Chlordane
| Units | Ref. | ||
|---|---|---|---|
| CAS | 000057-74-9 | - | - |
| Molecular formula | C10H6Cl8 | - | - |
| Molar weight | 409,78 | g mol-1 | - |
| Melting point | 108,8 | °C | [1] |
| Boiling point | 175 | °C | [2] |
| log KOW | 6,26 | - | [3] |
| Water solubility | 0,01299 | g m-3 | [3] |
| Vapor pressure | 0,000133 | Pa | [2] |
| Henry's law constant | 7,03E-5 | atm m3 mol-1 | [3] |
| log KOA | 8,922 | - | [3] |
| log KOC | 4,83 | - | [3] |
Chlordane is a persistent and bioaccumulative chlorinated cyclodiene. The technical grade chlordane is not a single chemical, but is a mixture of many related chemicals, of which about 10 are major components. Some of the major components are transchlordane, cischlordane, chlordene, heptachlor, and transnonachlor. Since the discovery of chlordane in 1945 by Julius Hyman of the Velsicol Corporation, it was used as a pesticide on agricultural crops, lawns, and gardens including vegetables, small grains, maize, other oilseeds, potatoes, sugarcane, sugar beets, fruits, nuts, cotton and jute. Chlordane was also extensively used as a fumigating agent. In the late 1970s and at the beginning of the 1980s many countries severely restricted or banned its use. Action to ban the use of chlordane has been taken among others in Austria, Belgium, Bolivia, Brazil, Chile, Columbia, Costa, Rica, Denmark, Dominican Republic, EU, Kenya, Korea, Lebanon, Liechtenstein, Mozambique, Netherlands, Norway, Panama, Paraguay, Philippines, Poland, Portugal, Santa Lucia, Singapore, Spain, Sweden, Switzerland, Tonga, Turkey, United Kingdom, Yemen and Yugoslavia. From 1983 until 1988, in the US, use of chlordane was only approved by the EPA to control termites in homes. The pesticide was applied underground around the foundation of homes to kill termites that come into contact with it.
Chlordane has been used as a broad-spectrum contact insecticide, mainly on non-agricultural crops and on animals. Under occupational exposure conditions, both inhalation and skin contact are relevant, if adequate preventive and protection measures are lacking
Chlordane is a persistent, non-systemic, contact and ingested insecticide with some fumigant action. It is used on land against formicidae, coleoptera, noctuidae larvae, saltatoria, subterranean termites (including Coptotermes spp.) and many other insect pests. It also controls household insects, pests of man and domestic animals, is used as a wood preservative, a protective treatment for underground cables and to reduce earthworm populations in lawns. It may be applied to soil, directly to foliage or as a seed treatment. Chlordane is on list of persistent organochlorine pesticides (POP) identified by UNEP Governing Council, for which international action is required to reduce the risks to human health and the environment (SC POPs). It is also subject to the prior informed consent procedure of UNEP and FAO.
Chlordane was first prepared in the 1940s by exhaustive chlorination of the cyclopentadiene-hexachlorocyclopentadiene adduct. It was first described as an insecticide in 1945 by Kearns. Chlordane is produced commercially by reacting hexachloro-cyclopentadiene with cyclopentadiene to form chlordene, which is then chlorinated to produce chlordane. Chlordane was first produced commercially in the USA in 1947. Production in the USA, in 1974, amounted to 9.5 million kg. Chlordane is not produced in Europe nor has it ever been manufactured in Japan. In Japan, the only permitted use of the compound is for the control of termites. It is also used against wood-boring beetles and in ant baits. Both the amounts of chlordane produced and used have decreased considerably in recent years. Chlordane has been used as an insecticide for more than 35 years. It is a versatile, broad spectrum, contact insecticide and is used mainly for non-agricultural purposes (primarily for the protection of structures, but also on lawn and turf, ornamental trees, and drainage ditches). Further- more, it is used on corn, potatoes, and livestock.
When used as a pesticide on crops, on lawns and gardens, and to control termites in houses, chlordane enters the environment. In soil, it attaches strongly to particles in the upper layers of soil and is unlikely to enter into groundwater. It is not known whether chlordane breaks down in most soils. If breakdown occurs, it is very slow. Chlordane is known to remain in some soils for over 20 years. Persistence is greater in heavy, clayey or organic soil than in sandy soil. Most chlordane is lost from soil by evaporation and is more rapid from light, sandy soils than from heavy soils. Half of the chlordane applied to the soil surface may evaporate in 2 to 3 days and when chlordane penetrates into the soil, evaporation is much slower. In water, some chlordane attaches strongly to sediment and particles in the water column and some is lost by evaporation. It is not known whether much breakdown of chlordane occurs in water or in sediment. In the atmosphere chlordane breaks down by reacting with light and with some chemicals in the atmosphere. However, it is sufficiently persistent that it may travel long distances and be deposited on land or in water far from its source. Chlordane or the chemicals that chlordane changes into accumulate in fish, birds, and mammals. Chlordane is still commonly found in some form in the fat of fish, birds, mammals, and almost all humans. Chlordane is stable to light under normal conditions. It is readily adsorbed on soil particles and therefore there is no significant migration through the soil profile or leaching into ground water. Some volatilisation into air from treated soils, and some run-off into surface waters can take place. Chlordane is fairly persistent in soil and sediments, especially in the form of its alpha- and gamma-isomers, which are, to a certain extent, translocated into crops grown on the soil. Limited bioaccumulation in the adipose tissue of terrestrial and aquatic organisms can take place. In general, concentration factors in mammals are less than 1. Chlordane is highly toxic to earthworms, which may present its greatest long-term hazard for the environment.
