Mirex
| Units | Ref. | ||
|---|---|---|---|
| CAS | 002385-85-5 | - | - |
| Molecular formula | C10Cl12 | - | - |
| Molar weight | 545.55 | g mol-1 | - |
| Melting point | 485 | °C | [1] |
| Boiling point | - | - | - |
| log KOW | 7.01 | - | [3] |
| Water solubility | 0.0004755 | g m-3 | [3] |
| Vapor pressure | 0.00013 | Pa | [2] |
| Henry's law constant | 1.28E-6 | atm m3 mol-1 | [3] |
| log KOA | 8.369 | - | [3] |
| log KOC | 5.552 | - | [3] |
Mirex (SC POPs) is a fully chlorinated organic compound, based on two linked five member carbon rings. It is highly stable, doesn't burn easily or react readily with acids, bases, chlorine or ozone. It was first synthesized in 1946 by Prins, but was not used in pesticide formulation until 1955. Mirex is manufactured by the dimerization of hexachlorocyclopentadiene in the presence of aluminium chloride. Because of its high melting point, mirex was used as a fire retardant in plastic, rubber, paint, paper and electronics. It is also used as a stomach insecticide. It has also been used to combat leaf cutters in South America, harvester termites in South Africa, mealy bug of pineapple in Hawaii.
Mirex is mainly used as a flame-retardant and as a stomach insecticide, mainly formulated into baits, for the control of ants, especially fire ants and harvester ants. The USA appears to be the main country in which mirex was used for pest control, but this use was discontinued in 1978.
Mirex was first synthesized in 1946 by Prins but was not used in pesticide formulations until 1955. Mirex is made by the dimerization of hexachlorocyclopentadiene in the presence of aluminum chloride (IARC). It is a stomach insecticide with little contact activity. The insecticidal use of mirex has been largely focused on the control of the imported fire ant Solenopsis saevissima richteri, in southeastern USA. The imported fire ant was introduced into the USA at the beginning of this century and for the first twenty years confined itself to the area around the port of Mobile, Alabama. However, a second wave of a closely related species (Solenopsis invicta) appeared in the late 1920s and spread throughout the south of the USA. Since then, the imported fire ant has infested some 76 million hectares in the southern USA. This pest can pose a nuisance as it can deliver a severe sting which often results in secondary infection. In addition, the mounds produced by the ants make farming difficult and can cause damage to farm machinery. To combat the problem, approximately 250 000 kg of mirex was applied to fields during 1962-75. Most of the mirex was in the form of 4X mirex bait, which consists of 0.3% mirex in 14.7% soybean oil mixed with 85% corncob grits. Preparations also came in 2X and 1X baits, which contained 0.15 and 0.1% mirex, respectively. Application of the 4X bait was designed to give a coverage of 4.2 g mirex/ha and was delivered by aircraft, helicopter or tractor. Another form of bait consists of microencapsulated mirex in soybean oil. Normal application rates are 750 mg active ingredient/kg for fire ant baits and 1500 mg/kg for harvester ant baits. Other pests are also sensitive to mirex, including the western hamster ant, the yellow-jacket and the Texas leaf-cutting ant. Mirex bait has been applied to pineapple-growing areas in Hawaii to control mealy bug, under permit from US EPA since 1970. In 1971, the US EPA cancelled all federal regulations permitting the use of mirex pending release of an environmental impact study. New regulations, issued by the US EPA in 1972, authorized the restricted use of mirex by permit only. Allied Chemical Corporation, which at the time was the sole producer of bait formulations, sold the registration for mirex and the right to produce, for one dollar, to the Mississippi Department of Agriculture. During the same year, the US EPA ordered a phasing-out of the use of mirex for pestpest control and brought in a ban with exemptions on June 30, 1978. Mississippi has since been trying to gain approval for a new compound under the generic name Ferriamicide. This bait contains long-chain alkyl amines and ferrous chloride in addition to mirex. With this composition, 80 - 90% of the mirex was claimed to degrade within 30 days, compared with the normal break-down time of 5 - 10 years. However, a Canadian study conducted in 1979 demonstrated that photomirex, a major break-down product of Ferriamicide, was considerably more toxic than mirex itself. Hence, the US EPA has withheld permission for the Mississippi Pest Control Program, pending review of the Canadian study. The literature indicates that the USA may be the only country to have used mirex in pest control. Mirex, under the name Dechlorane, is also used as a fire retardant in plastics, rubber, paint, paper, and electrical goods, and as a smoke-generating compound, when combined with zinc oxide and powered aluminum. Statistics show that between 1959 and 1975, 400 000 kg of mirex and 1 500 000 kg of Dechlorane were sold, of which 74% was used in the USA for non-agricultural purposes. Recently, non-agricultural mirex has been replaced in part by compounds such as Dechlorane plus, Dechlorane 4070, 510, 602, 603, and 604, all of which have similiar fire retardent properties. No recent consumption data for mirex in non-agricultural applications could be obtained. Unfortunately, complete information on the quantities of mirex produced in the USA and its fate is not available. In fact, as much as half of the mirex used between 1962-73 cannot be accounted for. Little information is also available on world-wide production and use, but patents for the use of mirex exist in several countries including Belgium, France, the Federal Republic of Germany, Japan, the Netherlands, and the United Kingdom.
