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The information in this profile may be out-of-date. It was last revised in 1996. EXTOXNET no longer updates this information, but it may be useful as a reference or resource.

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E X T O X N E T

Extension Toxicology Network

Pesticide Information Profiles

A Pesticide Information Project of Cooperative Extension Offices of Cornell University, Oregon State University, the University of Idaho, and the University of California at Davis and the Institute for Environmental Toxicology, Michigan State University. Major support and funding was provided by the USDA/Extension Service/National Agricultural Pesticide Impact Assessment Program.

EXTOXNET primary files maintained and archived at Oregon State University

Revised June 1996

Heptachlor

Trade and Other Names: Trade names include Biarbinex, Cupincida, Drinox, E 3314, Fennotox, Heptagran, Heptamul, Heptox, Termide, Velsicol 104.

Regulatory Status: Heptachlor is a moderately toxic compound in EPA toxicity class II. In 1988, the EPA canceled all uses of heptachlor in the U.S. Phase out of heptachlor use began in 1978. The only commercial use still permitted is for fire ant control in power transformers. Heptachlor is still available outside the U.S.

Chemical Class: organochlorine cyclodiene

Introduction: Heptachlor is an organochlorine cyclodiene insecticide, first isolated from technical chlordane in 1946. During the 1960s and 1970s, it was used primarily by farmers to kill termites, ants, and soil insects in seed grains and on crops, as well as by exterminators and home owners to kill termites. Before heptachlor was banned, formulations available included dusts, wettable powders, emulsifiable concentrates, and oil solutions. It acts as a nonsystemic stomach and contact insecticide. An important metabolite of heptachlor is heptachlor epoxide, which is an oxidation product formed from heptachlor by many plant and animal species.

Formulation: Before heptachlor was banned, formulations available included dusts, wettable powders, emusifiable concentrates, and oil solutions.

Toxicological Effects:

• Acute toxicity: Heptachlor is highly to moderately toxic compound via the oral route, with reported oral LD50 values of 100 to 220 mg/kg in rats, 30 to 68 mg/kg in mice, 116 mg/kg in guinea pigs, 100 mg/kg in hamsters, and 62 mg/kg in chickens [2,57]. It is moderately toxic via the dermal route as well, with reported dermal LD50 values of 119 to 320 mg/kg in rats, and greater than 2000 mg/kg in rabbits [9]. It is reported not to be a skin or eye irritant [9]. Heptachlor, like many organochlorines, may interfere with nerve transmission, and may also cause an increase in activity of the enzymes involved in the breakdown of foreign chemicals [57]. This may lead to serious toxicities from drugs taken for medical reasons. The acute toxicity of heptachlor epoxide, the main and most persistent of heptachlor's metabolites (see below), may be greater. Effects due to heptachlor exposure may include hyperexcitation of the central nervous system, liver damage, lethargy, incoordination, tremors, convulsions, stomach cramps or pain, and coma [2,57]. In humans exposed to chlordane, a closely-related organochlorine insecticide which usually contains 10% heptachlor, signs of neurotoxicity such as irritability, salivation, lethargy, dizziness, labored respiration, muscle tremors, and convulsions have been observed [2,57]. In severe cases, death may occur due to respiratory failure. Persons with underlying convulsive disorders or liver damage are at increased risk from exposure [2,57]. Prior to it being banned in the U.S. and in many other countries, the main routes of human exposure to heptachlor were via ingestion of residues in food or via inhalation in homes treated for termite control, especially where applications were done improperly [58].
• Chronic toxicity: Chronic exposure to heptachlor may cause the same effects as acute exposure. No effects were observed in rats fed dietary doses of 0.25 mg/kg/day over 2 years [57]. Increased mortality was observed in mice fed heptachlor/heptachlor epoxide for 2 years at dose levels 1.5 mg/kg/day [2,57]. When fed to dogs for 60 days, 0.1 mg/kg/day resulted in no observed adverse effects. Liver damage produced by doses of 0.35 mg/kg/day in rats over a 50-week period were reversible [57]. Changes which occurred in rat liver tissues after dosages of 0.35 mg/kg/day for 50 weeks returned to normal after 30 additional weeks without dosing [2]. The photoisomer of heptachlor (photoheptachlor) and the major metabolite of heptachlor (heptachlor epoxide) may both be more toxic than the parent compound [2].
• Reproductive effects: There is evidence that heptachlor and heptachlor epoxide are associated with infertility and improper development of offspring. Animal studies have shown that females were less likely to become pregnant when both males and females were fed heptachlor. Decreased postnatal survival was reported in the progeny of rats that were fed 0.25 mg/kg/day heptachlor for 60 days and during pregnancy [57]. Dosage of 6.9 mg/kg/day for 3 days significantly reduced fertility in rats and reduced the survival by one-third of young during the first weeks. A dose of 1 mg/kg/day had no adverse effects on reproduction. No increase in fetal mortality or malformations occurred when pregnant rats were given up to 20 mg/kg/day on days 7 to 17 of gestation [57]. Because the available data are inconclusive, it is not possible to make conclusions about possible reproductive effects of heptachlor in humans.
• Teratogenic effects: No teratogenic effects were observed rats, rabbits, chickens, and beagle dogs [58]. No increase in malformations occurred when pregnant rats were given up to 20 mg/kg/day on days 7 to 17 [2,57]. In studies where reproductive effects were noted (e.g., increased mortality), decreased viablility of offspring was observed [57]. In one study, rats born to mothers fed relatively low doses of heptachlor showed a tendency to develop cataracts shortly after their eyes opened, but these results have not been reproduced elsewhere [2,57]. In another study, doses of 5 mg/kg/day over 3 days produced developmental abnormalities in rats [2,57]. Overall, these data suggest that teratogenic effects in humans are unlikely at expected exposures.
• Mutagenic effects: Laboratory tests indicate that neither heptachlor nor heptachlor epoxide are mutagenic [57,58].
• Carcinogenic effects: It is reported that "a few large doses" of heptachlor given to suckling rats did not result in observable tumor incidence over an observation period of 106 to 110 weeks [2,57]. In another study, doses of approximately 1.2 mg/kg/day of either heptachlor or heptachlor epoxide increased the incidence of liver carcinomas in rats [2,57]. There is evidence that heptachlor promotes development of tumors in rats after initiation with a known tumor initiator [2,57]. Available evidence is not sufficient to assess the potential of heptachlor to cause cancer in humans.
• Organ toxicity: Results of animal tests show that chronic exposure to heptachlor or heptachlor epoxide adversely affect the liver, kidney, and red blood cells.

