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Heptachlor

Publication Date: 9/93

TRADE OR OTHER NAMES

Trade names include Drinox, Heptagran, H-34 Heptamul, Heptox, Goldcrest H-60 (2, 7)

REGULATORY STATUS

In 1988, the EPA canceled all uses of heptachlor in the United States. Phase out of heptachlor use began in 1978. The only commercial use still permitted is for fire ant control in power transformers (1, 9). Heptachlor is still available outside the United Sates (7, 10).

INTRODUCTION

Heptachlor is an organochlorine (cyclodiene) insecticide which was first isolated from technical chlordane in 1946. During the 1960s and 1970s, it was used primarily by farmers to kill insects in seed grains and on crops, as well as by exterminators and home owners to kill termites (1). Before heptachlor was banned, formulations available included dusts, wettable powders, emulsifiable concentrates, and oil solutions. It acts as a non-systemic stomach and contact insecticide (2, 10).

An important metabolite of heptachlor is heptachlor epoxide which is an oxidation product formed from heptachlor by many plant and animal species (1).

TOXICOLOGICAL EFFECTS

ACUTE TOXICITY

Heptachlor is highly toxic to humans and can be absorbed through the skin, lungs and gastrointestinal tract. It causes hyperexcitation of the central nervous system and damage to the liver. Poisoning symptoms observed in laboratory animals include lethargy, incoordination, tremors, convulsions, stomach cramps or pain, and coma. 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. In severe cases, death may occur due to respiratory failure. Persons with convulsive disorders or liver damage are at increased risk from exposure (11).

Heptachlor is stored in fatty tissues. Intense activity or starvation may mobilize the pesticide, resulting in the reappearance of toxic symptoms long after actual exposure (11).

Prior to it being banned in the United States 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 (1, 10).

Heptachlor is not a skin or eye irritant (5, NIOSH OSHA Occupat. Health Guide Chem. Hazards. 1981).

The organochlorines interfere with nerve transmissions. They also cause the body to produce more of the enzymes involved in the breakdown of certain chemicals. Because of this, exposure to heptachlor can lead to serious toxicities from drugs taken for medical reasons.

The amount of a chemical that is lethal to one-half (50%) of experimental animals fed the material is referred to as its acute oral lethal dose fifty, or LD50. The oral LD50 for heptachlor in rats is 40- 220 mg/kg, 30 to 68 mg/kg in mice, 116 mg/kg in guinea pigs,100 mg/kg in hamsters, and 62 mg/kg in chickens. The dermal LD50 in rats is 119-320 mg/kg, in guinea pigs is 1,000 mg/kg, and for rabbits is greater than 2,000 mg/kg. The inhalation LCLO in cats is 150 mg/m3.

The acute toxicity of heptachlor epoxide, the main and most persistent of heptachlor's metabolites, is greater. For example, the intravenous lethal doses for heptachlor and heptachlor epoxide are 40 and 10 mg/kg, respectively (1, 2, 7, 10, 11).

CHRONIC TOXICITY

Chronic exposure to heptachlor can cause the same symptoms as acute exposure. Increased mortality has been observed in both rats and mice fed heptachlor/heptachlor epoxide for two years. The LOAEL levels in these studies were 0.25 mg/kg/day for rats and 1.5 mg/kg/day for mice. When fed to dogs for 60 days, 0.1 mg/kg/day of heptachlor had no adverse effect. 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 (1, 2).

The EPA has established a lifetime health advisory level for heptachlor of 17.5 ug/l (ppb) and for heptachlor epoxide of 0.4 ug/l (ppb). This means that a person may drink water containing heptachlor or heptachlor epoxide at or below these levels daily over the course of their lifetime with no health effects. These lifetime health advisory levels do not account for the risk of cancer posed by exposure to heptachlor or heptachlor epoxide. The U.S. Public Health Service has published a health advisory which is based on cancer risk and which recommends the following limits for long-term exposure in drinking water: heptachlor, 0.0104 ppb; and heptachlor epoxide, 0.0006 ppb (1).

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 (1).

Dosage of 6.9 mg/kg/day for 3 days significantly reduced fertility in rats and reduced the survival of young during the first weeks by one- third. A dose of 1mg/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 (2).

Teratogenic Effects

No teratogenic effects were observed rats, rabbits, chickens and beagle dogs (5, 10). Baby rats born to mothers fed relatively low doses of heptachlor showed a tendency to develop cataracts shortly after their eyes opened (1, 14).

Mutagenic Effects

Laboratory tests indicate that neither heptachlor nor heptachlor epoxide are mutagenic (1, 5, Mut. Res. 116(3-4):185-216. 1983; Envir. Mutagen. 3(1):11-23. 1981).

Carcinogenic Effects

Chronic oral exposure to heptachlor/ heptachlor epoxide increased the incidence of liver carcinomas in rats. The Environmental Protection Agency has classified heptachlor and heptachlor epoxide as probable human carcinogens. The International Agency for Research on Cancer states that there is inadequate evidence that heptachlor causes cancer in humans, and only limited evidence that it causes cancer in animals (1).

