Polychlorinated biphenyls (PCBs) are a group of chlorinated hydrocarbon compounds that once were used widely as high-temperature insulators for transformers and other electric equipment and were also found in carbonless copy papers and some inks and paints. Since 1974, all uses in the United States have been confined to closed systems. Most PCB poisonings are chronic occupational exposures, with delayed-onset symptoms the first indication that an exposure has occurred. In 1977, the US Environmental Protection Agency (EPA) banned further manufacturing of PCBs because they are suspected carcinogens and highly persistent in the environment. The primary exposures occur from leaking transformers and other electric equipment, from hazardous waste sites, and environmentally from ingestion of contaminated water, fish, or wildlife.
Mechanism of toxicity. PCBs are irritating to mucous membranes. When burned, PCBs may produce the more highly toxic polychlorinated dibenzodioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs [See Dioxins]). It is difficult to establish the specific effects of PCB intoxication because PCBs are nearly always contaminated with small amounts of these compounds. PCBs, and particularly the PCDD and PCDF contaminants, are mutagenic and teratogenic and are considered probable human carcinogens.
Toxic dose. PCBs are well absorbed by all routes (skin, inhalation, and ingestion) and are widely distributed in fat; bioaccumulation occurs even with low-level exposure.
Inhalation. PCBs are mildly irritating to the skin at airborne levels of 0.1 mg/m3 and very irritating at 10 mg/m3. The ACGIH-recommended workplace limits (TLV-TWA) are 0.5 mg/m3 (for PCBs with 54% chlorine) and 1 mg/m3 (for PCBs with 42% chlorine) as 8-hour time-weighted averages. The air level considered immediately dangerous to life or health (IDLH) for either type is 5 mg/m3.
Ingestion. Acute toxicity after ingestion is unlikely; the oral 50% lethal dose (LD50) is 1–10 g/kg.
Acute PCB exposure may cause skin, eye, nose, and throat irritation.
Chronic exposure may cause chloracne (cystic acneiform lesions predominantly found on the face, posterior neck, axillae, upper back, and abdomen); the onset usually occurs 6 weeks or longer after exposure. Skin pigmentation, porphyria, elevated hepatic transaminases, and thyroid hormone abnormalities may occur.
Epidemiologic studies suggest that PCB exposure can be associated with neurobehavioral effects in newborns and children. Other effects include decreased birth weight and immune system effects in babies as a result of trans-placental transmission or breastfeeding by mothers exposed to elevated levels of PCBs. There is evidence that PCBs cause adverse estrogen activity in male neonates.
Diagnosis usually is based on a history of exposure and the presence of chloracne or elevated hepatic transaminases.
Specific levels. PCB serum and fat levels are poorly correlated with health effects. Serum PCB concentrations are usually less than 20 mcg/L; higher levels may indicate exposure but not necessarily toxicity.
Other useful laboratory studies include BUN, creatinine, and liver enzymes.
Emergency and supportive measures
Treat bronchospasm (See Hypoxia) if it occurs.
Monitor for elevated hepatic enzymes, chloracne, and nonspecific eye, GI, and neurologic ...