Dioxins occur as by-products in the manufacture of some organochlorides, in the incineration of chlorine-containing substances such as polyvinyl chloride (PVC), in the chlorine bleaching of paper, and from natural sources such as volcanoes and forest fires. There have been many incidents of dioxin pollution resulting from industrial emissions and accidents; the earliest such incidents were in the mid 19th century during the Industrial Revolution.
In PCDDs, chlorine atoms are attached to this structure at any of 8 different places on the molecule, at positions 1–4 and 6–9. There are 75 different PCDD congeners (that is, related dioxin compounds).
The toxicity of PCDDs depends on the number and positions of the chlorine atoms. Congeners that have chlorine in the 2, 3, 7, and 8 positions have been found to be significantly toxic. In fact, 7 congeners have chlorine atoms in the relevant positions which were considered toxic by the World Health Organization toxic equivalent (WHO-TEQ) scheme.
Occupational exposure is an issue for some in the chemical industries, historically for those making chlorophenols or chlorophenoxy acid herbicides or in the application of chemicals, notably herbicides. In many developed nations there are now emissions regulations which have dramatically decreased the emissions and thus alleviated some concerns, although the lack of continuous sampling of dioxin emissions causes concern about the understatement of emissions. In Belgium, through the introduction of a process called AMESA, continuous sampling showed that periodic sampling understated emissions by a factor of 30 to 50 times. Few facilities have continuous sampling.
Dioxins are produced in small concentrations when organic material is burned in the presence of chlorine, whether the chlorine is present as chlorideions or as organochlorine compounds, so they are widely produced in many contexts. According to the most recent US EPA data, the major sources of dioxins are broadly in the following types:
When first carried out in 1987, the original US EPA inventory of dioxin sources revealed that incineration represented more than 80% of known dioxin sources. As a result, US EPA implemented new emissions requirements. These regulations succeeded in reducing dioxin stack emissions from incinerators. Incineration of municipal solid waste, medical waste, sewage sludge, and hazardous waste together now produce less than 3% of all dioxin emissions. Since 1987, however, backyard barrel burning has showed almost no decrease, and is now the largest source of dioxin emissions, producing about one third of the total output.
In incineration, dioxins can also reform or form de novo in the atmosphere above the stack as the exhaust gases cool through a temperature window of 600 to 200°C. The most common method of reducing the quantity of dioxins reforming or forming de novo is through rapid (30 millisecond) quenching of the exhaust gases through that 400°C window. Incinerator emissions of dioxins have been reduced by over 90% as a result of new emissions control requirements. Incineration in developed countries is now a very minor contributor to dioxin emissions.
Tolerable daily, monthly or annual intakes have been set by the World Health Organization and a number of governments. Dioxins enter the general population almost exclusively from ingestion of food, specifically through the consumption of fish, meat, and dairy products since dioxins are fat-soluble and readily climb the food chain.
Children are passed substantial body burdens by their mothers, and breastfeeding increases the child's body burden. Dioxin exposure can also occur from contact with Pentachlorophenol (Penta) treated lumber as Pentachlorophenol often contains dioxins as a contaminant. Children's daily intakes during breast feeding are often many times above the intakes of adults based on body weight. This is why the WHO consultation group assessed the tolerable intake so as to prevent a woman from accumulating harmful body burdens before her first pregnancy. Breast fed children usually still have higher dioxin body burdens than non breast fed children. The WHO still recommends breast feeding for its other benefits. In many countries dioxins in breast milk have decreased by even 90% during the two last decades.
Dioxins are present in cigarette smoke. Dioxin in cigarette smoke was noted as "understudied" by the US EPA in its "Re-Evaluating Dioxin" (1995). In that same document, the US EPA acknowledged that dioxin in cigarettes is "anthropogenic" (man-made, "not likely in nature").
Dioxins are absorbed primarily through dietary intake of fat, as this is where they accumulate in animals and humans. In humans, the highly chlorinated dioxins are stored in fatty tissues and are neither readily metabolized nor excreted. The estimated elimination half-life for highly chlorinated dioxins (4–8 chlorine atoms) in humans ranges from 4.9 to 13.1 years.
The persistence of a particular dioxin congener in an animal is thought to be a consequence of its structure. Dioxins with no lateral (2, 3, 7, and 8) chlorines, which thus contain hydrogen atoms on adjacent pairs of carbons, can more readily be oxidized by cytochromes P450. The oxidized dioxins can then be more readily excreted rather than stored for a long time.