• Fate in humans and animals: Heptachlor is readily taken up through the skin, lungs, and gastrointestinal tract [57]. Once absorbed, it is systemically distibuted and moves into body fat [2,57]. In mammals, heptachlor is readily converted to its most persistent and toxic metabolite, heptachlor epoxide, in the liver [2,57]. Heptachlor epoxide is stored mainly in fatty tissue, but also in liver, kidney, and muscle tissues [57]. Rats fed diets containing 30 ppm had the highest concentration of heptachlor in their fatty tissues after 2 to 4 weeks. At 12 weeks after cessation of the exposure, heptachlor disappeared completely from fatty tissues, while heptachlor epoxide was found in the rats' fatty, liver, kidney, and muscle tissues [57]. Heptachlor is able to cross the placenta and has been found in human milk. Intense activity or starvation may mobilize the pesticide as body fat is burned, resulting in the reappearance of toxic symptoms long after uptake from the environment [58]. It is excreted in the urine and feces [2,58]. Heptachlor is generally not detectable in the human population, but heptachlor epoxide has been found in human fat, blood, organs, and milk [58]. In localities where heptachlor was used regularly, it has been found at higher concentrations in human milk than in dairy milk [58]. Rats retained 77% of heptachlor that they inhaled during a 30-minute period [9].

Ecological Effects:

