Polychlorinated dibenzo-furans,
(2,3,7,8,–TCDD)
| Units | Ref. | ||
|---|---|---|---|
| CAS | 001746-01-6 | - | - |
| Molecular formula | C12H4Cl4O2 | - | - |
| Molar weight | 321.98 | g mol-1 | - |
| Melting point | 295 | °C | [1] |
| Boiling point | 421.1 | °C | [2] |
| log KOW | 6.92 | - | [3] |
| Water solubility | 0.001103 | g m-3 | [3] |
| Vapor pressure | 2.02E-07 | Pa | [2] |
| Henry's law constant | 3.53E-06 | atm m3 mol-1 | [3] |
| log KOA | 9.489 | - | [3] |
| log KOC | 5.396 | - | [3] |
Polychlorinated dibenzopdioxins (PCDDs) are a family of 75 different compounds commonly referred to as polychlorinated dioxins or just dioxins. With general chemical formula of C12H8XClXO2, these compounds have varying harmful effects. The PCDD family is divided into eight groups of chemicals based on the number of chlorine atoms in the compound:
- mono-chlorinated dioxin
- di-chlorinated dioxin (DCDD)
- tri-chlorinated dioxin (TrCDD)
- tetra-chlorinated dioxin (TCDD)
- penta-chlorinated dioxin (PeCDD)
- hexa-chlorinated dioxin (HxCDD)
- hepta-chlorinated dioxin (HpCDD)
- octa-chlorinated dioxin (OCDD)
The chlorine atoms can be attached to the dioxin molecule at any one of eight positions. The name of each dioxin indicates both the number and the positions of the chlorine atoms. For example, the dioxin with four chlorine atoms at positions 2, 3, 7, and 8 on the dioxin molecule is called 2,3,7,8tetrachlorodibenzopdioxin or 2,3,7,8TCDD. 2,3,7,8TCDD is one of the most toxic to mammals of all PCDDs and has received the most attention and it serves as a prototype for the PCDDs. Dioxins with toxic properties similar to 2,3,7,8TCDD are called dioxinlike compounds. PCDDs (mainly 2,3,7,8TCDD) may be formed during the chlorine bleaching process used by pulp and paper mills. PCDDs occur as a contaminant in the manufacturing process of certain chlorinated organic chemicals, such as chlorinated phenols. 2,3,7,8TCDD is a byproduct formed during the manufacture of 2,4,5trichlorophenol (2,4,5TCP). 2,4,5TCP was used to produce hexachlorophene and the herbicide, 2,4,5trichlorophenoxyacetic acid (2,4,5T). In most industrialized countries the use of products contaminated with PCDDs has been greatly reduced. Chlorinated chemicals, like pentachlorophenol (PCP), used to preserve wood, do contain some of the more highly chlorinated PCDDs. The use of PCP has been restricted to certain manufacturing applications. PCDDs can enter your body when you breathe contaminated air, eat contaminated food, or have skin contact with contaminated soil or other materials. The most common way PCDDs can enter your body is by eating food contaminated with PCDDs Polychlorinated dibenzofurans (PCDFs) are a family of chemicals known as polychlorinated dibenzofurans or simply furans. These chemicals contain one to eight chlorine atoms attached to the carbon atoms of the parent chemical, dibenzofuran. The PCDF family contains 135 individual compounds (known as congeners) with varying harmful health and environmental effects. Of these 135 compounds, those that contain chlorine atoms at the 2,3,7,8-positions of the parent dibenzofuran molecule are especially harmful. Other than for laboratory use of small amounts of PCDFs for research and development purposes, these chemicals are not deliberately produced by industry. Most PCDFs are produced in very small amounts as unwanted impurities of certain products and processes utilizing chlorinated compounds. Only a few of the 135 PCDF compounds have been produced in large enough quantities so that their properties, such as colour, smell, taste, and toxicity could be studied. The few PCDF compounds that have been produced in those quantities are colourless solids. They do not dissolve in water very easily. There is no known use for these chemicals.