2,3,7,8-Tetrachlorodibenzodioxin (TCDD) is considered the most toxic of the congeners (for the mechanism of action, see 2,3,7,8-Tetrachlorodibenzodioxin and Aryl hydrocarbon receptor). Other dioxin congeners including PCDFs and PCBs with dioxin-like toxicity, are given a toxicity rating from 0 to 1, where TCDD = 1 (see Dioxins and dioxin-like compounds). This toxicity rating is called the Toxic Equivalence Factor concept, or TEF. TEFs are consensus values and, because of the strong species dependence for toxicity, are listed separately for mammals, fish, and birds. TEFs for mammalian species are generally applicable to human risk calculations. The TEFs have been developed from detailed assessment of literature data to facilitate both risk assessment and regulatory control. Many other compounds may also have dioxin-like properties, particularly non-ortho PCBs, one of which has a TEF as high as 0.1.
The total dioxin toxic equivalence (TEQ) value expresses the toxicity as if the mixture were pure TCDD. The TEQ approach and current TEFs have been adopted internationally as the most appropriate way to estimate the potential health risks of mixture of dioxins. Recent data suggest that this type of simple scaling factor may not be the most appropriate treatment for complex mixtures of dioxins; both transfer from the source and absorption and elimination vary among different congeners, and the TEF value is not able to accurately reflect this.
Dioxins build up primarily in fatty tissues over time (bioaccumulation), so even small exposures may eventually reach dangerous levels. In 1994, the US EPA reported that dioxins are a probable carcinogen, but noted that non-cancer effects (reproduction and sexual development, immune system) may pose a greater threat to human health. TCDD, the most toxic of the dibenzodioxins, is classified as a Group 1 carcinogen by the International Agency for Research on Cancer (IARC). TCDD has a half-life of approximately 8 years in humans, although at high concentrations, the elimination rate is enhanced by metabolism. The health effects of dioxins are mediated by their action on a cellular receptor, the aryl hydrocarbon receptor (AhR).
Exposure to high levels of dioxins in humans causes a severe form of persistent acne, known as chloracne. High occupational or accidental levels of exposures to dioxins have been shown by epidemiological studies to lead to an increased risk of tumors at all sites. Other effects in humans (at high dose levels) may include:
Recent studies have shown that high exposure to dioxins changes the ratio of male to female births among a population such that more females are born than males.
Dioxins accumulate in food chains in a fashion similar to other chlorinated compounds (bioaccumulation). This means that even small concentrations in contaminated water can be concentrated up a food chain to dangerous levels because of the long biological half life and low water solubility of dioxins.
Toxic effects in animals
While it has been difficult to establish specific health effects in humans due to the lack of controlled dose experiments, studies in animals have shown that dioxin causes a wide variety of toxic effects. In particular, TCDD has been shown to be teratogenic, mutagenic, carcinogenic, immunotoxic, and hepatotoxic. Furthermore, alterations in multiple endocrine and growth factor systems have been reported. The most sensitive effects, observed in multiple species, appear to be developmental, including effects on the developing immune, nervous, and reproductive systems. The most sensitive effects are caused at body burdens relatively close to those reported in humans.
Among the animals for which TCDD toxicity has been studied, there is strong evidence for the following effects:
The LD50 of dioxin also varies wildly between species with the most notable disparity being between the ostensibly similar species of hamster and guinea pig. The oral LD50 for guinea pigs is as low as 0.5 to 2 μg/kg body weight, whereas the oral LD50 for hamsters can be as high as 1 to 5mg/kg body weight, a difference of as much as thousandfold or more, and even among rat strains there may be thousandfold differences.
During the Vietnam war, between 1962 and 1971, the United States military sprayed 20,000,000 U.S. gallons (76,000,000L) of chemical herbicides and defoliants in Vietnam, eastern Laos and parts of Cambodia, as part of Operation Ranch Hand.
By 1971, 12% of the total area of South Vietnam had been sprayed with defoliating chemicals, which were often applied at rates that were 13 times as high as the legal USDA limit. In South Vietnam alone, an estimated 10 million hectares of agricultural land were ultimately destroyed. In some areas, TCDD concentrations in soil and water were hundreds of times greater than the levels considered safe by the U.S. Environmental Protection Agency.