• Effects on birds: Heptachlor is moderately to highly toxic to bird species; the reported acute oral LD50 in mallard ducks is 2080 mg/kg [53]. The reported 5-day dietary LC50 in Japanese quail is 99 ppm [54]. Other reported 8-day dietary LC50 values for heptachlor are 450 to 700 ppm in bobwhite quail, and 250 to 275 ppm in pheasants [9]. It is also reported to decrease the survivability of chicken eggs [17]. Heptachlor and its more potent metabolite, heptachlor epoxide, have been found in the fat of fish and birds. They have also been found in the liver, brain, muscle, and eggs of birds [58].
• Effects on aquatic organisms: Both heptachlor and the epoxide are very highly toxic to most fish species tested. The reported 96-hour LC50 values are: 5.3 to 13 ug/L in bluegill sunfish; 7.4 to 20 ug/L in rainbow trout, 6.2 ug/L in northern pike, 23 ug/L in fathead minnow and 10 ug/L in largemouth bass [55]. Heptachlor is also very highly toxic to freshwater aquatic invertebrates (like snails, worms, crayfish, etc.) [17,55]. Heptachlor is also toxic to marine aquatic life, but its toxicity varies highly from species to species; crustacean and younger life stages of fish and invertebrates are most sensitive [58]. Both heptachlor and heptachlor epoxide have been shown to bioconcentrate in aquatic organisms such as fish, mollusks, insects, plankton, and algae [57]. It has been found in several fish, molluscs, and other aquatic species at concentrations of 200 to 37,000 times the concentration of heptachlor in the surrounding waters [57,58].
• Effects on other organisms: Heptachlor is highly toxic to bees.

Environmental Fate:

• Breakdown in soil and groundwater: Heptachlor and heptachlor epoxide are highly persistent in soils, with a reported representative field half-life of 250 days [15]. Data collected in Mississippi, New Jersey, and Maryland showed a soil half-life for heptachlor of 0.4 to 0.8 years. The mean disappearance rates of heptachlor from soil ranged from 5.25 to 79.5% per year, depending upon the soil type and mode of application. The highest rates of degradation were observed in sandy soils following an application of a granular formulation. Soil incorporation also led to rapid disappearance rates in all soil types. Without incorporation, volatilization from soil surfaces, especially wet ones, is the major route of loss of heptachlor [58]. This compound has sometimes been detected in soil in trace amounts 14 to 16 years after application [58]. Heptachlor and its epoxide are moderately bound to soils [15] and should not be highly mobile [57,58]. Over their long residence times, even low mobility may result in appreciable movement and so heptachlor and its metabolite (heptachlor epoxide) may be considered to pose a risk of groundwater contamination over time [57,58]. Very low levels of heptachlor have been found in well water [58]. Heptachlor epoxide is not very susceptible to biodegradation, photolysis, oxidation, or hydrolysis in the environment [57].
• Breakdown in water: Heptachlor is almost insoluble in water, and will enter surface waters primarily though drift and surface run-off. In water, heptachlor readily undergoes hydrolysis to a compound which is then readily processed (preferentially under anaerobic conditions) by microoorganisms into heptachlor epoxide [2,3,6]. After hydrolysis, volatilization, adsorption to sediments, and photodegradation may be significant routes for disappearance of heptachlor from aquatic environments [57].
• Breakdown in vegetation: In plants, the major breakdown product of heptachlor is the epoxide [9]. Heptachlor is nonphytotoxic when used as directed [9].

Physical Properties:

• Appearance: Pure heptachlor is a white or light tan, crystalline solid with a mild camphor or cedar-like odor; the technical heptachlor is a soft wax [9].
• Chemical Name: 1,4,5,6,7,8,8-heptachloro-3a,4,7,7a-tetrahydro-4,7-methanoindene [9]
• CAS Number: 76-44-8
• Molecular Weight: 373.34
• Water Solubility: 0.056 mg/L [9]
• Solubility in Other Solvents: v.s. in acetone, alcohol, benzene, carbon tetrachloride, cyclohexanone, kerosene, and xylene [9]
• Melting Point: 95-96 C (pure); 46-74 C (technical) [9]
• Vapor Pressure: 53 mPa @ 25 C [9]
• Partition Coefficient: 5.44 [57]
• Adsorption Coefficient: 24,000 [15]

Exposure Guidelines:

• ADI: 0.0001 mg/kg/day [27]
• MCL: 0.0004 mg/L [8]
• RfD: 0.005 mg/kg/day [8]
• PEL: 0.5 mg/m3 (8-hour) (skin) [28]
• HA: Not Available
• TLV: Not Available

Basic Manufacturer:

Velsicol Chemical Corporation
10400 W. Higgins Road
Rosemont, IL 60018-5119

• Phone: 708-298-9000
• Emergency: Not Available
  

References:

References for the information in this PIP can be found in Reference List Number 6

DISCLAIMER: The information in this profile does not in any way replace or supersede the information on the pesticide product labeling or other regulatory requirements. Please refer to the pesticide product labeling.