Hexachlorobenzene (HCB)

Synonyms and Trade Names (partial list): Amaticin, Anticarie, Bunt-cure, Bunt-no-more, Co-op hexa, Granox, No bunt, Sanocide, Smut-go, Sniecotox.
Appearance: White monoclinic crystals or crystalline solid.


Hexachlorobenzene (HCB) is a fungicide that was first introduced in 1945 for seed treatment, especially for control of bunt of wheat. HCB is also a byproduct of the manufacture of industrial chemicals including carbon tetrachloride, perchlorethylene, trichloroethylene and pentachlorbenzene. It is a known impurity in several pesticide formulations, including pentachlorophenol and dicloram and may be present as an impurity in others. HCB is highly insoluble in water, and is soluble in organic solvents. It is quite volatile and can be expected to partition into the atmosphere as a result. It is very resistant to breakdown, has a high partition coefficient (KOW=3.03-6.42), and is known to bioconcentrate in the fat of living organisms as a result.

HCB is banned in Austria, Belgium, Czechoslovakia, Denmark, the EU, Germany, Hungary, Liechtenstein, Netherlands, Panama, Switzerland, Turkey, United Kingdom and the USSR. It is severely restricted or has been voluntarily withdrawn in Argentina, New Zealand, Norway and Sweden.

Usage in South East Asia


Used or Found in Country?

Years of Usage

Regulatory Controls








Never registered




Banned in 1988







Viet Nam


Banned in 1992

(table references)

Potential Effects on Humans

The most notable episode involving the effects of HCB on humans involves the ingestion of HCB treated seed grain in eastern Turkey between 1954 and 1959. The patients who ingested the treated seed experienced a range of symptoms including photosensitive skin lesions, hyperpigmentation, hirsutism, colic, severe weakness, porphyrinuria, and debilitation. Approximately 3,000-4,000 people developed porphyria turcica, a disorder of haem biosynthesis. Mortality was up to 14%. Mothers who ingested the seeds passed the HCB to their children by placental transfer and through maternal milk. Children born to these women developed "pembe yara" or pink sore, with a reported mortality rate of approximately 95%. A study of 32 individuals twenty years after the outbreak showed that porphyria can persist years after the ingestion of HCB. A small cross-sectional study of workers exposed to HCB did not find any evidence of cutaneous porphyria or any other adverse effects associated with exposure of 1 to 4 years.

IARC has concluded that while there is inadequate evidence for the carcinogenicity of HCB in humans, there is sufficient evidence in experimental animals. IARC has classified HCB as a possible human carcinogen (Group 2B).

Potential Effects on Animals

The acute toxicity of HCB to laboratory animals is quite low, with acute oral LD50 values in the range of more than 2,600 mg/kg body weight in rabbits and 4,000 mg/kg in mice. Porphyria, skin lesions, hyperexcitability and changes in weight, enzyme activities and morphology of the liver have been reported in association with subchronic toxicity of HCB. HCB has also been reported to stimulate the immune system in rats, and suppress the immune system of mice. HCB has also been reported to produce adverse effects on reproduction and reproductive tissue. Female rats fed HCB in the diet experienced offspring mortality, with a 21-day LD50 of 100 ppm.

A four-generation reproduction study in rats fed HCB in the diet was conducted. HCB affected reproduction by reducing the number of litters whelped, litter size and the number of pups surviving to weaning. In a separate study, HCB at a concentration of 100 mg/kg body weight/day was associated with cleft palate and some kidney malformations in CD-1 mice. HCB exposure in several studies in cynomologous monkeys has resulted in degenerative changes in the ovarian surface epithelium, suppression of serum progesterone, atrophy of thymic cortex, a reduction in the number of lymphocytes, degenerative changes in the ovaries and kidney and degenerative changes in the liver compatible with porphyria tarda.

HCB is unlikely to cause direct toxicological effects in aquatic animals at or below saturation concentrations (approximately 5 µg/L) in water. At an exposure concentration of 4.8 µg HCB/L for 32 days, there was no observed effect on embryonic through juvenile stages in developing fathead minnows (Pimephales promelas) giving a NOEC of 4.8 µg/L. The caldoceran Daphnia magna, the amphipods Hylella azeteca, and Gammarus lacustris, the annelid worm Lumbricus variegatus, and the fathead minnow Pimephales promelas were exposed to HCB at saturation concentration (5 µg/L) for 68 days. No effects on survival, growth or reproduction were observed.

Adult Japanese quail (Coturnix japonica) were fed diets containing HCB for 90 days, resulting in increased mortality at 100 µg/g diet and significantly reduced hatchability at 20 µg/g. At 5 µg/g increased liver weight, slight liver damage and increased faecal excretion of coproporphyrin were observed.

Experiments conducted in mink (Mustela vison) and European ferrets (Mustela putorius furo) with dietary HCB resulted in adult mortality are higher doses (125 and 625 mg HCB/kg diet) and decreased litter size, increased percentage of stillbirths, increased kit mortality and decreased kit growth. Mink were generally more susceptible than ferrets to the effects of HCB. Results from another study indicate that in utero exposure to HCB resulted in higher kit mortality than exposure via the mothers milk.


HCB is very persistent. Estimated half lives in soil from aerobic and anaerobic degradation range from 2.7 to 22.9 years. This persistence, combined with a high partition coefficient (log KOW = 3.03-6.42), provides the necessary conditions for HCB to bioconcentrate in organisms. Bioconcentration factors of 22,000 and 106,840 have been reported in fathead minnows and Lumbricus variegatus, respectively. The chemical properties of HCB (low water solubility, high stability, and semi-volatility) favour its long range transport, and HCB has been detected in Arctic air, water and organisms.

HCB is ubiquitous in the environment, and has been measured in foods of all types.

  • HCB was one of two organochlorines detected in all samples of Spanish meat and meat products surveyed with mean levels ranging from 8 ppb (fat weight) in pork products (cured ham) to 49 ppb in lamb, with a maximum level of 178 ppb in lamb.
  • HCB was detected in 13 of 241 serum samples from Colorado beef cattle in a monitoring program, with an average concentration of 3.1 ppb.
  • A survey of US pasteurized milk detected HCB in 8 of 806 composite milk samples.
  • A survey of foods from India found average concentrations of HCB ranging from 1.5 ng/g (fat weight) in both oils and milk to 9.1 ng/g in fish and prawns, with a maximum concentration of 28 ng/g in fish and prawns and an estimated daily intake of 0.13 µg/person.
  • Average HCB residues in foods from Vietnam ranged from 0.28 ng/g (fat weight) in pulses to 27 ng/g in caviar, with an estimated daily intake of 0.10 µg/person.

For more information:

Adapted from Persistent Organic Pollutants: Information on POPs, their alternatives and alternative approaches (United Nations Environmental Programme (UNEP) 1995).

Chemical structure of Hexachlorobenzene (HCB)
Source: UNEP
Hatfield Consultants The World Bank funded by the Canadian POPs Trust Fund through the      
Canadian International Development Agency
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