According to Vietnamese Ministry of Foreign Affairs, 4.8 million Vietnamese people were exposed to Agent Orange, resulting in 400,000 people being killed or maimed, and 500,000 children born with birth defects. The Red Cross of Vietnam estimates that up to 1 million people are disabled or have health problems due to Agent Orange contamination. The United States government has challenged these figures as being unreliable and unrealistically high.
In 1963, a dioxin cloud escaped after an explosion in a Philips-Duphar plant (now Solvay Group) near Amsterdam. The plant was so polluted with dioxin after the accident that it had to be dismantled, embedded in concrete, and dumped into the ocean.
Between 1965 and 1968 production of 2,4,5-trichlorophenol in SpolanaNeratovice plant in Czechoslovakia seriously poisoned about 60 workers with dioxins; after 3 years of investigation of the health problems of workers, Spolana stopped manufacture of 2,4,5-T (most of which was supplied to the US military in Vietnam). Several buildings of the Spolana chemical plant were heavily contaminated by dioxins. Unknown amounts of dioxins were flushed into the Elbe and Mulde rivers during the 2002 European flood, contaminating soil. Analysis of eggs and ducks found dioxin levels 15 times higher than the EU limit and a high concentration of dioxin-like PCBs in the village of Libiš. In 2004, the state health authority published a study which analysed the level of toxic substances in human blood near Spolana. According to the study, dioxin levels in Neratovice, Libiš and Tišice were about twice the level of the control group in Benešov. The quantity of dioxins near Spolana is significantly higher than the background levels in other countries. According to the US EPA, even a background level can pose a risk of cancer from 1:10000 to 1:1000, about 100 times higher than normal. The consumption of local fish, eggs, poultry, and some produce was prohibited because of post-flood contamination.
Also during 1965 through 1968, Dr. Albert M. Kligman was contracted by the Dow Chemical Company to perform threshold tests for TCDD on inmates at Holmesburg Prison in Philadelphia after Dow studies revealed adverse effects on workers at Dow's Midland, Michigan, plant were likely due to TCDD. A subsequent test by Dow in rabbit ear models when exposed to 4–8μg usually caused a severe response. The human studies carried out in Holmesburg failed to follow Dow's original protocol and lacked proper informed consent by the participants. As a result of poor study design and subsequent destruction of records, the tests were virtually worthless even though ten inmates were exposed to 7,500μg of TCDD.
In 1976, large amounts of dioxins were released in an industrial accident at Seveso, Italy, although no immediate human fatalities or birth defects occurred.
A chemical plant Khimprom in Ufa, Russia released phenol into the water tributaries in the Spring of 1990. An investigation revealed previously classified disposal of dioxin in manufacturing 2,4,5-Trichlorophenoxyacetic_acid. The Spring 1990 accident affected 670,000 people. Dioxin was found in tap water. It was assumed that it resulted from chlorophenol produced by a reaction with chlorine in water purification.
Explosions resulting from the terrorist attacks on the US on September 11, 2001, released massive amounts of dust into the air. The air was measured for dioxins from September 23, 2001, to November 21, 2001, and reported to be "likely the highest ambient concentration that have ever been reported [in history]." The United States Environmental Protection Agency report dated October 2002 and released in December 2002 titled "Exposure and Human Health Evaluation of Airborne Pollution from the World Trade Center Disaster" authored by the EPA Office of Research and Development in Washington states that dioxin levels recorded at a monitoring station on Park Row near City Hall Park in New York between October 12 and 29, 2001, averaged 5.6 parts per trillion, or nearly six times the highest dioxin level ever recorded in the U.S. Dioxin levels in the rubble of the World Trade Centers were much higher with concentrations ranging from 10 to 170 parts per trillion. The report did no measuring of the toxicity of indoor air.
In a 2001 case study, physicians reported clinical changes in a 30-year-old woman who had been exposed to a massive dosage (144,000 pg/g blood fat) of dioxin equal to 16,000 times the normal body level; the highest dose of dioxin ever recorded in a human. She suffered from chloracne, nausea, vomiting, epigastric pain, loss of appetite, leukocytosis, anemia, amenorrhoea and thrombocytopenia. However, other notable laboratory tests, such as immune function tests, were relatively normal. The same study also covered a second subject who had received a dosage equivalent to 2,900 times the normal level, who apparently suffered no notable negative effects other than chloracne. These patients were provided with olestra to accelerate dioxin elimination.