Release into the environment has occurred via effluents from manufacturing plants and sites where mirex was utilized as a fire resistant additive to polymers, and at points of application where it was used as a insecticide. Mirex is expected to persist in the environment despite the 1978 ban on its use in the US.
Mirex is a very persistent compound in the environment and is highly resistant to both chemical and biological degradation. The primary process for the degradation of mirex is photolysis in water or on soil surfaces. The primary photoreduction product of mirex in water is photomirex, which can also cause harmful health effects is more poisonous than mirex it self. Mirex has been detected in air, surface water, soil and sediment, aquatic organisms, and foodstuffs. Historically, mirex was released to the environment primarily during its production or formulation for use as a fire retardant and as a pesticide. Because mirex is a very hydrophobic compound with a low vapour pressure, atmospheric transport is unlikely. Atmospheric releases of mirex could result from airborne dust from the production and processing of mirex, combustion of mirexcontaining products, or volatilization of mirex applied as a pesticide. Little information was found on the degradation of mirex in the atmosphere. Mirex is expected to be stable against photogenerated hydroxyl radicals in the atmosphere. Based on a calculated soil sorption coefficient of 1,200 (5,800 experimental) for mirex, this compound will tightly bind to organic matter in soil and, therefore, will be highly immobile. Thus, mirex is most likely to enter surface waters as a result of soil runoff. In addition, most land applications of mirex to soils containing high organic content would result in very little leaching through soil to groundwater. However, leaching of mirex from some agricultural soils can occur as mirex has been detected in groundwater wells near agricultural areas. In soil or sediments, anaerobic biodegradation is also a major removal mechanism whereby mirex is slowly dechlorinated to the lomonohydro derivative. Aerobic biodegradation on soil is a very slow and minor degradation process. Twelve years after the application of mirex to soil, 50% of the mirex and mirexrelated compounds remained on the soil. Between 65-73% of the residues recovered were mirex and 36% were chlordecone, a transformation product. Mirex has been released to surface waters via waste waters discharged from manufacturing and formulation plants, in activities associated with the disposition of residual pesticides, and as a result of its direct use as a pesticide, particularly in the fire ant eradication programs. Mirex insecticide baits were dispersed by aerial applications, and mirex could be released into surface water directly or could reach surface waters via runoff. Because mirex binds tightly to organicrich soils, leaching to groundwater is not generally expected to occur.
