See also:
Heptaclor summary in Assessment report on POPs, Français, Español
Rotterdam Convention Decision Guidance Documents on Heptaclor: English, Français, Español

Chemical properties

CAS chemical name: 1,4,5,6,7,8,8-Heptachloro-3a,4,7,7a-tetrahydro-4,7-methanol-1H-indene.
Synonyms and Trade Names (partial list): Aahepta, Agroceres, Baskalor, Drinox, Drinox H-34, Heptachlorane, Heptagran, Heptagranox, Heptamak, Heptamul, Heptasol, Heptox, Soleptax, Rhodiachlor, Veliscol 104, Veliscol heptachlor.
CAS No.: 76-44-8;
Molecular formula: C10H5Cl7;
Formula weight: 373.32.
Appearance: White to light tan, waxy solid or crystals with a camphor-like odour.
Properties: Melting point: 95-96 C (pure), 46-74 C (technical); boiling point: 135-145 C at 1-1.5 mm Hg, decomposes at 760 mm Hg; KH; 2.3 x 10 -3 atm.mm3/mol; log KOC: 4.38; log KOW; 4.40-5.5; solubility in water: 180 ppb at 25 C; vapor pressure: 3 x 10-4 mm Hg at 20 C.

Heptachlor 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 binds readily to aquatic sediments and bioconcentrates in the fat of living organisms.

Historical Uses

Heptachlor is a non-systemic stomach and contact insecticide, used primarily against soil insects and termites. It has also been used against cotton insects, grasshoppers, some crop pests and to combat malaria.

The use of heptachlor has been banned in Cyprus, Ecuador, the EU, Portugal, Singapore, Sweden, Switzerland and Turkey. Its use is severely restricted in Argentina, Israel, Austria, Canada, Czechoslovakia, Denmark, Finland, Japan, New Zealand, Philippines, USA and USSR.

Human Health and Environmental Issues

Heptachlor is metabolised in animals to heptachlor epoxide, whose toxicity is similar to that of heptachlor, and which may also be stored in animal fat.

There is no information on accidental or suicidal intoxication by heptachlor in humans. Symptoms in animals include tremors and convulsions.

A study of workers from a plant involved in the production of heptachlor and endrin found a significant increase in bladder cancer . This result was unexpected as no know bladder carcinogens were used at the plant, however, the small number of deaths (3) makes interpretation of these findings difficult.

No deaths from liver or biliary tract cancer were observed, although mortality from cerebrovascular disease was higher than expected. There is limited evidence that cyclodienes such as heptachlor may affect immune responses.

The acute oral LD50 of heptachlor to laboratory animals is in the range of 40 mg/kg body weight in rats to 116 mg/kg in rabbits. Groups of male and female rats were administered daily doses of heptachlor orally beginning at 4 months of age, and continuing for 200 days. All the animals in the 50 and 100 mg/kg groups died by the 10th day of exposure. Three animals in the 5 mg/kg group and 1 in the control died before the end of the study. Beginning on the 50th day to the study, hyper-reflexia, dyspnoea and convulsions were observed in the rats exposed to 5 mg/kg. Histological examination revealed fatty degeneration of the liver cells and moderate fatty infiltration of the epithelium of the renal tubules in the 5 mg/kg exposed group. In a reproduction study, rats were fed diets containing heptachlor in their diet throughout three generations. Mortality of pups in the 10 mg/kg group was slightly increased during the second and third weeks after birth in the second generation only. No adverse effects were observed in the lower dose levels. WHO has reported no evidence of teratogenicity of heptachlor in rats and rabbits.

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

Heptachlor has been strongly implicated in the decline of several wild bird populations including Canada geese and the American Kestrel in the Columbia Basin in the US. A population of Canada geese at the Umatilla National Wildlife Refuge in Oregon experienced lowered reproductive success, and adult mortality. Heptachlor epoxide residues were detected in the brains of dead birds and in the eggs of nests with low success. The reproductive success of American Kestrels in the same area was also reduced. Heptachlor epoxide residues in the eggs were associated with reduced productivity. The presence of residues in the eggs indicates that heptachlor is transferred through the food chain, as Kestrels are not seed eaters, which was the presumed route of exposure for the geese. Concentrations on the treated seeds were lower than the recommended usage level indicating that effects on wildlife may occur, even if heptachlor is used responsibly.

The half life of heptachlor in temperate soil is up to 2 years. This persistence, combined with a high partition coefficient (KOW = 4.4-5.5), provides the necessary conditions for heptachlor to bioconcentrate in organisms. Bioconcentration factors of heptachlor and heptachlor epoxide in fathead minnows (Pimephales promelas) were 9,500 and 14,400, respectively.

The chemical properties of heptachlor (low water solubility, high stability, and semi-volatility) favour its long range transport, and heptachlor and its epoxide have been detected in arctic air, water and organisms.

WHO suggests that food is the major source of exposure of heptachlor to the general population. Heptachlor has been detected in the blood of cattle from both the US and Australia. Heptachlor was detected in 30 of 241 samples in American cattle, and violations of the MRL for heptachlor were detected in 0.02 % of Australian cattle. In both instances, heptachlor was among the most frequently detected organochlorine.

A daily intake of 0.25 µg/person/day (for heptachlor and heptachlor epoxide combined, based on a 60 kg person) was estimated for Vietnam, and of 0.07 µg/person/day (for heptachlor alone) for India.