1746-01-6

Basic information

• Product Name: 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN
• Synonyms: 2,3,6,7-Tetrachlorodibenzo-p-dioxin;2,3,7,8-Czterochlorodwubenzo-p-dwuoksyny;2,3,7,8-czterochlorodwubenzo-p-dwuoksyny(polish);2,3,7,8-TCDD;2,3,7,8-Tetrachlorodibenzo(b,e)(1,4)dioxan;2,3,7,8-tetrachlorodibenzo(b,e)(1,4)dioxin;2,3,7,8-Tetrachlorodibenzo[b,e][1,4]dioxin;2,3,7,8-Tetrachlorodibenzo-1,4-Dioxin
• CAS NO: 1746-01-6
• Molecular Formula: C₁₂H₄Cl₄O₂
• Molecular Weight: 321.97
• EINECS: 217-122-7
• Product Categories: Aromatics;Heterocycles
• Mol File: 1746-01-6.mol
• Article Data: 28

Chemical Properties

• Melting Point: 284-287°C
• Boiling Point: 407.62°C (rough estimate)
• Flash Point: 4 °C
• Appearance: /
• Density: 1.6430 (estimate)
• Vapor Pressure: 8.26E-07mmHg at 25°C
• Refractive Index: 1.6430 (estimate)
• Storage Temp.: Refrigerator
• Water Solubility: 0.0000000019 g/100 mL
• CAS DataBase Reference: 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN(CAS DataBase Reference)
• NIST Chemistry Reference: 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN(1746-01-6)
• EPA Substance Registry System: 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN(1746-01-6)

Safety Data

• Hazard Codes: F,Xn
• Statements: 11-38-48/20-63-65-67
• Safety Statements: 36/37-62-46
• RIDADR: 2811
• WGK Germany: 3
• HazardClass: 6.1(a)
• PackingGroup: I
• Hazardous Substances Data: 1746-01-6(Hazardous Substances Data)

Usage

Description

The term dioxins refers to chlorinated hydrocarbons containing a dibenzo-p-dioxin structure (two benzene rings conjoined at their para carbons by two oxygen molecules). The nomenclature for chlorinated dibenzodioxins (CDD) is based on the number and position of the chlorine molecules and include mono- (MCDD), di- (DCDD), tri- (TrCDD), tetra- (TCDD), penta- (PeCDD), hexa- (HxCDD), hepta- (HpCDD), and octachlorinated (OCDD) congeners. There are 75 congeners in total. The 2,3,7,8-tetrachlorodienzo-p-dioxin (2,3,7,8-TCDD) congener is the most familiar congener due in part to its toxicity in animal models, its widespread distribution and persistence in the environment, its bioaccumulation potential, and because most data pertain to this congener. Dioxins in pure form are colorless solids and are formed as combustion products. Dioxins may be formed during the combustion of organic material in the presence of halogens, especially chlorine (and bromine), during waste incineration and forest fires. They also occur as contaminants in herbicides. Dioxin was a contaminant of Agent Orange and possibly responsible for some of the adverse health effects associated with exposure to the defoliant. Dioxin was the poisoning agent in a high-profile political incident in 2004. Dioxin was ultimately identified as the cause of the disfiguring acne-like skin (chloracne) condition suffered by Ukrainian opposition leader Viktor Yushchenko a few months prior to the first presidential election. The suspicion was that the dioxin was placed into soup consumed by Mr Yushchenko. The acne-like skin condition is a recognized hallmark of dioxin poisoning in humans. The actual intake of dioxin in this incident is unknown.

Chemical Properties

Different sources of media describe the Chemical Properties of 1746-01-6 differently. You can refer to the following data:
1. White Solid
2. Tetrachlorodibenzo-p-dioxin is a white, needleshaped, crystalline solid.

Uses

Different sources of media describe the Uses of 1746-01-6 differently. You can refer to the following data:
1. A toxic polychlorinated dibenzo-p-dioxin detected in domestic meat and poultry.
2. With the exception of its use in research, it is ironic that there are no known uses for any of the dioxins. They are unintended byproducts of chemical manufacturing and combustion. There is no commercial manufacture of these compounds. The limited production of dioxins for use in research involves production by condensation of polychlorophenol or, for a specific dioxin, by chlorination of the parent dibenzo-p-dioxin.