In 2004, in a notable individual case of dioxin poisoning, Ukrainian politician Viktor Yushchenko was exposed to the second-largest measured dose of dioxins, according to the reports of the physicians responsible for diagnosing him. This is the first known case of a single high dose of TCDD dioxin poisoning, and was diagnosed only after a toxicologist recognized the symptoms of chloracne while viewing television news coverage of his condition.
In the early 2000s, residents of the city of New Plymouth, New Zealand, reported many illnesses of people living around and working at the Dow Chemical plant. This plant ceased production of 2,4,5-T in 1987.
DuPont has been sued by 1,995 people who claim dioxin emissions from DuPont's plant in DeLisle, Mississippi, caused their cancers, illnesses or loved ones' deaths; of these only 850 were pending as of June 2008. In August 2005, Glen Strong, an oyster fisherman with the rare blood cancer multiple myeloma, was awarded $14 million from DuPont, but the ruling was overturned June 5, 2008, by a Mississippi jury who found DuPont's plant had no connection to Mr. Strong's disease. In another case, parents claimed dioxin from pollution caused the death of their 8-year-old daughter; the trial took place in the summer of 2007, and a jury wholly rejected the family's claims, as no scientific connection could be proven between DuPont and the family's tragic loss. DuPont's DeLisle plant is one of three titanium dioxide facilities (including Edgemoor, Delaware, and New Johnsonville, Tennessee) that are the largest producers of dioxin in the country, according to the US EPA's Toxic Release Inventory. DuPont maintains its operations are safe and environmentally responsible.
In 2007, thousands of tonnes of foul-smelling refuse were piled up in Naples, Italy and its surrounding villages, defacing entire neighbourhoods. Authorities discovered that polychlorinated dibenzodioxins levels in buffalo milk used by 29 mozzarella makers exceeded permitted limits; after further investigation they impounded milk from 66 farms. Authorities suspected the source of the contamination was from waste illegally disposed of on land grazed by buffalo. Prosecutors in Naples placed 109 people under investigation on suspicion of fraud and food poisoning. Sales of Mozzarella cheese fell by 50% in Italy.
In December 2008 in Ireland dioxin levels in pork were disclosed to have been between 80 and 200 times the legal limit. All Irish pork products were withdrawn from sale both nationally and internationally.
In this case the dioxin toxicity was found to be mostly due to dioxin-like polychlorinated dibenzofurans and polychlorinated biphenyls, and the contribution from actual polychlorinated dibenzodioxins was relatively low. It is thought that the incident resulted from the contamination of fuel oil used in a drying burner at a single feed processor, with PCBs. The resulting combustion produced a highly toxic mixture of PCBs, dioxins and furans, which was included in the feed produced and subsequently fed to a large number of pigs.
According to data in 2009, in 2005 the production of dioxin by the steel industry ILVA in Taranto (Italy) accounted for 90.3 per cent of the overall Italian emissions, and 8.8 per cent of the European emissions.
German dioxin incident: In January 2011 about 4700 German farms were banned from making deliveries after self-checking of an animal feed producer had showed levels of dioxin above maximum levels. This incident appeared to involve PCDDs and not PCBs. Dioxins were found in animal feed and eggs in many farms. The maximum values were exceeded twofold in feed and maximally fourfold in some individual eggs. Thus the incident was minor as compared with the Belgian crisis in 1999, and delivery bans were rapidly cleared.
The analyses used to determine these compounds' relative toxicity share common elements that differ from methods used for more traditional analytical determinations. The preferred methods for dioxins and related analyses use high resolution gas chromatography/mass spectrometry (HRGC/HRMS). Concentrations are determined by measuring the ratio of the analyte to the appropriate isotopically labeled internal standard.
Also novel bio-assays like DR CALUX are nowadays used in identification of dioxins and dioxin-like compounds. The advantage in respect to HRGC/HRMS is that it is able to scan many samples at lower costs. Also it is able to detect all compounds that interact with the Ah-receptor which is responsible for carcinogenic effects.
Polychlorinated dibenzofurans (PCDFs) – A group of compounds, produced by the same conditions as dioxins and commonly co-present with dioxins in contamination incidents. They have the same toxic mode of action and are included in the toxic equivalent scheme for the purposes of assessing dioxin levels.
Chemetco – this former copper smelter is cited in an academic study as one of the 10 highest ranking sources of dioxin pollution reaching Nunavut in the Canadian Arctic
Polychlorinated biphenyls – A group of compounds historically used in the manufacture of electrical transformers certain members of which can also contribute to dioxin-like toxicity. These dioxin like compounds are also included in the toxic equivalent scheme when measuring dioxin levels.
