E X T O X N E T
Extension Toxicology Network
A Pesticide Information Project of Cooperative Extension Offices of
Cornell University, Michigan State University, Oregon State University, and
University of California at Davis. Major support and funding was provided
by the USDA/Extension Service/National Agricultural Pesticide Impact
Publication Date: 9/93
TRADE OR OTHER NAMES
In addition to chlordane, common names have included chlordan and
clordano. Trade names include Belt, Chlor Kil, Chlortox, Corodane, Gold
Crest C-100, Kilex Lindane, Kypchlor, Niran, Octachlor, Octa-Klor,
Synklor, Topiclor 20 , Toxichlor, Velsicol 1068 (1, 2).
Because of concern about the risk of cancer, all use of chlordane
was canceled in April, 1988. Between July, 1983 and April 1988, the
only permitted use for chlordane was for control of subterranean
termites. Before 1983, chlordane had been used to control insects on a
wide variety of crops. Chlordane is no longer distributed in the United
States. The only commercial use still permitted is for fire ant control
in power transformers (13, 4, 5, 6, 11). Pesticide products containing
chlordane must bear the signal word "Warning" (2).
Chlordane is a persistent organochlorine insecticide. It kills
insects when ingested and on contact. Formulations previously
available or available outside of the United States include dusts,
emulsifiable concentrates, granules, oil solutions, and wettable powders
Chlordane is moderately to highly toxic through all routes of
exposure. Symptoms usually start within 45 minutes to several hours
after exposure to a toxic dose. Convulsions may be the first sign of
poisoning or they may be preceded by nausea, vomiting and gut pain.
Initially, poisoning victims may appear agitated or excited, but later
they may become depressed, uncoordinated, tired or confused. Other
symptoms reported in cases of chlordane poisoning include headaches,
dizziness, vision problems, irritability, weakness or muscle twitching.
In severe cases, respiratory failure and death may occur. Complete
recovery from a toxic exposure to chlordane is possible if proper
medical treatment is administered (1, 10, 11, 19).
Chlordane is very irritating to the skin and eyes (21).
Because chlordane induces liver microsomal enzymes, many
interactions between medical drugs and this pesticide occur. Among
these are decreased effectiveness of oral anticoagulants,
phenylbutazone, chlor-promazine, cortisol and other steroids (including
birth control pills), diphenhydramine (Benadryl). Increased activity of
thyroxin (thyroid hormone) may also occur (22).
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 chlordane in rats is 200
to 700 mg/kg, for mice is 145 to 430 mg/kg, for rabbits is 20 to 300
mg/kg, and for hamsters is 1,720 mg/kg. The oral LDLO for humans is 29
to 40 mg/kg. The LDLO is the lowest dose which causes death. The dermal
LDLO for humans is 428 mg/kg. The dermal LD50 for rabbits is 780 mg/kg,
and for rats is 530 to 690 mg/kg. The lethal concentration fifty, or
LC50, is that concentration of a chemical in air or water that kills
half of the experimental animals exposed to it for a set time period.
The 4-hour inhalation LD50 for cats is 100 mg/m3 (1, 2, 3, 12).
In addition to the symptoms described for acute exposure, chronic
exposure to chlordane may cause jaundice in humans. Studies of workers
in plants where chlordane was manufactured reported no increase in the
mortality rate over that of the general population and no increase in
any specific cause of death attributable to exposure to chlordane.
Inhalation was the most likely route of exposure to chlordane for these
workers. There were no gastrointestinal symptoms and no deaths observed
in rats or monkeys exposed intermittently to air concentrations of 10 mg
chlordane/m3 over 90 days. However, liver lesions and changes in blood
serum occurred in rats exposed to 1.0 mg/m3. Increased kidney weights
occurred in rats exposed to 10 mg/m3. For monkeys, increased liver
weight occurred at 10 mg/m3 (11).
Animal studies have shown that consumption of chlordane has caused
damage to the liver and the central nervous system (5, 6). In a two-
year feeding study with rats, a near-lethal dose of 300 mg/kg produced
eye and nose hemorrhaging, severe changes in the tissues of the liver,
kidney, heart, lungs, adrenal gland and spleen. In this same study, no
adverse effects were observed in rats fed 5 mg/kg. In a long-term
feeding study with mice, body weight loss, increased liver weight, and
death occurred at doses of 22 to 63.8 mg/kg. In a two-year feeding study
with dogs, the NOAEL was 0.075 mg/kg/day (3 mg/kg diet). Dogs fed doses
of 15 and 30 mg/kg diet exhibited increased liver weights and changes in
organ tissues (9).
Fertility was reduced by about 50% in mice injected with chlordane
at 22 mg/kg once a week for 3 weeks (9).
It is not known if chlordane causes birth defects (11). No toxic
effects on fetuses and no teratogenic effects were observed in rats born
to dams fed chlordane at 5 to 300 mg/kg diet for two years. Pups nursed
by dams ingesting very high dietary doses of chlordane at 150 and 300
mg/kg developed dose-related symptoms of toxicity (9).
