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Heptachlor is an organochlorine cyclodiene insecticide isolated from technical chlordane. It is available in the form of white crystals or a tan-colored waxy solid with a characteris- tic camphor-like or cedar-like odor. It is sparingly soluble or insoluble in water, but fairly soluble in acetone, benzene, ethanol, xylene, and other organic solvents. It is used for the control of termites, ants, and soil insects in cultivated and non-cultivated soils. Heptachlor epoxide is formed in nature when heptachlor is released into the environment and mixes with oxygen. Heptachlor epoxide remains in the soil for long periods of time. Heptachlor and heptachlor epoxide may also be present at numerous hazardous waste sites. Although the use of heptachlor is restricted, exposure to the general population does occur through the ingestion of contaminated food.

white crystalline solid

ChEBI: A cyclodiene organochlorine insecticide that is 3a,4,7,7a-tetrahydro-1H-4,7-methanoindene substituted by chlorine atoms at positions 1, 4, 5, 6, 7, 8 and 8. Formerly used to kill termites, ants and other insects in agricultural and domes ic situations.

Formerly as insecticide for control of cotton boll weevil.

HEPTACHLOR is a white to light tan waxy looking solid. Noncombustible. Insoluble in water. Can cause illness by inhalation, skin absorption and/or ingestion. The primary hazard is the threat posed to the environment. Immediate steps should be taken to limit its spread to the environment. Used as an insecticide.

Susceptible to epoxidation. Insoluble in water. Slowly losses hydrogen chloride in the presence of alkaline solution.

HEPTACHLOR is incompatible with strong alkalis. Corrosive to metals. Can react with iron and rust to form toxic gases. Can react vigorously with oxidizing materials. Susceptible to epoxidation . May be incompatible with many amines, nitrides, azo/diazo compounds, alkali metals, and epoxides.

Inhalation of dust causes irritability, tremors, and collapse. Ingestion causes nausea, vomiting, diarrhea, and irritation of the gastrointestinal tract. Contract with dust causes irritation of eyes and moderate irritation of skin.

Special Hazards of Combustion Products: Irritating hydrogen chloride fumes may form in fire.

Toxic by ingestion, inhalation, and skin absorption; use has been restricted and discontinued except for termite control. Possible carcinogen.

Exposures to heptachlor epoxide cause adverse health effects to animals and humans. Exposure to heptachlor is toxic by mouth, by skin contact, as well as by inhalation of dust from powder concentrates. Heptachlor acts as a CNS stimulant. Prolonged period of expo- sures to high concentrations of heptachlor cause headache, dizziness, nausea, vomiting, weakness, irritability, salivation, lethargy, respiration distress, muscle tremors, convul- sions, and paralysis. Severe cases of poisoning lead to respiratory failure and death. In fact, seizures and cortical excitability are the prime CNS symptoms following acute hepta- chlor exposure. The photoisomer of heptachlor (photoheptachlor) and the major metabo- lite of heptachlor, namely, heptachlor epoxide are more toxic than the parent compound. Heptachlor induces tremors, convulsions, paralysis, and hypothermia in rats and young calves. The poisoned animals showed muscle spasms in the head and neck region, convul- sive seizures, elevated body temperatures, and engorged brain blood vessels. Humans exposed to heptachlor in the home during termite control operations showed signs of neurotoxicity, i.e., irritability, salivation, lethargy, dizziness, labored respiration, muscle tremors, convulsions, and death due to respiratory failure. Heptachlor interfered with nerve transmission, caused hyperexcitation of the CNS, lethargy, incoordination, tremors, convulsions, stomach cramps or pain, leading to coma and death.

Colorless to light tan, waxy or crystalline, nonflammable solid with a camphor-like odor

Heptachlor may be synthesized by reacting chlordene with N-bromosuccinimide to give the intermediate 1-bromochlordene followed by chlorination with hydrogen chloride in nitromethane in the presence of aluminum trichloride.