Acute inhalation, oral, and dermal exposure data in humans have identified neurological, gastrointestinal, hematological, and respiratory effects, and jaundice as the presenting symptoms in persons exposed to high doses. High level oral exposure to chlordane may be lethal. The data suggests that the target organs for acute exposure in humans are the central nervous system and live. Specific levels associated with effects in these organs in acutely exposed humans are not known. Acute inhalation data in rats have identified a level associated with mortality. Acute oral and dermal exposure data in animals have identified LD50 values and levels associated with mortality in rats, hamsters, and mice. Acute oral data also have identified the liver and the central nervous system as target organs in rats. The animal data confirmed the target organs in humans, and, based on similar target organs and metabolic pathways, the rat appears to be an appropriate model for toxicity in humans. An acute oral MRL of 0.001 mg.kg.day was derived from a LOAEL of 1 mg.kg.day for developmental effects in the offspring of mice exposed to chlordane in the diet during the third trimester of pregnancy. The pharmacokinetic data in animals, which indicate that absorption occurs following exposure by any route, and the human effects data indicate that the central nervous system and liver would be the target organs of dermal exposure. The World Health Organization has classified hexachlorobenzene as Class II moderately azardous. No data were located for human oral or dermal intermediate duration exposure. Intermediateduration inhalation exposure data in rats, mice, and monkeys have identified the lungs, hematological system, liver, central nervous system, thyroid, and possibly the thymus in female rats, as the target organs. Intermediateduration oral studies have identified levels in rats, mice, and rabbits associated with death, and identified the liver, central nervous system, and developing immune system as target organs. Intermediateduration dermal exposure induces convulsions and liver necrosis in mice and hyperkeratosis of the skin of guinea pigs. Itermediateduration inhalation MRL of 0.0002 mg/m3 was derived based on a NOAEL for hepatic effects in rats exposed to chlordane intermittently for 90 days. An intermediate duration oral MRL of 0.0006 mg.kg.day was derived based on a NOAEL of 0.055 mg.kg.day for hepatic effects in rats given chlordane in the diet for 30 months. Chronic toxicity inhalation data include two case report studies of blood dyscrasia, and several studies of humans living in chlordanetreated homes or exposed to chlordane during its manufacture or during its use as a pesticide. Dermatitis, migraine headaches, unspecified skin neoplasms, and unspecified ovarian and uterine disease have been associated with chronic inhalation exposure to chlordane. A chronicduration inhalation MRL of 0.00002 mg/m3 was derived from the NOAEL for hepatic effects in rats exposed to chlordane intermittently for 90 days. Elevated serum levels of hepatic enzymes associated with liver damage were found in pesticide applicators. No studies of chronic oral exposure to chlordane were located for humans. Chronicduration dermal data in humans are limited to a report of seizures in a nursery owner who handled soil containing chlordane. Chronicduration animal exposure data, located only for oral exposure, have identified levels in rats and mice associated with reduced survival, and identify the liver and central nervous system as target organs. A chronicduration oral MRL of 0.0006 mg.kg.day was derived based on the NOAEL for hepatic effects in rats given chlordane in the diet for 30 months. Chlordane induced liver tumors in mice, and chlordane has not been sufficiently studied for reproductive effects. No chronic inhalation studies of chlordane in animals were located. The epidemiology studies and various case reports revealed no convincing evidence of chlordanes carcinogenicity in humans, except for a weak association with leukemia and neuroblastoma. Oral studies in animals have confirmed that chlordane induces liver tumors in mice, but not rats, exposed to high levels. Chronicduration inhalation and dermal studies were not located, but it seems likely that the carcinogenicity of chlordane in mice is not routedependent, because the pharmacokinetic data in animals indicate that absorption occurs following any route of exposure, and because the liver is a target organ for noncancer effects regardless of route of exposure. Most genotoxicity tests with chlordane yielded negative results, suggesting an epigenetic mechanism of carcinogenicity. The Department of Health and Human Services (DHHS) determined that chlordane may reasonable be anticipated to be a human carcinogen. The International Agency for Research on Cancer (IARC) determined that chlordane may possibly cause cancer in humans. According to the U.S. EPA Carcinogen List there is a sufficient evidence of chlordane carcinogenicity from animal studies with inadequate or no data from epidemiologic studies in humans, there for it is classified as a Category B2, Probable human carcinogen.
- AOAC Official Method 990.06 Organochlorine Pesticide in Water. Gas Chromatographic Method. 2005 AOAC International
- AOAC Official Method 990.06 Organochlorine Pesticide Contamination of Pesticide Formulations. ThinLayer Chromatographic Method. 2005 AOAC International
- EPA Method 8081A: Organochlorine Pesticides by Gas Chromatography (and ECD)
- EPA Method 8270C: Semivolatile Organic Compounds by Gas Chromatography/Mass Spectrometry (GC/MS)
- ISO 6468 (1996) Water quality Determination of certain organochlorine insecticides, polychlorinated biphenyls and chlorobenzenes Gas chromatographic method& after liquidliquid extraction
- ISO 10382 (2002): Soil quality Determination of organochlorine pesticides and polychlorinated biphenyls Gaschromatographic method with electron capture detection
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[3] US EPA. [2009]. Estimation Programs Interface Suite™ for Microsoft® Windows, v 4.00]. United States Environmental Protection Agency, Washington, DC, USA
[4] IPCS: Intox Databank, http://www.intox.org/databank/index.htm
[5] ATSDR: Agency for toxic substances and disease registery, http://www.atsdr.cdc.gov/
[6] TOXNET: TOXikology Data NETwork TOXNET - http://toxnet.nlm.nih.gov/
[7] IRZ: Integrovaný registr znečišťování životního prostředí (IRZ) : http://www.irz.cz/
[8] National Safety Council, http://www.nsc.org/index.htm
[9] Databáze Eurochem, http://www.eurochem.cz