Organ Toxicity

The liver is the organ which is most sensitive to the acute toxic effects of heptachlor. Test animals fed heptachlor or heptachlor epoxide have shown enlarged livers and damage to liver tissues, damage to kidney tissues, and increased numbers of red blood cells (1, 5, 15).

Fate in Humans and Animals:

In mammals, heptachlor is readily converted to its most persistent and toxic metabolite, heptachlor epoxide. Metabolism occurs in the liver. Heptachlor epoxide is stored mainly in fatty tissue, but also in liver, kidney and muscle tissues. Rats fed diets containing 30 mg/kg had the highest concentration of heptachlor in their fatty tissues after two to four weeks. Twelve 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. Heptachlor epoxide has also been found to accumulate in the fatty tissues of humans, dogs and chickens. Heptachlor is generally not detectable in the human population, but heptachlor epoxide has been found in human fat, blood, organs and milk. It is excreted in the urine and feces (2, 6, 10, 13, 14).

Heptachlor is able to cross the placenta and has been found in human milk. In localities where heptachlor was used regularly, it has been found at higher concentrations in human milk than in dairy milk (1, 2, 6, 10, 13, 14).

Rats retained 77% of heptachlor that they inhaled during a 30-minute period (2).

ECOLOGICAL EFFECTS

Effects on Birds

Heptachlor appears to be fairly low in toxicity to birds such as mallards (4). It decreases the survivability of chicken eggs (14). Effects on Aquatic Organisms

Heptachlor is toxic to sea urchins. It causes abnormal embryos to be produced (14). Heptachlor is toxic to freshwater fish and aquatic invertebrates (like snails, worms, crayfish, etc.). Both heptachlor and heptachlor epoxide have been shown to bioconcentrate in aquatic organisms, especially fish and mollusks (1).

Effects on Other Animals (Nontarget species)

Heptachlor is toxic to aquatic life, but its toxicity varies highly from species to species. Marine crustacean and younger life stages of fish and invertebrates are most sensitive (10).

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. Heptachlor, like all organochlorines, has a strong tendency to bioaccumulate. Fish, insects, plankton and algae accumulate heptachlor. It has been found in several fish and other aquatic species at concentrations of 200 to 37,000 times the concentration of heptachlor in the surrounding waters (3, Callahan. Water-Rel. Environ. Fate Priority Pollut. 1979; EPA 1981).

ENVIRONMENTAL FATE

Breakdown of Chemical in Soil and Groundwater

Heptachlor and heptachlor epoxide are highly persistent in soils. Heptachlor epoxide is not very susceptible to biodegradation, photolysis, oxidation, or hydrolysis in the environment. The soil half- life of heptachlor is 6 months to 3.5 years, but trace levels have been detected in soil 14 and 16 years after application. Heptachlor epoxide can migrate into crops grown on soils last treated 5 to 15 years ago. 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 rate was observed in sandy soil following an application of a granular formulation. Soil incorporation also lead to rapid disappearance rates in all soil types. Heptachlor adsorbs strongly to soil and therefore resists leaching to groundwater (1, 3, 10).

Without incorporation, volatilization from soil surfaces, especially wet ones, is the major route of loss of heptachlor from soils. Ninety percent of the heptachlor applied to bare moist soil was volatilized within 2 to 3 days following application. Under anaerobic conditions, biodegradation may be significant (1, 3, 10, Appl. Ecol. 17(2):295-307. 1980).

The cyclodiene insecticides are all possible groundwater pollutants. This is especially true of the very persistent epoxides (such as endrin and heptachlor epoxide). Very low levels of heptachlor have been found in well water.

Breakdown of Chemical in Water

Heptachlor is almost insoluble in water (8) and is therefore unlikely to contaminate groundwater. In sunlit water, it will remain active for about 1 day, otherwise it may last from 2-10 days (EPA 1985). After one week, 75% of the heptachlor entering the Little Miami River in Ohio disappeared. After 2 weeks, the heptachlor was 100% degraded. Chemical hydrolysis is expected to be the main fate of heptachlor in water, with half-lives of 233.1 hours in buffered water and 4.48 days at pH 7 in 99:1 water: ethanol. After hydrolysis, volatilization, adsorption to sediments and photodegradation may be significant routes for disappearance of heptachlor from aquatic environments (3).

Breakdown of Chemical in Vegetation

Sunlight will breakdown heptachlor, but it tends to be stable to light, moisture, air and moderate heat (5, 14, EPA 1985).

Soil microbes break down most of the heptachlor in moist soil (WHO Envir. Health Criteria. 1984). Heptachlor is usually metabolized to the epoxide. Heptachlor epoxide is at least as toxic as heptachlor (EPA 1985).