Production Methods

2,3,7,8-TCDD is not commercially produced except for its use as a research chemical. 2,3,7,8-TCDDis a contaminant of 2,4,5-trichlorophenol (2,4,5-TCP), the herbicide 2-(2,4,5- trichlorophenoxy)propionic acid [Silvex], the herbicide 2,4,5-trichlorophenoxyacetic acid (2,4,5-T), the wood preservative pentachlorophenol, hexachlorophene, hexachlorobenzene, and polychlorodiphenyl ethers. 2,3,7,8-TCDD is also produced by incineration of municipal, hospital, and toxic wastes and sludges and wood that contain chlorinated compounds and materials, of polyvinylchloride containing plastics, by paper and pulp bleaching, during PCB electrical transformer fires, during the hot processes of dye and pigment manufacturing, and smelter emissions. It is not imported into the United States. The major source of 2,3,7,8-TCDDwas in the manufacture of 2,4,5-trichlorophenoxyacetic acid (2,4,5-T), which was introduced in the late 1940s. Prior to 1965, commercial 2,4,5-T contained up to 30 mg/kg (ppm) 2,3,7,8-TCDD but it was reduced to 0.01 ppm in the mid-1980s. Its use peaked in the 1970s, and has been phased out in Europe and the United States. The levels of 2,3,7,8-TCDD in the Vietnam War herbicide Agent Orange (1:1 mixture of the n-butyl esters of 2,4,5-T and (2,4-dichlorophenoxy)acetic acid (2,4-D)) varied considerably from 0.02 to 47 mg/kg (ppm). In the 1960s, the level of 2,3,7,8-TCDD could have been as high as 100 mg/kg in Agent Orange. In the 1980s, all producers claimed that 2,3,7,8-TCDD concentrations were less than 0.1 mg/kg. 2,3,7,8-TCDD and other PCDDs are formed by hot industrial, thermal, and photochemical processes that involve chlorinated organics.

General Description

White crystals or tan crystalline powder.

Air & Water Reactions

Insoluble in water.

Reactivity Profile

2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN reaacts when exposed to ultraviolet light in solution in isooctane or n-octanol. Undergoes catalytic perchlorination .

Health Hazard

Chlorinated dibenzo-p-dioxins (CDDs) cause chloracne, may cause hepatotoxicity, immunotoxicity, reproductive toxicity, developmental toxicity, and central nervous system toxicity, and are considered to be a human carcinogen. The most obvious health effect in humans for exposure to CDDs is chloracne, a severe skin disease characterized by follicular hyperkeratosis (comedones) occurring with or without cysts and pustules.2–4 Unlike adolescent acne, chloracne may affect almost every follicle in an involved area, and it may be more disfiguring than adolescent acne.

Fire Hazard

Literature sources indicate that 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN is nonflammable.

Pharmacology

TCDD and other chlorinated dibenzodioxins, dibenzofurans, and planar PCBs are thought to operate through a common mechanism. For humans and rodents, there is an initial binding to the aryl hydrocarbon (Ah) receptor. Binding to the receptor is a necessary (but not sufficient) event for the biological response. TCDD induces many responses, including induction of gene expression, altered metabolism, altered cell growth and differentiation, and disruption of steroid hormone and growth factor signal transduction pathways. The very diversity of tissue-selective and species-selective responses elicited by TCDD requires that the receptor (Ah) is part of a multicomponent system, and it is unlikely that the differences in dose-response are related solely to differences in Ah receptor concentrations or affinities in various species or tissues (29). It is considered that there is an inducible protein-binding site in the liver (30,31) known as CYP1A1 (30–34) because TCDD was not sequestered in the liver of transgenic mice that lack P450 1A2 gene.

Safety Profile

Confirmed carcinogen with experimental carcinogenic, neoplastigenic, tumorigenic, and teratogenic data. One of the most toxic synthetic chemicals. A deadly experimental poison by ingestion, skin contact, and intraperitoneal routes. Human systemic effects by skin contact: allergic dermatitis. Experimental reproductive effects. Human mutation data reported. An eye irritant. TCDD is the most toxic member of the 75 dioxins. It causes death in rats by hepatic cell necrosis. Death can follow a lethal dose by weeks. Acute and subacute exposure result in wasting, hepatic necrosis, thymic atrophy, hemorrhage, lymphoid depletion, chloracne. A by-product of the manufacture of polychlorinated phenols. It is found at low levels in 2,4,5-T, 2,4,5-trichlorophenol, and hexachlorophene. It is also formed during various combustion processes. Incineration of chemical wastes, including chlorophenols, chlorinated benzenes, and biphenyl ethers, may result in the presence of TCDD in flue gases, fly ash, and soot particles. It is immobile in contaminated soil and may be retained for years. TCDD has the potential for bio-accumulation in animals. An accident in Seveso, Italy, and inadvertent soil contamination in Mmouri have resulted in abandonment of the contaminated areas. When heated to decomposition it emits toxic fumes of Cl-.