Related Research Articles
A polychlorinated biphenyl (PCB) is an organic chlorine compound with the formula C12H10−xClx. Polychlorinated biphenyls were once widely deployed as dielectric and coolant fluids in electrical apparatus, carbonless copy paper and in heat transfer fluids.
The Seveso disaster was an industrial accident that occurred around 12:37 PM on July 10, 1976, in a small chemical manufacturing plant approximately 20 kilometres (12 mi) north of Milan in the Lombardy region of Italy. It resulted in the highest known exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in residential populations, which gave rise to numerous scientific studies and standardized industrial safety regulations. The EU industrial safety regulations are known as the Seveso II Directive. This accident was ranked eighth in a list of the worst man-made environmental disasters by Time magazine in 2010.
Chloracne is an acne-like eruption of blackheads, cysts, and pustules associated with exposure to certain halogenated aromatic compounds, such as chlorinated dioxins and dibenzofurans. The lesions are most frequently found on the cheeks, behind the ears, in the armpits and groin region.
Polybrominated diphenyl ethers or PBDEs, are a class of organobromine compounds that are used as flame retardants. Like other brominated flame retardants, PBDEs have been used in a wide array of products, including building materials, electronics, furnishings, motor vehicles, airplanes, plastics, polyurethane foams, and textiles. They are structurally akin to the polychlorinated biphenyls (PCBs) and other polyhalogenated compounds, consisting of two halogenated aromatic rings. PBDEs are classified according to the average number of bromine atoms in the molecule. The health hazards of these chemicals have attracted increasing scrutiny, and they have been shown to reduce fertility in humans at levels found in households. Their chlorine analogs are polychlorinated diphenyl ethers (PCDEs). Because of their toxicity and persistence, the industrial production of some PBDEs is restricted under the Stockholm Convention, a treaty to control and phase out major persistent organic pollutants (POPs).
The term flame retardants subsumes a diverse group of chemicals which are added to manufactured materials, such as plastics and textiles, and surface finishes and coatings. Flame retardants are activated by the presence of an ignition source and are intended to prevent or slow the further development of ignition by a variety of different physical and chemical methods. They may be added as a copolymer during the polymerisation process, or later added to the polymer at a moulding or extrusion process or applied as a topical finish. Mineral flame retardants are typically additive while organohalogen and organophosphorus compounds can be either reactive or additive.
Persistent organic pollutants (POPs), sometimes known as "forever chemicals" are organic compounds that are resistant to environmental degradation through chemical, biological, and photolytic processes. Because of their persistence, POPs bioaccumulate with potential adverse impacts on human health and the environment. The effect of POPs on human and environmental health was discussed, with intention to eliminate or severely restrict their production, by the international community at the Stockholm Convention on Persistent Organic Pollutants in 2001.
Xenoestrogens are a type of xenohormone that imitates estrogen. They can be either synthetic or natural chemical compounds. Synthetic xenoestrogens include some widely used industrial compounds, such as PCBs, BPA, and phthalates, which have estrogenic effects on a living organism even though they differ chemically from the estrogenic substances produced internally by the endocrine system of any organism. Natural xenoestrogens include phytoestrogens which are plant-derived xenoestrogens. Because the primary route of exposure to these compounds is by consumption of phytoestrogenic plants, they are sometimes called "dietary estrogens". Mycoestrogens, estrogenic substances from fungi, are another type of xenoestrogen that are also considered mycotoxins.
2,4,5-Trichlorophenoxyacetic acid, a synthetic auxin, is a chlorophenoxy acetic acid herbicide used to defoliate broad-leafed plants. It was developed in the late 1940s and was widely used in the agricultural industry until being phased out, starting in the late 1970s due to toxicity concerns. Agent Orange, a defoliant used by the British in the Malayan Emergency and the U.S. in the Vietnam War, was equal parts 2,4,5-T and 2,4-D. 2,4,5-T itself is toxic with a NOAEL of 3 mg/kg/day and a LOAEL of 10 mg/kg/day. Additionally, the manufacturing process for 2,4,5-T contaminates this chemical with trace amounts of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). TCDD is a carcinogenic persistent organic pollutant with long-term effects on the environment. With proper temperature control during production of 2,4,5-T, TCDD levels can be held to about .005 ppm. Before the TCDD risk was well understood, early production facilities lacked proper temperature controls and individual batches tested later were found to have as much as 60 ppm of TCDD.