Polychlorinated dibenzodioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) are by-products of combustion and of various industrial processes, and they are widely present in the environment.
PCDDs and PCDFs are not produced commercially. These compounds are in fact formed as trace amounts of undesired impurities in the manufacture of other chemicals such as chlorinated phenols and their derivatives, chlorinated diphenyl ethers, and polychlorinated biphenyls (PCBs). There is no known technical use for the PCDDs and PCDFs.
Dioxins and furans are released into the air during combustion processes such as industrial and municipal waste incineration (including burning of household waste in some areas), metal recycling and refining (smelting) and burning of fuels like wood, coal, gasoline, or oil. Dioxins and furans can also be formed from natural sources (for example, during forest fires). Chlorine bleaching of pulp and paper, certain types of chemical manufacture and processing and other industrial processes all can create small quantities of dioxins and furans.
Currently, PCDDs are primarily released to the environment during combustion of fossil fuels (coal, oil, and natural gas) and wood, and during incineration processes, municipal and medical solid waste and hazardous waste incineration. While incineration may be the primary current source of release of PCDDs into the environment, the levels of PCDDs produced by incineration are extremely low. PCDDs are associated with ash generated in combustion and incineration processes. Emissions from incinerator sources vary greatly and depend on management practices and applied technologies. PCDDs also have been detected at low concentrations in cigarette smoke, homeheating systems, and exhaust from cars running on leaded gasoline or unleaded gasoline, and diesel fuel. Burning of many materials that may contain chlorine, such as plastics, wood treated with pentachlorophenol (PCP), pesticidetreated wastes, other polychlorinated chemicals (polychlorinated biphenyls or PCBs), and even bleached paper can produce PCDDs and even home frying. PCDDs enter the environment as mixtures containing a variety of individual components and impurities. In the environment they tend to be associated with ash, soil, or any surface with a high organic content, such as plant leaves. In air and water, a portion of the PCDDs may be found in the vapour or dissolved state, depending on the amount of particulate matter, temperature, and other environmental factors. PCDDs are known to occur naturally. They are naturally produced from the incomplete combustion of organic material by forest fires or volcanic activity. PCDDs are not intentionally manufactured by industry, except in small amounts for research purposes. Small amounts of PCDFs can enter the environment from a number of sources. Accidental fires or breakdowns involving capacitors, transformers, and other electrical equipment (e.g., fluorescent light fixtures) that contain polychlorinated biphenyls (PCBs) are known to release high levels of furans formed by thermal degradation. PCDFs are also produced as unwanted compounds during the manufacture of several chlorinated chemicals and consumer products, such as wood treatment chemicals, some metals, and paper products. When the waste water, sludge, or solids from these processes are released into waterways or soil in dumpsites, they become contaminated with PCDFs. Furans also enter into the environment from burning municipal and industrial waste in incinerators. The exhaust from cars that use leaded gasoline, which contains chlorine, releases small amounts of these compounds in the environment. Small amounts of PCDFs may also enter into the environment from burning of coal, wood, or oil for home heating and production of electricity. Many of these chemicals or processes that produce PCDFs in the environment are either being slowly phased out or strictly controlled. Furans in air are present mostly as solid particles and to a much lesser extent as vapour. Some of the PCDFs present in air return to the land and water by settling, snow, and rainwater. An amount of PCDFs in the vapour phase is destroyed by reacting with certain chemical agents, called hydroxyl radicals, naturally present in the atmosphere. Depending on the congener, furans may remain in air for an average of more than 10 days. Once in the air, they can be carried long distances. Polychlorinated dibenzofurans tend to stick to suspended particles and settled particles in lakes and rivers and can remain at the bottom of lakes and rivers for several years. PCDFs can build up in fish, and the amount of the compounds in fish can be tens of thousands times higher than the levels in water. The PCDFs in water can get into birds or other animals and humans that eat fish containing PCDFs. Furans bind strongly to soil and are not likely to move from the surface soil into groundwater. In some instances, PCDFs from some waste landfills may reach underground water. PCDFs are more likely to move from soil to water or other soils by soil erosion and flooding. The breakdown or loss of PCDFs in soil occurs over years, so PCDFs remain in soil for years. Most PCDFs found in plants are probably deposited by air. Cattle that eat plants contaminated by PCDFs will build up some of the PCDFs in their bodies. Some will enter the milk and meat of cattle.
