| | HEPTACHLOR Basic information |
| Product Name: | HEPTACHLOR | | Synonyms: | 1,4,5,6,7,8,8-HEPTACHLORO-3A,4,7,7A-TETRAHYDRO-4,7-METHANOINDENE;VELSICOL 104(R);E3314;E3314(R);DRINOX(R);CUPINCIDA;FENNOTOX;(-)-HEPTACHLOR | | CAS: | 76-44-8 | | MF: | C10H5Cl7 | | MW: | 373.32 | | EINECS: | 200-962-3 | | Product Categories: | 2000/60/EC;Pesticides;2000/60/ECMore...Close...;Alpha sort;Baby Food Directives 13/2003 EC&14/2003 ECPesticides;CyclodienesPesticides&Metabolites;European Community: ISO and DIN;H;HA -HTMethod Specific;H-MAlphabetic;Insecticides;Method Specific;Oeko-Tex Standard 100;PesticidesMethod Specific;ASTM 4947: Analysis of Chlordane and Heptachlor in AirPesticides;ASTM Air Monitoring | | Mol File: | 76-44-8.mol |  |
| | HEPTACHLOR Chemical Properties |
| Melting point | 96℃ | | Boiling point | 458.95°C (rough estimate) | | density | 1.6 g/cm3 | | vapor pressure | 2.33(x 10-4 mmHg) at 25 °C (subcooled liquid vapor pressure calculated from GC retention time data, Hinckleyet al., 1990) | | refractive index | 1.5407 (estimate) | | Fp | 11 °C | | storage temp. | APPROX 4°C
| | Water Solubility | 0.056 mg l-1 (25-29 °C) | | form | neat | | Merck | 13,4675 | | Henry's Law Constant | 0.19(x 10-3 atm?m3/mol) at 5 °C, 0.31 at 15 °C, 0.40 at 20 °C, 0.61 at 25 °C, 0.82 at 35 °C:in 3% NaCl solution: 0.52
at 5 °C, 0.82 at 15 °C, 1.33 at 25 °C, 2.09 at 35 °C (gas stripping-GC, Cetin et al., 2006) | | Exposure limits | NIOSH REL: TWA 0.5 mg/m3, IDLH 35 mg/m3; OSHA PEL: TWA 0.5 mg/m3; ACGIH TLV: TWA 0.5 mg/m3.
| | Stability: | Stable. Non-combustible. Incompatible with strong alkali, oxidizing agents. Corrodes many metals. | | IARC | 2B (Vol. Sup 7, 53, 79) 2001 | | EPA Substance Registry System | Heptachlor (76-44-8) |
| | HEPTACHLOR Usage And Synthesis |
| Description | Heptachlor is a soft, white to light tan, waxy, non-combustible, crystalline solid with a
camphor-like odour. Heptachlor is a member of the cyclodiene group of chlorinated insecticides
(aldrin, dieldrin, endrin, chlordane, heptachlor, and endosulfan) and has a long
history following World War II. It was registered as a commercial pesticide in 1952 for
foliar, soil, and structure applications and for malarial control programmes; after 1960,
it was used primarily in soil applications against agricultural pests and to a lesser extent
against termites.
Heptachlor is available commercially as a dust, a dust concentrate, an emulsifiable concentrate,
a wettable powder, or in oil solutions. It is corrosive to metals and reacts with iron
and rust to form hydrogen chloride gas. Heptachlor is incompatible with many amines,
nitrides, azo/diazo compounds, alkali metals, and epoxides but is stable under normal
temperatures and pressures. It may burn, but does not ignite readily. Heptachlor at high
heat and temperature produces highly toxic, corrosive fumes of hydrogen chlorine gas and toxic oxides of carbon. An important metabolite of heptachlor is heptachlor epoxide
which is an oxidation product formed from heptachlor by many plant and animal species.
Heptachlor is almost insoluble in water but soluble in ether, acetone, benzene, and many
other organic solvents. | | Chemical Properties | white crystalline solid | | Chemical Properties | 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. | | Physical properties | Colorless to light tan, waxy or crystalline, nonflammable solid with a camphor-like odor | | Uses | Heptachlor is used for the control of termites, ants, household
insects and soil insects. It is also applied as a seed treatment, soil treatment
or directly to foliage. | | Uses | Insecticide for termite control. | | Uses | Formerly as insecticide for control of cotton boll weevil. | | Definition | 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. | | Preparation | 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. | | General Description | 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. | | Air & Water Reactions | Susceptible to epoxidation. Insoluble in water. Slowly losses hydrogen chloride in the presence of alkaline solution. | | Reactivity Profile | 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. | | Hazard | Toxic by ingestion, inhalation, and skin
absorption; use has been restricted and discontinued except for termite control. Possible carcinogen. | | Health Hazard | 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. | | Health Hazard | 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. | | Health Hazard | Highly toxic to animals; toxic symptoms —tremors, convulsions, and liver necrosis; alsocauses blood dyscrasias; oral LD50 value(rats): 40 mg/kg; caused liver cancers inmice; no evidence of human carcinogenicity;RCRA Waste Number P059; exposure limit:TLV-TWA (skin) 0.5 mg/m3 (ACGIH).
Exposure of laboratory animals to heptachlor has shown to alter the levels and function of dopamine transporter producing dopaminergic neurotoxin (Caudle et al.2005). In an earlier study Kirby et al. (2001)investigated neurotoxicity of heptachlor inmice treated by intraperitoneal injection threetimes in 2-week period at dose levels of3–100 mg/kg. Their studies indicated thatheptachlor exerted selective effects on striatal dopaminergic neurons and played arole in the etiology of idiopathic Parkinson’s disease.. | | Fire Hazard | Special Hazards of Combustion Products: Irritating hydrogen chloride fumes may form in fire. | | Environmental Fate | 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. | | Metabolic pathway | 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. | | Solubility in organics | 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). | | Solubility in water | 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). | | Degradation | 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). | | Toxicity evaluation | 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. |
| | HEPTACHLOR Preparation Products And Raw materials |
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