Evaluates the risks to human health and the environment posed by exposure to hexachlorobenzene (HCB). HCB has historically had many industrial and agricultural uses, including extensive use as a seed dressing to prevent fungal disease on grains. Although concerns about effects on health and the environment prompted many countries to discontinue production in the 1970s, inadvertent production continues in the form of by products and impurities generated during the manufacture of chlorinated solvents, chlorinated aromatics, and chlorinated pesticides. Other continuing sources of this highly persistent chemical include application of contaminated pesticides, incomplete incineration of chlorine containing wastes, and release from old dumpsites. A discussion of the environmental behavior of HCB cites properties, including its resistance to degradation, mobility and lipid solubility that help explain its detection in all environmental compartments and its presence in the adipose tissues of virtually all members of the general population. Studies indicate that HCB undergoes significant bioaccumulation and biomagnification in the food chain. Concerning environmental levels and human exposure, food is determined to be the principal route of exposure for the general population. Although HCB is widely dispersed in ambient air, concentrations are generally low. The contribution of levels in drinking water to total exposure is likewise estimated to be low. Limited data suggest that when poor industrial hygiene is practiced, workers in certain occupations may be exposed to higher concentrations than the general population. A review of data on the kinetics and metabolism of HCB in experimental animals concludes that the chemical is readily absorbed by the oral route and poorly via the skin. Studies demonstrate that HCB is slowly metabolized and eliminated, accumulates in lipid rich tissues, crosses the placental barrier, and is present in breast milk. The most extensive section evaluates findings from the numerous studies of toxic effects in laboratory animals. Convincing studies demonstrate that HCB is carcinogenic in animals and has adverse non neoplastic effects, at relatively low doses, on a wide range of organs and systems, including the liver, lungs, kidneys, thyroid, reproductive tissues, and nervous and immune systems. The evaluation of effects on human health draws on numerous reviews of an accidental poisoning incident in Turkey that occurred in 1955 1959, when HCB treated wheat grain was ground into flour and used to produce bread, and resulted in more than 600 cases of porphyria cutanea tarda with a high mortality rate. In this incident, clinical manifestations of poisoning included disturbances in porphyrin metabolism, dermatological lesions, hyperpigmentation, hypertrichosis, enlarged liver, enlargement of the thyroid gland and lymph nodes, and osteoporosis or arthritis. Nursing infants of exposed mothers developed a disorder called pembe yara, or pink sore, and most died within a year. Follow up of survivors at 20 and 30 years revealed persistent abnormalities. The report found no adequate epidemiological studies of cancer in exposed populations, including workers. On the basis of clinical evidence from the poisoning incident supported by animal data demonstrating adverse effects at several sites in several species at relatively low doses, the report calls for measures to reduce the environmental burden of HCB and concludes that alternatives should be found for any continuing present uses. The following health based guidance values for the total daily intake of HCB in humans were proposed: for non neoplastic effects, 0.17 micrograms/kg body weight/day; for neoplastic effects, 0.16 micrograms/kg body weight/day.