A griculturalChemical; Tumorigen， Mutagen; Reproductive Effector.Those involved in the manufacture, formulation, and appli-cation of this insecticide for control of cotton boll weevil.Registration of heptachlor-containing pesticides has beencanceled by the US EPA with the exception of its use fortermite control outside of dwellings by in-ground (subsur-face) insertion. Infants have been ex posed to heptachlor andheptachlor epoxide through mothers' milk, cows' milk, andcommercially prepared baby foods. It appears that infantsraised on mothers’ milk run a greater risk of ingestingheptachlor epoxide than if they were fed cows' milk and/orcommercially prepared baby food. Persons living and work-ing in or near heptachlor-treated areas have a particularlyhigh inhalation exposure potential. Heptachlor has beenfound in at least 206 of the 1 662 current or former EPANational Priorities List (NPL) sites. Heptachlor epoxide hasbeen found in at least 195 NPL sites.

If this chemical gets into the eyes, remove anycontact lenses at once and irri gate immediately for at least15 min, occasionally lifting upper and lower lids. Seek med-ical attention immediately. If this chemical contacts theskin, remove contaminated clothing and wash immediatelywith soap and water. Seek medical attention immediately. Ifthis chemical has been inhaled, remove from exposure,begin rescue breathing (using universal precautions, includ-ing resuscitation mask) if breathing has stopped and CPR ifheart action has stopped. Transfer promptly to a medicalfacility. When this chemical has been swallowed, get medi-cal attention. Give large quantities of water and induce :vomiting. Do not make an unconscious person vomit.Note to physician: For severepoisoning，do not useBAL .[British Anti-Lewisite， dimercaprol, dithiopropanol (C3HgOS2)] as it is contraindicated or ineffective in poisoningfrom iron.

Biological. Many soil microorganisms were found to oxidize heptachlor to heptachlor epoxide (Miles et al., 1969). In addition, hydrolysis produced hydroxychlordene with subsequent epoxidation yielding 1-hydroxy-2,3-epoxychlordene (Kearney and Kaufman, 1976). Heptachlor reacted with reduced hematin forming chlordene, which decomposed to hexachlorocyclopentadiene and cyclopentadiene (Baxter, 1990). In a model ecosystem containing plankton, Daphnia magna, mosquito larva (Culex pipiens quinquefasciatus), ?sh (Cambusia af?nis), alga (Oedogonium cardiacum) and snail (Physa sp.), heptachlor degraded to 1-hydroxychlordene, 1-hydroxy-2,3-epoxychlordene, hydroxychlordene epoxide, heptachlor epoxide and ?ve unidentified compounds (Lu et al., 1975). In foursuccessive 7-day incubation periods, heptachlor (5 and 10 mg/L) was recalcitrant to degradation in a settled domestic wastewater inoculum (Tabak et al., 1981). When heptachlor (10 ppm) in sewage sludge was incubated under anaerobic conditions at 53°C for 24 hours, complete degradation was achieved (Hill and McCarty, 1967).
In a mixed bacterial culture under aerobic conditions, heptachlor was transformed to chlordene, 1-hydroxychlordene, heptachlor epoxide and chlordene epoxide in low yields (Miles et al., 1971). Heptachlor rapidly degraded when incubated with acclimated, mi
Soil. Heptachlor reacted with reduced hematin forming chlordene which decomposed to hexachlorocyclopentadiene and cyclopentadiene (Baxter, 1990). The reported half-life in soil is 9–10 months (Hartley and Kidd, 1987).
Heptachlor was rapidly converted to 1-hydroxychlordene in eight dry soils having low moisture contents. Under these conditions, heptachlor epoxide was not identified (Bowman et al., 1965).
Following application to an Ohio soil, only 7% of the applied amount had volatilized after 170 days (Glotfelty et al., 1984). Harris (1969) concluded that heptachlor has a very low tendency to leach in soils.

Heptachlor is quite stable and resistant to environmental degradation. Metabolic processes by which it undergoes transformation are epoxidation, hydrolysis and dechlorination. It is transformed into a variety of products, many of which differ from one another only in stereochemical features while retaining the carbon skeleton and the chlorinated norbornene moiety. The main biological metabolite is exoepoxyheptachlor. Products formed by sensitised photolysis have caged structures and undergo reactions that are typical of this class.