Chlorinated hydrocarbon insecticides are, in general, not mutagenic
(1). Fifteen out of 17 mutagenicity tests performed have shown that
chlordane is not mutagenic (9). No dominant lethal changes were found
when male mice were administered dosages of 50 or 100 mg/kg (1).
The EPA has ruled that chlordane is a probable human carcinogen.
Chlordane has caused liver cancer in laboratory animals given high doses
of the pesticide over the course of their lifetimes. A study was done
on workers at a manufacturing plant who had been exposed to chlorinated
hydrocarbons for 34 years, including chlordane. No increase in any type
of cancer was found (5, 9, 23). One feeding study with mice showed
increased incidence of liver tumors, but later tests on both rats and
mice showed no increase in the incidence of liver tumors.
The EPA has established an Acceptable Daily Intake of 0.03
micrograms per liter (ppb) for chlordane. An individual consuming
drinking water containing this level of chlordane over their entire
lifetime would have approximately a one-in-a-million chance of
developing cancer as a direct result of drinking water containing
In clinical studies of acute or chronic exposure to chlordane, the
effects most frequently observed are central nervous system effects and
blood disorders (9). Chlordane causes damage to blood vessels,
especially in the gut and heart (Vet Tox. 1981. Clarke). Kidney damage
has also been reported (NIOSH-OSHA 1981). Chlordane may also cause
blood diseases (aplastic anemia, acute leukemia) (IARC Monographs V2057,
1972). Liver cancer in mice, and liver and kidney damage in humans are
possible (8). Inhalation studies with chlordane at 0 to 10 ug/l for 90
days showed some alterations of the liver in rats, but no effects were
observed in monkeys (1).
Fate in Humans and Animals
Chlordane is absorbed into the body through the lungs, stomach and
skin. It is stored in fatty tissues as well as in the kidneys,
muscles, liver and brain (8). Chlordane has been found in human fat
samples at concentrations of 0.03 to 0.4 mg/kg in residents of the
United States (11). Chlorinated hydrocarbons stored in fatty tissues
can become released into circulation if these fatty tissues are
metabolized, as in starvation or intense activity (1). Chlordane that
is not stored in the body is excreted through the urine and feces.
Chlordane has been found in human breast milk (7, 9).
Rats that breathed chlordane vapor for 30 minutes retained 77% of
the total amount inhaled. Rabbits that received four doses of chlordane
stored it in fatty tissues, the brain, kidneys, liver and muscles (1).
Excretion of orally administered chlordane is relatively slow and
can take days to weeks. Removal from the blood stream is also
relatively slow. The biological half-life of chlordane in the blood
serum of a four-year-old child who drank an emulsifiable concentrate of
chlordane was 88 days. In adults, the half-life can be as short as 3 to
4 days (7). In another accidental poisoning of a 20-month-old child,
the half-life was 21 days. Chlordane accumulates in the fatty tissues,
muscles, kidneys, liver, heart, brain, and other organs of mammals, fish
and birds (9, 18).
Chlordane was used for approximately 40 years before all commercial
uses in the United States were canceled in 1988. Its main uses involved
direct application to soils. Because chlordane is very persistent
bioaccumulates in organisms and the environment, it remains present in
the environment for a period of time (9). Studies done in the late
1970's showed that the fatty tissues of land and water wildlife
contained large amounts of cyclodiene insecticides, including chlordane
(NRC Drinking Water and Health, 1977).
Effects on Birds
Chlordane is highly toxic to birds. The LD50 for bobwhite quail is
83 mg/kg. The 8-day dietary LD50 for chlordane in mallard ducks is 858
ppm of the diet, 331 ppm in bobwhite quail, and 430 ppm in pheasant (2,
18, Lethal Diet Tox. Environ Poll. Birds. 1975).
Effects on Aquatic Organisms
Chlordane is highly toxic to fresh water invertebrates and fish.
The 96-hour LC50 for bluegill is 57 to 74.8 ug/liter, and 42 to 90
ug/liter for rainbow trout (1, 8, 18).
Chlordane bioaccumulates in bacteria and in marine and freshwater
fish species (11).
Effects on Other Animals (Nontarget Species)
Chlordane is highly toxic to bees and earthworms (11).
Breakdown of the Chemical in Soil and Groundwater
In soils, chlordane is very persistent. Its soil half-life is 4
years, and it may persist in soils for as long as 20 years. Several
studies have found chlordane residues in excess of 10% of the initially
applied amount 10 years or more after application (11). Sunlight may
break down a small amount of the chlordane exposed to light (8), but
where application sites are limited to soil injection, photodegradation
is not possible. Volatilization may be the only major route of removal
from soils (11). Chlordane does not chemically degrade (hydrolyze) and
is not subject to biodegradation in soils. Despite its persistence,
chlordane has a low potential for groundwater contamination because it
is both insoluble in water and rapidly binds to soil particles making it
highly immobile within the soil profile. Chlordane molecules usually
remain adsorbed to clay particles or to soil organic matter in the top
soil layers and slowly volatilize into the atmosphere (11). However,
low levels of chlordane (0.01 to 0.001 ug/l) have been detected in both
ground and surface waters in areas where chlordane was heavily used (6,
9). Sandy soils will allow the passage of chlordane to groundwater
(NIH/EPA 1985, 16).