No information is available regarding the effects of acuteduration exposure to mirex in humans following inhalation, oral, or dermal exposure. A large number of studies have been published for acuteduration oral exposure of rats and mice to mirex, many of them addressing interactions with other chemicals, such as the halogenated hydrocarbons, and adaptive liver effects. However, no information could be located for acuteduration inhalation or dermal exposure. Mirex may lead to death after oral exposure, depending upon dose; some evidence exists that pregnant rats may be more sensitive to the lethal effects of mirex. The main targets of mirex toxicity following acute exposure by the oral route are the liver, nervous system, developing fetus, and eyes. Impaired hepatobiliary excretion and hepatic glycogen depletion have been described as the major hepatic effects. Tremors, hyperactivity or lethargy, and weakness were observed following acuteduration oral exposure to large doses of mirex. Prenatal acuteduration exposure to mirex resulted in cardiac and visceral anomalies, cataracts, increased resorptions, and lethality of offspring. Cataract formation in newborns occurs after early postnatal exposure. Diarrhoea, resulting from gastric irritation, has also been found with acuteduration oral mirex administration, especially in dying animals. The dose at which this effect occurs is not clear. Alterations in blood flow, in addition to changes in membranebound enzymes responsible for electrolyte flux in cardiac cells, occurs after acute oral exposure. The physiological significance of these changes to the experimental animal is not known. Thyroid toxicity has also been documented in rats, in addition to adrenal hypertrophy and hyperfunction. There was no indication that mirex was genotoxic in a dominant lethal assay. It is not possible to determine the target organ for mirex toxicity after inhalation or dermal exposure due to the complete lack of data in these areas for this duration of exposure. No acuteduration inhalation MRL could be derived for mirex because no inhalation data could be located. No acuteduration oral MRL was derived for mirex because serious effects, like heart block and arrhythmias in fetuses from dams exposed during gestation, were observed at the lowest dose tested. The World Health Organization has not listed mirex in WHO Acute Hazard Rankings because as an active ingredient is believed to be obsolete or discontinued for use as a pesticide.Studies performed by the U.S. EPA placed mirex formulations in Acute Toxicity Rankings in a Category 2, Moderately Toxic No information is available regarding the toxicity of intermediateduration exposure of humans to mirex by any route of administration. Information regarding exposure of animals to mirex for an intermediate duration is available for the oral route. Animals exposed orally to mirex for an intermediate period of time demonstrated increased lethality according to dose and species where mice and dogs may be more sensitive. Data from inhalation or dermal exposure to mirex could not be located; therefore, the concentration or dose that would be likely to cause death after these exposure routes cannot be established. The target organs of toxicity to orally administered mirex appear to be the liver, gastrointestinal system, and thyroid. Liver toxicity with intermediateduration oral exposure to mirex is similar to that occurring after acuteduration exposure, with the exception that lower doses cause hepatotoxicity. The most prominent hepatic effects are impaired biliary excretion and liver histopathology. Mild diarrhoea occurred in two studies in rats; in one study with mice, severe diarrhoea and haemorrhage of the intestines indicated a gastrointestinal origin for the disturbance. Histopathological changes in the thyroid have been reported after intermediateduration oral exposure of animals; however, no change in serum thyroid hormone levels was found. Adrenal effects have been seen that are consistent with increased lipid utilization. Body weight decreases have been found in intermediateduration oral studies using mirex. No adverse cardiovascular effects were found in one study; however, the data reported from this study were limited. No renal toxicity was found after intermediateduration oral exposure to mirex, but these studies are flawed. No reports could be located describing the musculoskeletal effects of intermediateduration oral mirex administration. No evidence for carcinogenicity in exposed humans was found in the available literature.Animal studies provide sufficient evidence that mirex and its metabolite (chlordecone) are carcinogenic after oral exposure. Carcinogenic potential has not been tested by the inhalation or dermal routes. Effects after inhalation exposure are unlikely because of low volatility. Evidence suggests that chlordecone and mirex are epigenetic carcinogens, and a twostage initiationpromotion study in rats provides strong evidence for liver tumour promotion activity of chlordecone. The Department of Health and Human Services (DHHS) determined that mirex may reasonable be anticipated to be a human carcinogen. The International Agency for Research on Cancer (IARC) determined that mirex may possibly cause cancer in humans. US EPA has not listed mirex on its Carcinogens List.
- AOAC Official Method 990.06 Organochlorine Pesticides in Water. Gas Chromatographic Method. 2005 AOAC International
- AOAC Official Method 990.06 Organochlorine Pesticide Contamination of Pesticide Formulations. Thin-Layer 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 liquid-liquid extraction
- ISO 10382 (2002): Soil quality - Determination of organochlorine pesticides and polychlorinated biphenyls - Gas chromatographic 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/