Acute exposure of humans to 2,3,7,8TCDD can cause chloracne and hepatic effects. Specifying the route of exposure in these human cases is difficult because the individuals were probably exposed by a combination of routes. Furthermore, human data did not provide any information regarding exposure levels and coexposure to other chemicals confounds the results. Also, in most cases, the exposed subjects were examined long after exposure occurred. Acute oral exposure to 2,3,7,8TCDD caused delayed type of death in all animal species tested, and LD50 values have been determined for rats, rabbits, guinea pigs, and hamsters. Furthermore, an acute LD50 was calculated for rats and mice exposed to a mixture of 1,2,3,6,7,8HxCDD and 1,2,3,7,8,9HxCDD. No deaths were observed with other congeners (2,7DCDD, 1,2,3,4,6,7,8HpCDD, 1,2,3,4,6,7,8,9OCDD) tested, and 2,3,7,8TCDD proved to be the most toxic dioxin. However, interspecies and interstrain differences were found in the susceptibility to PCDDs. Systemic effects observed in animals after acute oral exposure to 2,3,7,8TCDD included cardiovascular, gastrointestinal, hematological, hepatic, renal, endocrine, dermal effects, and body weight loss. Hepatic and body weight effects were the main signs of 2,3,7,8TCDD toxicity and occurred also after exposure to a mixture of 1,2,3,6,7,8HxCDD and 1,2,3,7,8,9HxCDD. Immunological effects were observed following low oral doses of 2,3,7,8TCDD, and an acute oral MRL was based on a NOAEL for immunological effects. Limited data were located regarding effects in animals after acute inhalation exposure to PCDDs. No information was located regarding health effects of other congeners in humans, and limited data exist about effects caused by an acute exposure to these congeners in animals. Several epidemiological studies of phenoxy herbicide and chlorophenol producers found increases in cancer mortality in populations exposed to 2,3,7,8TCDD. Exposure to this compound has been especially associated with the development of softtissue sarcoma after a prolonged latency period. The human data suggest that 2,3,7,8TCDD may be a human carcinogen, however, the interpretation of many of these studies is limited by confounding factors (e.g., small cohorts, short latency periods, coexposure to other chemicals, inadequate exposure data). There are no reliable human studies on the carcinogenicity of other PCDDs. Animal studies provided sufficient evidence that 2,3,7,8TCDD is a carcinogen after oral and dermal exposure. Furthermore, 2,3,7,8TCDD has promoting ability on tumours initiated by diethylnitrosourea. Similarly, chronic oral exposure of rodents to a mixture of 1,2,3,6,7,8HxCDD and 1,2,3,7,8,9HxCDD or to 2,7DCDD resulted in carcinogenic effects. No studies were located regarding cancer effects in animals following inhalation exposure to PCDDs. Essentially all of the information pertaining to health effects of PCDFs in humans is from the Yusho and Yu-Cheng rice oil poisoning incidents. No definite information is available on human health effects of acute oral exposure to PCDFs because exposure during these incidents predominately involved intermediate-duration exposure. Information on humans exposed to PCB fires, particularly PCB mixtures not containing chlorinated benzenes (which can form PCDDs), could possibly help characterize health effects of PCDFs following acute dermal and/or inhalation exposure. Health effects associated with the Binghamton State Office Building electrical transformer fire cannot be attributed solely to PCDFs or any of the other components of the soot due to the mixture of chemicals, which included chlorinated benzenes and PCDDs, and other confounding factors. Relatively little information is available on systemic effects of acute duration oral exposure to PCDFs in animals. Several effects have been observed, including histopathologic and possible functional changes in the kidneys and gastrointestinal tract and evidence of wasting and anaemia. Many of these effects