Breakdown of Chemical in Water
Chlordane does not degrade rapidly in water. It can exit aquatic
systems by adsorbing to sediments or by volatilization. It can
completely adsorb to sediments in water-sediment systems in as little as
6 days. The volatilization half-life for chlordane in lakes and ponds
is estimated to be less than 10 days. In one test, 85% of the chlordane
applied to river water remained after two weeks and persisted at that
level for another six weeks (11).
Chlordane has been detected in surface water, groundwater,
suspended solids, sediments, bottom detritus, drinking water, sewage
sludge, and urban run-off, but not in rain water. Concentrations
detected in surface water have been very low, while those found in
suspended solids and sediments are always higher (<0.03 to 580 ppb).
The presence of chlordane in drinking water has almost always been
associated with an accident, such as back siphoning during tank mixing
Breakdown of Chemical in Vegetation
No information found.
PHYSICAL PROPERTIES AND GUIDELINES
Technical chlordane is actually a mixture of at least 23 different
components including chlordane isomers, other chlorinated hydrocarbons
and by-products. It is a viscous, colorless or amber-colored liquid
with a chlorine-like odor. Although it is stable in acid and alkaline
conditions normally encountered during formulation and use, it is
unstable in the presence of weak alkali (1, 2, 11, 12).
In the presence of heat, chlordane breaks down into very toxic
gases, including toxic fumes of phosgene, toxic and corrosive fumes of
chlorine and oxides of carbon (12).
Chlordane is corrosive to iron, zinc and various protective
coatings, including plastics and rubber (8, 12).
The flash point of chlordane is quite low (100-199 degrees F)
(Bureau of Explosives; Emergency Handling of Hazardous Materials in
Surface Transport. 1981). The fumes, or vapors may travel to a source
of ignition and then flash back. Containers of chlordane may explode in
the heat of a fire. Vapor explosion and poisonings are possible
indoors, outdoors, or in sewers. Run-off to sewer may create a fire or
explosion hazard (13).
Chlordane decomposes in the presence of weak alkaline reagents and
should not be formulated with any solvent, carrier, diluent or
emulsifier which is alkaline. Chlordane poses a fire and explosion
hazard in the presence of strong oxidizers (14, 12, Merck Index 10th Ed.
Occupational Exposure Limits:
|OSHA TWA (skin): ||0.5 mg/m3
|ACGIH TWA (skin): ||0.5 mg/m3
|NIOSH recommended TWA (skin): ||0.5 mg/m3
|CAS #: ||57-74-9
|Specific gravity: ||1.59 to 1.63 gm/m3 (1)
|H20 solubility: ||Insoluble in water (2, 19).
|Solubility in other solvents: ||Soluble in most organic solvents, including petroleum oils (1, 2).
|Boiling point: ||175 degrees C (347 degrees F) at 2 mm Hg (12, 20); 118 degrees C at 0.66 mm Hg (14)
|Melting point: ||104-107 degrees C (1, 17).
|Flash point: ||56 degrees C (11)
|Vapor pressure: ||1 x 10 to the minus 5 power mm Hg at 22 degrees C (2, 20).
|Oil: ||water partition coefficient - 2.78 (Callahan. water-rel. environ. fate priority pollut. 1979).
|Odor: ||Penetrating, aromatic, pungent, chlorine-like odor. (Chris. hazardous chem. data manual. 1978).
|Koc: ||3.49-4.64 for pure chlordane (11)
|Chemical Class/Use: ||Chlorinated hydro-carbon/Organochlorine; Chlorinated cyclodiene
Velsicol Chemical Corporation
5600 N. River Rd.
Rosemont, IL 60018-5119
Review by Basic Manufacturer:
Comments solicited: November, 1992
Hayes, W.J. and E.R. Laws (ed.). 1990. Handbook of Pesticide
Toxicology, Vol. 3, Classes of Pesticides. Academic Press, Inc., NY.
Meister, R.T. (ed.). 1992. Farm Chemicals Handbook '92. Meister
Publishing Company, Willoughby, OH.
NIOSH RTECS Online File # 83/8307
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Politics, Trade: Controlling Chemical Residues in Agricultural Products:
A report to the Prime Minister. Australian Government Publishing
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chemistry, degradation, and mode of action. 2nd Ed. Vols. 1 & 2. New
York: M. Dekkar.
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Services. Bethesda, MD: NLM.
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chemicals and drugs. 9th Ed. Rahway, NJ: Merck.
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