PHYSICAL PROPERTIES AND GUIDELINES

Pure heptachlor is a white or light tan, crystalline solid with a mild camphor or cedar-like odor. Technical heptachlor is a soft wax (1, 2). It is corrosive to metals (8). It reacts with iron and rust to form hydrogen chloride gas (11, NIOSH OSHA Occupa. Health Guide of Chem. Hazards. 1981).

Heptachlor is stable under normal temperatures and pressures. It may burn, but does not ignite readily. Contact with strong oxidizers, excessive heat, sparks or open flame should be avoided. If overheated, heptachlor produces highly toxic, corrosive fumes of hydrogen chlorine gas and toxic oxides of carbon (11, 12).

Occupational Exposure Limits:

The odor threshold: 0.02 ppm (11).
ACGIH: 0.5 mg/m3 8-hour TWA (skin)
OSHA: 0.5 mg/m3 TWA (skin)
NIOSH: 0.5 mg/m3 recommended TWA (skin)
NIOSH: 0.5 mg/m3; airborne concentrations of 100 mg/m3 or more are immediately threatening to life or health (1)

Physical Properties:

CAS #: 76-44-8
H20 solubility: virtually insoluble, 0.056 ppm (2, 10)
Boiling point: 135-145 degrees C (275-293 degrees F) at 1.5 mm Hg (1)
Melting point: 95-96 degrees C (203-205 degrees F) (pure); 46-74 degrees C (technical) (2, 16).
Solubility in other solvents:
Solubility (g/100 ml):
Solventat 27 degrees C
Acetone 75
Alcohol 119
Benzene 106
Carbon tetrachloride 112
Cyclohexanone 119
Kerosene 189
Xylene 102 (2, 16)
Flash point: non-combustible (Bureau of Explosives; Emer. Handling of Haz. Mat'ls in Surface Transportation. 1981).
Vapor pressure: 3 x 10 to the minus 4 power mm Hg (2, 17)
Chemical Class/Use: Organochlorine insecticide
Oil: water partition coefficient: 3.87-5.44 (log) (EPA 1985)

BASIC MANUFACTURER

Velsicol Chemical Company
5600 N. River Rd.
Rosemont, IL 60018-5119

Review by Basic Manufacturer:

Comments solicited: November, 1992
Comments received:

REFERENCES

  1. Agency for Toxic Substances and Disease Registry. 1989. Toxicological Profile for Heptachlor/Heptachlor Epoxide, ATSDR/TP-88/16. ATSDR, US. Public Health Service, Washington, DC.
  2. Hayes, W.J. and E.R. Laws (ed.). 1990. Handbook of Pesticide Toxicology, Vol. 3, Classes of Pesticides. Academic Press, Inc., NY.
  3. Howard, P.H. 1989. Handbook of Environmental Fate and Exposure Data for Organic Chemicals, Vol. 3, Pesticides. Lewis Publishers, Inc., Chelsea, MI.
  4. Tucker, R. 1970. Handbook of toxicity of pesticides to wildlife. USDI Fish & Wildlife Service.
  5. Worthing, C.R. (ed.). 1987. The pesticide manual: A world compendium. 8th Ed. The British Crop Protection Council. Croydon, England.
  6. Hayes, Wayland, Jr. 1982. Pesticides studied in man. Baltimore, MD: Williams & Wilkins.
  7. Meister, R.T. (ed.). 1992. Farm Chemicals Handbook '92. Meister Publishing Company, Willoughby, OH.
  8. Hartley, D. and H. Kidd, (eds.) 1983. The agrochemicals handbook. Nottingham, England: Royal Society of Chemistry.
  9. US EPA. 1990 (Feb.). Suspended, Canceled, and Restricted Use Pesticides. Office of Compliance Monitoring, Office of Pesticides and Toxic Substances, US EPA, Washington, DC.
  10. World Health Organization. 1984. Environmental Health Criteria 38: Heptachlor. WHO, Geneva, Switzerland.
  11. Occupational Health Services, Inc. 1991 (March 19). MSDS for Heptachlor. OHS, INc., Secaucus, NJ.
  12. Sax, N.I. 1975. Dangerous properties of industrial materials. 4th Ed. New York: Van Nostrand Reinhold Co.
  13. Hallenbeck, W.H. & K.M. Cunningham-Burns. 1985. Pesticides and human health. New York: Springer-Verlag.
  14. TOXNET. 1985. National library of medicine's toxicology data network. Hazardous Substances Databank. Public Health Service. National Institute of Healtyh. U.S. Department of Health and Human Services. Bethesda, MD: NLM.
  15. Gosselin, R.E. 1984. Clinical toxicology of commercial products. 5th Ed. Baltimore, MD: Williams & Wilkins.
  16. Windholz, M. (ed.) 1976. The Merck Index: an encyclopedia of chemicals and drugs. 9th Ed. Rahway, NJ: Merck.
  17. Sunshine, I. 1969. Handbook of analytical toxicology. Cleveland, OH: Chemical Rubber Co.