occurred at lethal or other high doses, although effects in the guinea pig, which is the most sensitive species tested in acute oral studies, are relatively well characterized. Since acute toxicity of furans may depend more on total dose, rather than frequency of dosing, and is characteristically delayed in expression, some information from intermediate duration oral studies is relevant to acute exposure. Data on effects in animals following acute dermal or inhalation exposure to PCDFs are not available, although mobilization of PCDFs from adipose tissue to target organs is likely to be similar, regardless of the route of exposure. Acute dermal studies are relevant because skin is a route of concern for exposure at or near hazardous waste sites, particularly due to possibilities for brief contact. Acute inhalation studies are unlikely to be relevant, due to the low potential for inhalation exposure in the vicinity of hazardous waste sites and ambient air. Most of the existing toxicity information for PCDFs is available from intermediate duration studies of orally-exposed humans following Yusho and Yu-Cheng poisoning and animals. Dermal and ocular effects; mild anaemia; mild and transient hepatic alterations, including increased serum levels of triglycerides and liver enzymes and related ultrastructural changes; and bronchitis and other respiratory effects secondary to infection, were most consistently observed in the exposed humans. Although some estimates of doses associated with some effects of Yusho and Yu-Cheng exposure are available, these probably do not reflect the most sensitive toxic end points, as indicated by studies in rats, guinea pigs, and monkeys. Some systemic effects of intermediate duration oral PCDFs exposure in animals are consistent with the effects observed in humans, but the animal studies better characterize progression of certain effects (e.g., liver toxicity) and have identified other systemic effects (e.g., wasting syndrome, stomach mucosal lesions). Hepatic effects in rats were used as a basis for an intermediate-duration oral MRL. Because of limitations in the database, it is unclear whether different species should be used for studying effects on different target organs. The only information available on systemic toxicity of intermediate duration dermal exposure is from a study in mice, which found effects in the stomach and liver and on body weight, however, these data are suggestive of similar effects by both dermal and oral routes. No data were located regarding effects in animals after intermediate-duration inhalation exposure, but inhalation is a minor route of concern for humans. No information is available on effects in humans or animals following chronic exposure to PCDFs by any route. A retrospective mortality study of Yusho victims and an informal survey of Yu-Cheng deaths provides inconclusive evidence of liver cancer. An intermediate duration study in mice showed no skin neoplastic activity following dermal application of 2,3,4,7,8-pentaCDF or 1,2,3,4,7,8-hexaCDF alone, although these congeners as well as 2,3,7,8-tetraCDF promoted development of mouse skin neoplasms. These congeners also promoted development of liver tumours in rats following subcutaneous injection, providing further evidence of tumour promotion by PCDFs. Results of a 2-year carcinogenicity study in which 2,3,4,7,8-pentaCDF or 1,2,3,4,7,8-hexaCDF were administered to rats by 1 single or 4 weekly subcutaneous injections are inconclusive due to small numbers of tested animals.
- US EPA Method 8290: Polychlorinated Dibenzodioxins (PCDDs) and Polychlorinated Dibenzofurans (PCDFs) by HighResolution Gas Chromatography/HighResolution Mass Spectrometry (HRGC/HRMS)
[1] Lide, D.R., Editor (2003) Handbook of Chemistry and Physics. 84th Edition, CRC Press, Boca Raton, Florida.
[2] Schroy, J.M., Hileman, F.D., Cheng, S.C. (1985b) Physical/chemical of 2,3,7,8-TCDD. Chemosphere 14, 873–886.
[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/
