57-74-9 Usage
Description
Chlordane, a viscous, amber-colored liquid, is a persistent organochlorine insecticide that was widely used in the United States from 1948 to 1988. It is a mixture of many structurally related compounds, including trans-chlordane, cis-chlordane, chlordene, heptachlor, and trans-nonachlor. Chlordane is known for its effectiveness in killing insects when ingested and on contact.
Uses
Used in Agricultural Industry:
Chlordane is used as an insecticide for controlling a broad spectrum of pests, particularly in the production of crops such as corn, maize, and citrus. It was also used for termite control in homes and gardens, as well as for controlling soil insects during crop production.
Used in Residential and Commercial Applications:
Chlordane is used as a wood preservative, protective treatment for underground cables, and to reduce earthworm populations in lawns. It is effective against various insect pests, including Formicidae, Coleoptera, Noctuidae larva, Saltatoria, and subterranean termites, and is used to control household insects and pests of man and domestic animals.
Used in Industrial Applications:
Chlordane is used as an insecticide and fumigant in industrial settings, particularly for fire ant control in power transformers.
Hazard
A possible carcinogen. Toxic by ingestion,
inhalation, and skin absorption. Liver damage.
Health Hazard
Highly toxic to humans by ingestion; moderately toxic in test animals; skin absorption or inhalation of its vapors can producepoisoning effects; exhibits acute, delayed,and chronic effects; symptoms include nausea, vomiting, abdominal pain, irritation,confusion ataxia, tremor, and convulsions;delayed development of liver disease andblood disorder also reported (U.S. EPA1988); human death may result from ingestion of 10–20 g of pure compound or topical skin application of 50 g in 30 minutes;moderately irritating to skin; oral LD50value in rats ~300 mg/kg; exposure limit0.5 mg/kg: exposure limit 0.5 mg/m3 (skin);RCRA Waste Number U036; US EPA listedextremely hazardous substance; LD50 data inliterature inconsistent:LD50 oral (rat): 200–600 mg/kgLD50 oral (rabbit): 100 mg/kgLD50 skin (rat): 690 mg/kg.
Health Hazard
Exposures to chlordane cause adverse health effects and poisoning to animals and
humans. The acute oral LD50 values of technical grade chlordane for the rat range from
137 to 590 mg/kg and acute dermal LD50 for the rabbit is 1720 mg/kg. Signs of acute
chlordane intoxication include ataxia, convulsions, and cyanosis followed by death due
to respiratory failure. Rats treated by gavage with 100 mg/kg once a day for 4 days had
increased absolute liver weights; fatty infi ltration of the liver; and increased serum triglycerides, creatine phosphokinase, and lactic acid dehydrogenase. Sheep treated by stomach
tube with 500 mg/kg showed signs of intoxication, but recovered fully within 5–6 days; a
dose of 1000 mg/kg resulted in death after 48 h.
Ingestion of chlordane induces vomiting, dry cough, agitation and restlessness, hemorrhagic gastritis, bronchopneumonia, muscle twitching, convulsions, and death among
humans. Non-lethal, but accidental poisoning of children has resulted in convulsions,
excitability, loss of coordination, dyspnea, and tachycardia. Recovery, however, was complete. Ingestion of chlordane contaminated water (1.2 g/L) caused symptoms of gastrointestinal and neurological disorders. Chronic inhalation of chlordane produced symptoms
of poisoning that included, but were not limited to, sinusitis, bronchitis, dermatitis, neuritis, migraine, gastrointestinal distress, fatigue, memory defi cits, personality changes, Exposures to chlordane cause adverse health effects and poisoning to animals and
humans. The acute oral LD50 values of technical grade chlordane for the rat range from
137 to 590 mg/kg and acute dermal LD50 for the rabbit is 1720 mg/kg. Signs of acute
chlordane intoxication include ataxia, convulsions, and cyanosis followed by death due
to respiratory failure. Rats treated by gavage with 100 mg/kg once a day for 4 days had
increased absolute liver weights; fatty infi ltration of the liver; and increased serum triglycerides, creatine phosphokinase, and lactic acid dehydrogenase. Sheep treated by stomach
tube with 500 mg/kg showed signs of intoxication, but recovered fully within 5–6 days; a
dose of 1000 mg/kg resulted in death after 48 h.