At 27 °C (g/L): acetone (750), benzene (1,060), carbon tetrachloride (1,120), cyclohexanone (1,190), alcohol (45), xylene (1,020) (Windholz et al., 1983). Soluble in ether, kerosene, and ligroin (U.S. EPA, 1985).

At 27 °C (g/L): acetone (750), benzene (1,060), carbon tetrachloride (1,120), cyclohexanone (1,190), alcohol (45), xylene (1,020) (Windholz et al., 1983). Soluble in ether, kerosene, and ligroin (U.S. EPA, 1985).

Color Code- Blue: Health Hazard/Poison: Storein a secure poison location. Prior to working with thischemical you should be trained on its proper handling andstorage. Store in tightly closed containers in a cool, well-ventilated area. Protect storage containers from physicaldamage. Where possible, automatically pump liquid fromdrums or other storage containers to process containers. Aregulated, marked area should be established where thischemical is handled, used, or stored in compliance withOSHA Standard 1910.1045.

Heptachlor (organochloride pesticides， solid,toxic, n.0.s.) requires a shipping label of “POISONOUS/TOXIC MATERIALS.”It falls in Hazard Class 6.1 andPacking Group II.

Heptachlor (1) is stable in daylight, air, moisture and moderate heat (up to 160 °C). It is not readily dehydrochlorinated but it is susceptible to epoxidation. It is hydrolysed in water to 1-hydroxychlordene (5).
Irradiation in hexane or cyclohexane at 253.7 nm gave two isomeric monodechlorination products (2 and 3). In acetone, the sole product was a compound with a cage structure (4) (Zabik et aE., 1970). In mixtures of cyclohexane and acetone, smaller quantities of 4 were obtained and the major product 6 was formed in which a chlorine atom has been replaced by a cyclohexyl moiety. The conversion of 1 into 4 by irradiation in acetone is parallelled by the acetone-sensitised photoreactions of chlordene, β-chlordane, chlordane, and β-dihydroheptachlor which also form analogous cage structures. Under these conditions, heptachlor epoxide (7) formed caged structures containing a ketonic group (9 and 10) (Fischler and Korte, 1969).
A ketonic photoproduct (8), isomeric with heptachlor epoxide, was obtained when 1 was exposed to light of wavelengths >280 nm in acetone solution or on bean plants. Compounds 9 and 10 were also isolated from the reaction mixture and these were also produced by irradiation of compound 8, indicating that it is an intermediate in the photochemical reaction (Ivie et al., 1972).

The primary target for heptachlor and the other cyclodiene insecticides is the central nervous system. The mode of action as a noncompetitive antagonist acting on the chloride ion channel of the γ aminobutyric acid (GABAA) receptor became evident more than 30 years after the discovery of heptachlor. When activated by GABA, the GABAA receptor increases Cl- conductance into the neurons and prevents excessive nerve stimulation. Heptachlor interferes with the passage of Cl- ions by binding to the Cl- channel of the receptor and thereby blocking the actions of GABA. Seizures, vomiting, and convulsions are typical symptoms associated with antagonism with GABA. Molecular modeling indicates that heptachlor epoxide also blocks the brain GABA-gated chloride channels. Heptachlor is implicated in causing long-lasting changes in brain functions, possibly by altering the expression of GABAA receptor during the mammalian development.
Liver is another target of heptachlor toxicity (hepatocytomegaly, necrosis, steatosis, and tumors). However, the mechanism is unknown. Heptachlor induces hepatic cytochrome P-450 enzymes. In rat hepatocytes and mouse hepatoma cells, heptachlor and heptachlor epoxide initiated signal transduction processes characteristic for known mitogens, i.e., alteration of cellular Ca2+ levels and induction protein kinase C and mitogen-activated protein kinases. In mice, heptachlor epoxide causes downregulation of protein kinase C in the liver and induces the activator protein-1 DNA binding, both are critical factors in tumor promotion.

Reacts with strong oxidizers. Attacksmetal .Forms hydrogen chloride gas withiron and rustabove 74℃.