This is a complete list of polychlorinated biphenyl (PCB) congeners.
1,4-Dioxin (also referred as dioxin or p-dioxin) is a heterocyclic, organic, non-aromatic compound with the chemical formula C4H4O2. There is an isomeric form of 1,4-dioxin, 1,2-dioxin (or o-dioxin). 1,2-Dioxin is very unstable due to its peroxide-like characteristics.
More thorough treatise of all groups with similar actions and binding to aryl hydrocarbon reeceptor is given in Dioxins and dioxin-like compounds.
Environmental toxicology is a multidisciplinary field of science concerned with the study of the harmful effects of various chemical, biological and physical agents on living organisms. Ecotoxicology is a subdiscipline of environmental toxicology concerned with studying the harmful effects of toxicants at the population and ecosystem levels.
Octachlorodibenzodioxin is one of polychlorinated dibenzodioxins (PCDDs).
Dioxins and dioxin-like compounds (DLCs) are a group of chemical compounds that are persistent environmental pollutants (POPs). Some of them are highly toxic, but the toxicity among them varies 30,000-fold. They are grouped together, because their mechanism of action is the same. They activate aryl hydrocarbon receptor, albeit with very different binding affinities, leading to high differences in toxicity and other effects. They are mostly by-products of burning or various industrial processes - or, in case of dioxin-like PCBs and PBBs, unwanted minor components of intentionally produced mixtures. They include:
Polyhalogenated compounds (PHCs) are any compounds with multiple substitutions of halogens. They are of particular interest and importance because they bioaccumulate in humans, and comprise a superset of which has many toxic and carcinogenic industrial chemicals as members. PBDEs, PCBs, dioxins (PCDDs) and PFCs are all polyhalogenated compounds. They are generally non-miscible in organic solvents or water, but miscible in some hydrocarbons from which they often derive.
Chlorinated polycyclic aromatic hydrocarbons (Cl-PAHs) are a group of compounds comprising polycyclic aromatic hydrocarbons with two or more aromatic rings and one or more chlorine atoms attached to the ring system. Cl-PAHs can be divided into two groups: chloro-substituted PAHs, which have one or more hydrogen atoms substituted by a chlorine atom, and chloro-added Cl-PAHs, which have two or more chlorine atoms added to the molecule. They are products of incomplete combustion of organic materials. They have many congeners, and the occurrences and toxicities of the congeners differ. Cl-PAHs are hydrophobic compounds and their persistence within ecosystems is due to their low water solubility. They are structurally similar to other halogenated hydrocarbons such as polychlorinated dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and polychlorinated biphenyls (PCBs). Cl-PAHs in the environment are strongly susceptible to the effects of gas/particle partitioning, seasonal sources, and climatic conditions.
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a polychlorinated dibenzo-p-dioxin with the chemical formula C 12H 4Cl 4O 2. Pure TCDD is a colorless solid with no distinguishable odor at room temperature. It is usually formed as an unwanted product in burning processes of organic materials or as a side product in organic synthesis.
Toxic equivalency factor (TEF) expresses the toxicity of dioxins, furans and PCBs in terms of the most toxic form of dioxin, 2,3,7,8-TCDD. The toxicity of the individual congeners may vary by orders of magnitude.
Persistent, bioaccumulative and toxic substances (PBTs) are a class of compounds that have high resistance to degradation from abiotic and biotic factors, high mobility in the environment and high toxicity. Because of these factors PBTs have been observed to have a high order of bioaccumulation and biomagnification, very long retention times in various media, and widespread distribution across the globe. Majority of PBTs in the environment are either created through industry or are unintentional byproducts.
1,2,3,4,6,7,8-Heptachlorodibenzo-para-dioxin (often referred to as 1,2,3,4,6,7,8-HpCDD) is a polychlorinated derivative of dibenzo-p-dioxin and can therefore be categorized as polychlorinated dibenzo-p-dioxin (PCDD), a subclass of dioxins which includes 75 congeners. HpCDD is the dibenzo-p-dioxin which is chlorinated at positions 1, 2, 3, 4, 6, 7, and 8. It is a polycyclic heterocyclic organic compound, since HpCDD contains multiple cyclic structures (two benzene rings connected by a 1,4-dioxin ring) in which two different elements (carbon and oxygen) are members of its rings. HpCDD has molecular formula C12HCl7O2 and is an off-white powder, which is insoluble in water.
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