improving, 40% were unchanged, and 10% were 

 worse. Even among those said to be improving, many still complained of 

 headaches, fatigue, weakness and numbness of the limbs, and weight loss. 

 Impurities in the Kanechlor 400 mixture included polychlorinated dibenzofurans 

 and dioxins at levels up to 5 ppm, and these may be responsible, in part, for 

 the observed symptoms in victims. 



Mutagenic, carcinogenic, and teratogenic properties of PCBs are 

 documented. Certain PCB congeners, such as 4-chlorobiphenyl , were highly 

 mutagenic to Salmonella typhimurium in Ames tests (EPA 1980). Aroclor 1221 

 was less mutagenic, while Aroclors 1254 and 1268 were essentially inactive. 

 In general, mutagenic activity tends to decrease with increasing chlorination 

 (EPA 1980). The carcinogenic effects of PCBs have been established in mice 

 and rats with various Aroclor and Kanechlor PCBs and these, in turn, may 

 enhance the carcinogenicity of other chemicals (EPA 1980). Experimental data 

 clearly shows that commercial PCBs cause liver damage which leads to putative 

 preneoplastic changes and hepatocellular carcinomas; however, these lesions 

 are observed only after lengthy (11 to 21 months) exposures to relatively high 

 doses (100 to 1,200 ppm in diets) of these chemicals (NAS 1979; Safe 1984). 

 PCBs were also shown to inhibit the growth of experimental tumors in rats (EPA 

 1980); administration of Aroclor 1254 (either dietary or injected) for 5 days 

 before or after tumor inoculation was more effective than administration 

 between days 5 and 10. Teratogenic effects of PCBs observed in monkeys and 

 rabbits include abnormal skull formation of fetuses exposed to high levels of 

 Aroclor 1254 in utero, and retarded growth (EPA 1980). 



Aroclor 1254 at dietary levels of 25 to 100 ppm for up to 3 weeks can 

 significantly reduce sleeping times in animals that normally aestivate or 



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