Ingestion of chlordane induces vomiting, dry cough, agitation and restlessness, hemorrhagic gastritis, bronchopneumonia, muscle twitching, convulsions, and death among
humans. Non-lethal, but accidental poisoning of children has resulted in convulsions,
excitability, loss of coordination, dyspnea, and tachycardia. Recovery, however, was complete. Ingestion of chlordane contaminated water (1.2 g/L) caused symptoms of gastrointestinal and neurological disorders. Chronic inhalation of chlordane produced symptoms
of poisoning that included, but were not limited to, sinusitis, bronchitis, dermatitis, neuritis, migraine, gastrointestinal distress, fatigue, memory defi cits, personality changes, decreased attention span, numbness or paresthesias, blood dyscrasias, disorientation, loss
of coordination, dry eyes, and seizures. Chlordane-treated laboratory rats showed blood
diseases, including aplastic anemia and acute leukemia
Trade name
A SPON-CHLORDANE?; BELT?; CD 68?; CHLORINDAN?; CHLOR KIL?; CHLORODANE?; CORODANE?; CHLORTOX?; DOWCHLOR?[C]; DOW-KLOR?[C]; GOLD CREST?[C]; KILEX LINDANE?; HCS 3260?; KYPCHLOR?; M 140?; M 410?; NIRAN?; OCTACHLOR?; OKTATERR?; OMS 1437?; ORTHO-KLOR?[C]; SD 5532?; SHELL SD-5532?[C]; SYNKLOR?; TAT?; TAT CHLOR? 4; TERMEX?; TOPICHLOR? 20; TOPICLOR?; TOXICHLOR?; VELSICOL? 1068[C]
Safety Profile
Confirmed carcinogen
with experimental carcinogenic data. Poison
to humans by ingestion and possibly other
routes. An experimental poison by ingestion,
inhalation, intravenous, and intraperitoneal
routes. Moderately toxic by skin contact.
Human systemic effects by ingestion or skin
contact: tremors, convulsions, excitement,
ataxia (loss of muscle coordination), and
gastritis. Experimental teratogenic and
reproductive effects. Human mutation data
reported. Combustible liquid. It is no longer
permitted for use as a termiticide in homes.
A central nervous system stimulant whose
exact mode of action is unknown, but it may
involve microsomal enzyme stimulation.
Animals poisoned by this and related compounds show an extremely marked loss
of appetite and neurological symptoms. The
fatal dose to humans is unknown. It has
,
been estimated to be between 6 and 60 g
(0.2 and 2 ounces). One person receiving
~~Oan accidental slan application of 25%
solution (amounting to somethmg over 30
g of technical chlordane) developed
symptoms withm about 40 minutes and
ded, apparently of respiratory failure, before
medical attention was obtained. In two
patients, death followed exposure to low
ingestion doses of chlordane (2-4 g). On
microscopic examination, both patients
showed severe chronic fatty degeneration of
the liver, characteristic of chronic
alcoholism. Although these two fatalities
cannot be attributed exclusively to
chlordane, they are entirely consistent with
previous observations that the toxicity of
other chlorinated hydrocarbons is much
enhanced in the presence of chronic liver
damage. The dangerous chronic dose in
humans is unknown.
small doses exhibit hyperexcitabiltty,
tremors, and convulsions, and those that
survive long enough show marked anorexia
and loss of weight. Symptoms in animals
frequently occur withm an hour of the
administration of a large dose, but death
often is delayed for several days depending
on the dosage and route of administration.
In any event, symptoms are of longer
duration with chlordane than with DDT
under similar condtions.
are essentially normal, except that the
insecticide is found in tissues by means of
bioassay. A method for specific, quantitative
chemical analysis for chlordane is now
available using small amounts of
subcutaneous fat. Chronically poisoned
animals show degenerative changes in the
liver and kidney tubules.
emits toxic fumes of Cl-.
Experimental animals exposed to repeated
Laboratory analyses on poisoned animals
When heated to decomposition chlordan
Carcinogenicity
IARC has concluded that there is inadequate
evidence for carcinogenicity of chlordane to humans and sufficient evidence for its carcinogenicity
to animals.Chlordane was not mutagenic to bacteria.
Environmental Fate
Biological. In four successive 7-day incubation periods, chlordane (5 and 10 mg/L)
was recalcitrant to degradation in a settled domestic wastewater inoculum (Tabak et al.,
1981).
Soil. The actinomycete, Nocardiopsis sp., isolated from soil extensively degraded pure
cis- and trans-chlordane to dichlorochlordene, oxy-chlordane, heptachlor, heptachlor endoepoxide, chlordene chlorohydrin and 3-hydroxy-trans-chlordane. Oxychlordane is slowly
degraded to 1-hydroxy-2-chlorochlordene (Beeman and Matsumura, 1981). The reported
half-life in soil is approximately one year (Hartley and Kidd, 1987).
The percentage of chlordane remaining in a Congaree sandy loam soil after 14 years
was 40% (Nash and Woolson, 1967).
Chlordane did not degrade in settled domestic wastewater after 28 days (Tabak et al.,
1981).
Plant. Alfalfa plants were sprayed with chlordane at a rate of 1 lb/acre. After 21 days,
95% of the residues had volatilized (Dorough et al., 1972).
Photolytic. Chlordane should not undergo direct photolysis since it does not absorb
UV light at wavelengths greater than 280 nm (Gore et al., 1971).
