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Chlordane

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).

REGULATORY STATUS

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).

INTRODUCTION

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 (2).

TOXICOLOGICAL EFFECTS

ACUTE TOXICITY

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).

CHRONIC TOXICITY

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). Reproductive Effects

Fertility was reduced by about 50% in mice injected with chlordane at 22 mg/kg once a week for 3 weeks (9).

Teratogenic Effects

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).

Mutagenic Effects

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).

Carcinogenic Effects

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 chlordane (5).

Organ Toxicity

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).

ECOLOGICAL EFFECTS

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).

ENVIRONMENTAL FATE

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 operations (11).

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. 1983).

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

Physical Properties:

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

BASIC MANUFACTURER

Velsicol Chemical Corporation
5600 N. River Rd.
Rosemont, IL 60018-5119

Review by Basic Manufacturer:

Comments solicited: November, 1992
Comments received:

REFERENCES

  1. Hayes, W.J. and E.R. Laws (ed.). 1990. Handbook of Pesticide Toxicology, Vol. 3, Classes of Pesticides. Academic Press, Inc., NY.
  2. Meister, R.T. (ed.). 1992. Farm Chemicals Handbook '92. Meister Publishing Company, Willoughby, OH.
  3. NIOSH RTECS Online File # 83/8307
  4. Australian Science and Technology Council. 1989 (May). Health, Politics, Trade: Controlling Chemical Residues in Agricultural Products: A report to the Prime Minister. Australian Government Publishing Service, Canberra.
  5. US Environmental Protection Agency. 1989 (Jan.). Health Advisory Summary: Chlordane. US EPA, Washington, DC.
  6. US Environmental Protection Agency. 1990 (Fall). National Pesticide Survey: Chlordane. Offices of Water and of Pesticides and Toxic Substances, US EPA, Washington, DC.
  7. Kearney, P.C. & D.D. Kaufman (eds.). 1975. Herbicides: chemistry, degradation, and mode of action. 2nd Ed. Vols. 1 & 2. New York: M. Dekkar.
  8. Hartley, D. and H. Kidd, (eds.). 1983. The agrochemicals handbook. Nottingham, England: Royal Society of Chemistry.
  9. US Environmental Protection Agency. 1987 ( March 31). Chlordane: Health Advisory. Office of Drinking Water, US EPA, Washington, DC.
  10. Aldrich, F.D. and J.H. Holmes. 1969 (July). Acute chlordane intoxication in a child: Case report with toxicological data. Archives of Environmental Health 19: 129-132.
  11. Agency for Toxic Substances and Disease Registry. 1989 (Dec). Toxicological Profile for Chlordane (ATSDR/TP-89/06). US Dept. of Commerce, National Technical Information Service, Springfield, VA.
  12. Occupational Health Services, Inc. 1991 (April 10). MSDS for Chlordane. OHS Inc., Secaucus, NJ.
  13. Department of Transportation. 1984. Emergency Response Guidebook: Guidebook for hazardous materials incidents. Washington, DC: U.S. DOT.
  14. Hallenbeck, W.H. & K.M. Cunningham-Burns. 1985. Pesticides and human health. New York: Springer-Verlag.
  15. US Environmental Protection Agency. 1990 (Feb.). Suspended, Canceled, and Restricted Use Pesticides. Office of Compliance Monitoring, Office of Pesticides and Toxic Substances, US EPA, Washington, DC.
  16. TOXNET. 1985. National library of medicine's toxicology data network. Hazardous Substances Databank. Public Health Service. National Institute of Health. U.S. Department of Health and Human Services. Bethesda, MD: NLM.
  17. World Health Organization. 1984. Environmental Health Criteria 34: Chlordane. WHO, Geneva, Switzerland.
  18. US Environmental Protection Agency. 1986 (Dec). Chemical Fact Sheet for Chlordane, 109. Office of Pesticide Programs, US EPA, Washington, DC.
  19. Windholz, M. (ed.) 1976. The Merck Index: an encyclopedia of chemicals and drugs. 9th Ed. Rahway, NJ: Merck.
  20. Sunshine, Irving. 1969. Handbook of analytical toxicology. Cleveland, OH: Chemical Rubber Co.
  21. NIOSH OSHA Pocket Guide to Chemical Hazards.
  22. Martin, E.W. 1971. Hazards of medication: a manual on drug interactions, incompatibilities, contraindications, and adverse effects. Philadelphia, PA: Lippincott Press.
  23. Occupational Health Safety. 9 (8). 1980