Polychlorinated biphenyls (PCBs) are mixtures of up to 209 different chlorinated compounds that once were used widely as high-temperature insulators for transformers and other electric equipment. They were also found in carbonless copy papers, inks, paints, caulks, sealants and ceiling tiles. Many commercial PCB mixtures are known in the United States by the trade name Aroclor. Since 1974, all uses in the United States have been confined to closed systems. Most PCB poisonings are chronic occupational or environmental 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. Exposure occurs through the consumption of meat, fish, and dairy because of biomagnification up the food chain, as well as by inhalation in contaminated indoor or outdoor environments. PCBs were widely used in building materials from 1950s to 1979, and remain present in buildings that were constructed or renovated during that period. Since many schools in use today were built or renovated during that era, they present a potential risk of exposure to children and staff.

PCB metabolites may induce DNA strand breaks, resulting in cellular injury. PCBs are irritating to mucous membranes. When burned, PCBs may produce the more highly toxic polychlorinated dibenzodioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs). PCBs, and particularly the PCDD and PCDF contaminants, are mutagenic and teratogenic and are considered human carcinogens by the International Agency for Research on Cancer.

PCBs are either oily liquids or solids that are colorless to light yellow. Some can exist as a vapor in air. PCBs have no known smell or taste. PCBs are well absorbed by all routes (skin, inhalation, and ingestion) and are widely distributed in fat; bioaccumulation occurs even with low-level exposure.

1. 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 (TLVTWA) 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.
2. Ingestion. Acute toxicity after ingestion is unlikely; the oral 50% lethal dose (LD₅₀) is 1-10 g/kg.

1. Acute PCB exposure may cause skin, eye, nose, and throat irritation.
2. 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.
3. Epidemiologic studies suggest that PCB exposure is associated with decreased IQ and other neurobehavioral effects in newborns and children. Other effects include decreased birth weight and immune system effects in babies as a result of transplacental transmission or breastfeeding by mothers exposed to elevated levels of PCBs. Exposure to PCBs early in life has been shown in children to be associated with reductions of serum concentrations of antibodies against diphtheria and tetanus vaccinations. There is evidence that PCBs cause adverse estrogen activity in male neonates.

Usually is based on a history of exposure and the presence of chloracne or elevated hepatic transaminases.

1. 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.
2. Other useful laboratory studies include BUN, creatinine, and liver enzymes.

1. Emergency and supportive measures
   1. Treat bronchospasm if it occurs.
   2. Monitor for elevated hepatic enzymes, chloracne, and nonspecific eye, GI, and neurologic symptoms.
2. Specific drugs and antidotes. There is no specific antidote.
3. Decontamination
   1. Inhalation. Remove the victim from exposure and give supplemental oxygen if available.
   2. Skin and eyes. Remove contaminated clothing and wash exposed skin with soap and water. Irrigate exposed eyes with copious tepid water or saline.
   3. Ingestion. Administer activated charcoal orally if conditions are appropriate (see Table I-37,). Gastric lavage is not necessary after small-to-moderate ingestions if activated charcoal can be given promptly.
4. Enhanced elimination. There is no role for dialysis, hemoperfusion, or repeat-dose charcoal. Lipid-clearing drugs (eg, clofibrate and resins) have been suggested, but insufficient data exist to recommend them. Administration of the nonabsorbable fat substitute olestra has been described for dioxin poisoning, but human data are limited.