SUBSTANCES-OF-ABUSE
OCCUPATIONAL & ENVIRONMENTAL TOXICOLOGY

Hexachlorobenzene Fact Sheet

Source of Exposure

Hexachlorobenzene is employed widely as a fungicide and is found frequently as a by-product in similar products. It is used to control smut disease in cereal grains such as seed and wheat. Risk of exposure occurs from its unavoidable presence in the manufacture of chlorinated solvents, such as perchloroethylene. Exposure may also result from dietary intake of contaminated food or water. Trade names include Anti Carie, Bent-Cure.

Symptoms

One of the primary toxic effects of HCB is cutaneous porphyria involving blistering and epidermolysis of the face and hands. (standard) Acute exposure may cause nausea, dizziness, tremors, and convulsions and loss of consciousness. These poisons are absorbed across the gut and interfere with the transmission of nerve impulses. This neurologic interference can produce weakness, apprehension, excitability and disorientation in an exposed patient. Additional symptoms may be irregular or depressed respiration as well as myocardial irritability. Many forms of the pesticide may be delivered in petroleum solvents that may contribute to respiratory depression upon exposure.

Blood Concentrations

Hexachlorobenzene can be found in approximately 95% of the general population with an average serum concentration of 0.5 PPB (EHS data).

Toxic Levels

Hexachlorobenzene has a relatively low toxicity. A chemical worker who had developed cutaneous lesions on his hands and face had developed blood levels of 383 µg/L. After removal from exposure for one year, the workers blood concentrations declined to 268 µg/L. (Courtney, 1929) Individuals who have been sensitized may manifest negative health effects at concentrations well within the ranges considered safe for the average population.

Metabolism

Information on the metabolism of HCB in humans is limited. However, studies in rats have shown that 7% of a single dose is eliminated in urine and 27% is eliminated in feces as metabolites over a four week period. HCB is metabolized into pentachlorophenol, pentachlorobenzene, tetrachlorohydroquinone, chlorophenol and trichlorophenol. The half life of HBC is estimated at approximately 60 days.

Summary

Classification:   Chlorinated Pesticide
Population Average:   0.5 PPB
Frequency Per 100:   95%
Onset of Symptoms:   23 ppb (whole blood)
Death Data:   not available
Half Life:   60 Days
LD 50:   (oral-rat) 10,000 mg/kg

References

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Baselt,, R.C. , Disposition of Toxic Drugs and Chemicals in Man, 2nd Ed. Davis, CA: Biomedical Publications, 1982.

Brady, M.N. and Siyali, D.S. "Hexachlorobenzene in human body fat", Med J Aust 1: 158-161, 1972.

Burns, J.E., Miller, F.M., Gomes, E.D. and Albert, R.A. "Hexachlorobenzene exposure from contaminated DCPA in vegetable spraymen", Arch Env Health 29: 192-194, 1974.

Burns, J.E. and Miller, F.M. "Hexachlorobenzene contamination: its effects in a Louisiana population", Arch Env Health 30: 44-48, 1975.

Cam, C. and Nigogosyan, G. "Acquired toxic porphyria cutanea tarda due to hexachlorobenzene". J Am Med Asso 183: 90-93, 1963.

Committee on Toxicology, An Assessment of the Health Risks of Seven Pesticides Used for Termite Control, Washington, D.C: National Academy Press, 1982.

Courtney, K.D. "Hexachlorobenzene (HCB): a review", Env Res. 20: 225-266, 1979.

Currier, M.F., McClimans, C.D. and Barna-Lloyd, G. "Hexachlorobenzene blood levels and the health status of men employed in the manufacture of chlorinated solvents", J Tox Env Health 6: 367-377, 1980.

Davignon, L. F. , St. Pierre, J. , Charest, G. , and Tourangeau, F. J. "A study of the chronic effects of insecticides in man", in Canadian Med Assoc. 92: 507-602, 1965.

DeMatteis, F., Prior, B. E. and Rimington, C "Nervous and biochemical disturbances following hexachlorobenzene intoxication", Nature 191: 363-366, 1961.

Harris, C.R., and Sans, W.W. "Pesticides in soil"', Pest Monitoring J. 5: 259-267, 1971.

Morgan, D.P. Recognition and Management of Pesticide Poisonings, 3rd Ed., United States Environmental Protection Agency EPA-540/9-80-0059 Washington, D.C. U.S. Government Printing Office, January, 1982.

Peters, H.A. "Hexachlorobenzene poisoning in Turkey", Fed Proc. 35: 2400-240, 1976.

Richter, E and Schmid, A. "Hexachlorbenzolgehalt im Vollblut von Kindern:, Arch Tox. 35: 141-147, 1976.

Schmid, R. "Cutaneous porphyria in Turkey", New Eng J Med. 263: 397 - 398, 1960.

Seba, D.B., Milam, M.J. and Laseterl, J.L. "Uptake, measurement and elimination of synthetic chemicals by man", in Borstoff, J. and Challacombe, S.J. (Eds.), Food Allergy and Intolerance, London: Bailliere Tindall, 1987.

Siyali, D.S. "Hexachlorobenzene and other organochloride pesticides in human blood", Med J Aust. 2: 1063-1066, 1972.

Tocci, P.M., Mann, J.B., Davies, J.E., Edmundson, W.F. "Biochemical differences found in persons chronically exposed to high levels of pesticides", Ind Med. 38: 40-47, 1969.