HCB is a white crystalline solid that has negligible solubility in water but sparingly soluble in organic solvents. It is most soluble in halogenated solvents like chloroform, less soluble in esters and hydrocarbons, and even less soluble in short chain alcohols. Its vapour pressure is 1.09×10−5 mmHg at 20 °C. Its flash point is 242 °C and it sublimes at 322 °C.
Safety
Hexachlorobenzene is an animal carcinogen and is considered to be a probable human carcinogen. After its introduction as a fungicide in 1945, for crop seeds, this toxic chemical was found in all food types. Hexachlorobenzene was banned from use in the United States in 1966. This material has been classified by the International Agency for Research on Cancer as a Group 2B carcinogen. Animal carcinogenicity data for hexachlorobenzene show increased incidences of liver, kidney and thyroid cancers. Chronic oral exposure in humans has been shown to give rise to a liver disease, skin lesions with discoloration, ulceration, photosensitivity, thyroid effects, bone effects and loss of hair. Neurological changes have been reported in rodents exposed to hexachlorobenzene. Hexachlorobenzene may cause embryolethality and teratogenic effects. Human and animal studies have demonstrated that hexachlorobenzene crosses the placenta to accumulate in foetal tissues and is transferred in breast milk. HCB is very toxic to aquatic organisms. It may cause long term adverse effects in the aquatic environment. Therefore, release into waterways should be avoided. It is persistent in the environment. Ecological investigations have found that biomagnification up the food chain does occur. Hexachlorobenzene has a half life in the soil of between 3 and 6 years. Risk of bioaccumulation in an aquatic species is high.
Toxicology
Oral LD50 : 10,000 mg/kg
Oral LD50 : 4,000 mg/kg
Inhalation LC50 : 3600 mg/m3
Material has relatively low acute toxicity but is toxic because of its persistent and cumulative nature in body tissues in rich lipid content.
Unique Exposure Incident
In Anatolia, Turkey between 1955 and 1959, during a period when bread wheat was unavailable, 500 people were fatally poisoned and more than 4,000 people fell ill by eating bread made with HCB-treated seed that was intended for agriculture use. Most of the sick were affected with a liver condition called porphyria cutanea tarda, which disturbs the metabolism of hemoglobin and results in skin lesions. Almost all breastfeeding children under the age of two, whose mothers had eaten tainted bread, died from a condition called "pembe yara" or "pink sore", most likely from high doses of HCB in the breast milk. In one mother's breast milk the HCB level was found to be 20 parts per million in lipid, approximately 2,000 times the average levels of contamination found in breast-milk samples around the world. Follow-up studies 20 to 30 years after the poisoning found average HCB levels in breast milk were still more than seven times the average for unexposed women in that part of the world, and 150 times the level allowed in cow's milk. In the same follow-up study of 252 patients, 20–30 years postexposure, many subjects had dermatologic, neurologic, and orthopedic symptoms and signs. The observed clinical findings include scarring of the face and hands, hyperpigmentation, hypertrichosis, pinched faces, painless arthritis, small hands, sensory shading, myotonia, cogwheeling, enlarged thyroid, and enlarged liver. Urine and stool porphyrin levels were determined in all patients, and 17 have at least one of the porphyrins elevated. Offspring of mothers with three decades of HCB-induced porphyria appear normal.
