Aroclor® 1254 is a polychlorinated biphenyl (PCB) mixture containing approximately 21% C12H6Cl4, 48% C12H5Cl5, 23% C12H4Cl6, and 6% C12H3Cl7 with an average chlorine content of 54% (USAF 1989). PCBs are inert, thermally and physically stable, and have dielectric properties. In the environment, the behavior of PCB mixtures is directly correlated to the degree of chlorination. Aroclor® is strongly sorbed to soil and remains immobile when leached with water; however, the mixture is highly mobile in the presence of organic solvents (USAF 1989). PCBs are resistant to chemical degradation by oxidation or hydrolysis. However, biodegradation, especially of lower chlorinated PCBs, can occur (USAF 1989). PCBs have high bioconcentration factors, and due to lipophilicity, especially of highly chlorinated congeners, tend to accumulate in the fat of fish, birds, mammals, and humans (ATSDR 1995).
PCBs are absorbed after oral, inhalation, or dermal exposure and are stored in adipose tissue. The location of the chlorine atoms on the phenyl rings is an important factor in PCB metabolism and excretion. The major route of PCB excretion is in the urine and feces; however, more important is the elimination in human milk. Metabolites are predominately found in urine and bile, while small amounts of the parent compound are found in the feces. Biliary excretion appears to be the source of fecal excretion (ATSDR 1995).
Accidental human poisonings and data from occupational exposure to PCBs suggest initial dermal and mucosal disturbances followed by systemic effects that may manifest themselves several years post-exposure. Initial effects are enlargement and hypersecretion of the Meibomian gland of the eye, swelling of the eyelids, pigmentation of the fingernails and mucous membranes, fatigue, and nausea. These effects were followed by hyperkeratosis, darkening of the skin, acneform eruptions, edema of the arms and legs, neurological symptoms, such as headache and limb numbness, and liver disturbance (USAF 1989).
Hepatotoxicity is a prominent effect of Aroclor® 1254 that has been well characterized (EPA 1995a). Effects included hepatic microsomal enzyme induction, increased serum levels of liver-related enzymes indicative of hepatocellular damage, liver enlargement, lipid deposition, fibrosis, and necrosis. Groups of 16 adults (11.1 +/-4.1 years at study initiation) female rhesus monkeys ingested gelatin capsules containing 0, 0.005, 0.02, 0.04, or 0.08 mg/kg/day Aroclor® 1254 daily for more than 5 years (Arnold et al. 1993 a,b; Truelove et al. 1990). Increases in the incidence of inflamed and/or prominent Meibomian glands; increased incidences of ocular exudate; changes in finger and/or toe nails; decreases in IgG and IgM antibody levels; decreases in the percent of helper T-lymphocytes; increases in suppressor T-lymphocyte count; a decrease in helper/suppressor ratio; and decreases in reticulocyte count, serum cholesterol, total bilirubin, and alpha-1+ alpha-2-globulins were observed in treated monkeys. A chronic oral reference dose (RfD) of 2E-05 mg/kg/day for Aroclor® 1254 was calculated from a lowest-observed-adverse-effect level (LOAEL) of 0.0005 mg/kg/day derived from the above study (EPA 1995a). The subchronic oral RfD is 5E-05 mg/kg/day (EPA 1995b).
Data are suggestive but not conclusive concerning the carcinogenicity of PCBs in humans. The EPA has not determined a weight-of-evidence classification or slope factor for Aroclor® 1254 specifically. However, hepatocellular carcinomas in three strains of rats and two strains of mice have led the EPA (1995c) to classify PCBs as group B2, probable human carcinogen. The carcinogenicity slope factor (q1*) for oral exposure to PCBs is 7.7 (mg/kg/day)-1 based on an increase of hepatocellular tumors in female Sprague-Dawley rats treated with Aroclor® 1260. A drinking water unit risk of 2.2E-4 (µg/L)-1 for PCBs was calculated based on the q1* (EPA 1995c).