Chemical/Physical. In an alkaline medium or solvent, carrier, diluent or emulsifier
having an alkaline reaction, chlorine will be released (Windholz et al., 1983). Technical
grade chlordane passed over a 5% platinum catalyst at 200°C resulted in the formation of
tetrahydrodicyclopentadiene (Musoke et al., 1982).
Chlordane (1 mM) in methyl alcohol (30 mL) underwent dechlorination in the presence
of nickel boride (generated by the reaction of nickel chloride and sodium borohydride).
The catalytic dechlorination of chlordane by this method yielded a pentachloro derivative
as the major product having the empirical formula C10H9Cl5 (Dennis and Cooper, 1976).
Chlordane is subject to hydrolysis via the nucleophilic substitution of chlorine by
hydroxyl ions to yield 2,4,5,6,7,8,8-heptachloro-3a,4,7,7a-tetrahydro-4,7-methano-1Hindene which is resistant to further hydrolysis (Kollig, 1993). The hydrolysis half-life at
pH 7 and 25°C was estimated to be >197,000 years (Ellington et al., 1988).
Emits very toxic fumes of chlorides when heated to decomposition (Lewis, 1990)
Metabolic pathway
Chlordane undergoes a variety of metabolic processes including oxidation,
reductive dechlorination, hydrolysis and epoxidation. These
reactions afford products involving alteration of the cyclopentane
ring; the norbornyl moiety generally remains unaffected except in photochemical
reactions when bridged compounds may be formed or
dechlorination may occur. Hydroxylation at position 3 is effected by
microsomal mixed function oxidases to form 3-hydroxychlordane
(12). Dehydration of this compound gives 1,2-dichlorochlordene (13),
a key metabolic intermediate in the formation of oxychlordane and
other metabolites. A second metabolic pathway involves dehydrochlorination
to form heptachlor (2). Dechlorination affords 1-chlorodihydrochlordene
(7). Hydrolysis gives 1-chloro-2-hydroxychlordene
chlorohydrin (6) which may be metabolised to monochlorodihydroxy
and trihydroxy derivatives of dihydrochlordene (Nomeir and Hajjar,
1987).
Degradation
Acetone-sensitised photolysis of cis-chlordane (1) gave bridged derivatives
to which cage-like structures (19a or 19b) have been assigned. The
isomeric trans-chlordane (1) failed to yield bridged products because the
double bond in these compounds interacts with the endo-chlorine atom
(Fischler and Korte, 1969). However, it was later reported that with transchlordane
(l),bridging did occur forming 20 involving carbon-1 which
has a non-interfering exo-chlorine atom.
Unsensitised photolysis of trans-chlordane (1) in aqueous organic
solvents at wavelengths less than 300 nm gave two isomeric monodechlorinated
products (21a and 2) and ultimately the bis-dechlorination
product (Vollner et al. 1969; Ivie et al. 1972). When cis-chlordane (1) was
irradiated as a solid film, up to 70% was converted after 16-20 hours
irradiation into a mixture of products, more than half of which were
bridged isomers (depending on conditions, the dechlorinated compounds
may also form bridged compounds). These transformations are shown in
Scheme 1.
Chlordane is decomposed by alkalis with the loss of chlorine.
Toxicity evaluation
Technical chlordane is a viscous, amber liquid (bp
175 ?C/267 Pa, vp 1.3 mPa at 25 ?C) soluble in water to
about 9 μg/L. It has rat LD50s of 335, 430 (oral), and 840,
690 (dermal) mg/kg. Technical chlordane contains about
60% of the isomers and 10–20% of heptachlor.
Check Digit Verification of cas no
The CAS Registry Mumber 57-74-9 includes 5 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 2 digits, 5 and 7 respectively; the second part has 2 digits, 7 and 4 respectively.
Calculate Digit Verification of CAS Registry Number 57-74:
(4*5)+(3*7)+(2*7)+(1*4)=59
59 % 10 = 9
So 57-74-9 is a valid CAS Registry Number.
InChI:InChI=1/C10H8Cl8/c11-3-1-2-4(5(3)12)9(16)7(14)6(13)8(2,15)10(9,17)18/h2-7H,1H2
57-74-9Relevant articles and documents
Physical, chemical, and isotopic (atomic) labels
-
, (2008/06/13)
Chemical or isotopic labels are added to, e.g., a potentially lethal drug formulation, to generate a unique chemical fingerprint. Combinations of chemical additives are mixed with the drug to aid in their isolation and identification, especially when such drugs are used for illicit purposes. When stable isotopes are incorporated into lethal drugs, the labeling process conveys a very unique internal chemical signature and greatly aids in the identification of the parent drug in body fluids and tissues. When heath-care providers become aware that certain drugs can now be easily tracked and identified in a victim, individuals may be reluctant to utilize these agents for ill purposes.