E X T O X N E T
Extension Toxicology Network
A Pesticide Information Project of Cooperative Extension Offices of
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University of California at Davis. Major support and funding was provided
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Pesticide
Information
Profile
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Heptachlor
Publication Date: 9/93
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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):
| Solvent | at 27 degrees C |
| Acetone | 75 |
| Alcohol | 119 |
| Benzene | 106 |
| Carbon tetrachloride | 112 |
| Cyclohexanone | 119 |
| Kerosene | 189 |
| Xylene | 102 (2, 16) |
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| 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
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.
Hayes, W.J. and E.R. Laws (ed.). 1990. Handbook of Pesticide
Toxicology, Vol. 3, Classes of Pesticides. Academic Press, Inc., NY.
Howard, P.H. 1989. Handbook of Environmental Fate and Exposure
Data for Organic Chemicals, Vol. 3, Pesticides. Lewis Publishers, Inc.,
Chelsea, MI.
Tucker, R. 1970. Handbook of toxicity of pesticides to wildlife.
USDI Fish & Wildlife Service.
Worthing, C.R. (ed.). 1987. The pesticide manual: A world
compendium. 8th Ed. The British Crop Protection Council. Croydon,
England.
Hayes, Wayland, Jr. 1982. Pesticides studied in man. Baltimore,
MD: Williams & Wilkins.
Meister, R.T. (ed.). 1992. Farm Chemicals Handbook '92. Meister
Publishing Company, Willoughby, OH.
Hartley, D. and H. Kidd, (eds.) 1983. The agrochemicals handbook.
Nottingham, England: Royal Society of Chemistry.
US EPA. 1990 (Feb.). Suspended, Canceled, and Restricted Use
Pesticides. Office of Compliance Monitoring, Office of Pesticides and
Toxic Substances, US EPA, Washington, DC.
World Health Organization. 1984. Environmental Health Criteria
38: Heptachlor. WHO, Geneva, Switzerland.
Occupational Health Services, Inc. 1991 (March 19). MSDS for
Heptachlor. OHS, INc., Secaucus, NJ.
Sax, N.I. 1975. Dangerous properties of industrial materials.
4th Ed. New York: Van Nostrand Reinhold Co.
Hallenbeck, W.H. & K.M. Cunningham-Burns. 1985. Pesticides and
human health. New York: Springer-Verlag.
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.
Gosselin, R.E. 1984. Clinical toxicology of commercial products.
5th Ed. Baltimore, MD: Williams & Wilkins.
Windholz, M. (ed.) 1976. The Merck Index: an encyclopedia of
chemicals and drugs. 9th Ed. Rahway, NJ: Merck.
Sunshine, I. 1969. Handbook of analytical toxicology.
Cleveland, OH: Chemical Rubber Co.
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criticism of unnamed products implied. Most of this information is historical
in nature and may no longer be applicable.
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