Potential Exposure

TCDD is primarilly a research chemical. As noted above, TCDD is an inadvertent contaminant in herbicide precursors and thus in the herbicides themselves. It is also formed during various combustion processes including the incineration of chemical wastes (chlorophenols, chlorinated benzenes, and biphenyl ethers). It may be found in flue gases, fly ash, and soot particles. It is highly persistent in soil, and contamination may be retained for years. TCDD is the most toxic of all the dioxins, and has the potential for bio-accumulation in animals. Thus, it is applied in herbicide formulations, but is not used per se. It has been estimated that approximately 2 million acres in the United States have been treated for weed control on one or more occasions with approximately 15 million pounds of TCDD contaminated 2,4,5,-T, 2,4,-D, or combinations of the two.

Carcinogenicity

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is known to be a human carcinogen based on sufficient evidence of carcinogenicity from studies in humans, both epidemiological and on the mechanism of carcinogenesis. TCDD was first listed in the Second Annual Report on Carcinogens as reasonably anticipated to be a human carcinogen. Subsequently, a number of studies were published that examined cancer in human populations exposed to TCDD occupationally or through industrial accidents. A concerted research effort examined the molecular and cellular events that occur in tissues of humans and animals exposed to TCDD. Based on the new information, the listing was revised to known to be a human carcinogen in the January 2001 addendum to the Ninth Report on Carcinogens.

Source

Although not produced commercially, TCDD is formed as a by-product in the synthesis of 2,4,5-trichlorophenol. TCDD was found in 85% of soil samples obtained from a trichlorophenol manufacturing site. Concentrations ranged from approximately 20 ng/kg to 600 g/kg (Van Ness et al., 1980). TCDD may be present in the herbicide 2,4-D which contains a mixture of dichloro-, trichloro-, and tetrachlorodioxins. TCDD is commonly found as a contaminant associated with pulp and paper mills (Boddington, 1990). In addition, during the manufacture of 2,4,5-T and silvex from trichlorophenol, TCDD was found at concentrations averaging 20 parts per billion (Newton and Snyder, 1978). TCDD is unintentionally formed during the combustion of domestic and industrial waste (Czuczwa and Hites, 1984, 1986) and bleaching of paper pulp by chlorine compounds (Buser et al., 1989; Swanson et al., 1988). Drinking water standard (final): MCLG: zero; MCL: 3 x 10-5 μg/L (U.S. EPA, 2000). In Canada, the Ontario Ministry of Environment has established an Interim Drinking Water Objective of 10 parts per quadrillion (Boddington, 1990). In addition, the U.S. EPA (2000) recommended a DWEL of 4 x 10-5 μg/L.

Environmental fate

Biological. After a 30-d incubation period, the white rot fungus Phanerochaete chrysosporium was capable of oxidizing TCDD to carbon dioxide. Mineralization began between the third and sixth day of incubation. The production of carbon dioxide was highest between 3 to 18 d of incubation, after which the rate of a carbon dioxide produced decreased until the 30th day. It was suggested that the metabolism of TCDD and other compounds, including p,p′-DDT, benzo[a]pyrene, and lindane, was dependent on the extracellular lignin-degrading enzyme system of this fungus (Bumpus et al., 1985). A half-life of 418 d was calculated based on die away test data (Kearney et al., 1971). In a laboratory sediment-water system incubated under anaerobic conditions, the half-life of TCDD was 500 to 600 d (Ward and Matsumura, 1978). Soil. In shallow and deep soils, reported half-lives were 10 and 100 yr, respectively (Nauman and Schaum, 1987). Due to its low aqueous solubility, TCDD will not undergo significant leaching by runoff (Helling et al., 1973). Surface Water. Plimmer et al. (1973) reported that the photolysis half-life of TCDD in a methanol solution exposed to sunlight was 3 h. Volatilization half-lives of 32 and 16 d were reported for lakes and rivers, respectively (Podoll et al., 1986). Photolytic. Pure TCDD did not photolyze under UV light. However, in aqueous solutions containing cationic (1-hexadecylpyridinium chloride), anionic (sodium dodecyl sulfate), and nonionic (methanol) surfactants, TCDD decomposed into the end product tentatively identified as 2-phenoxyphenol. The times required for total TCDD decomposition using the cationic, anionic, and nonionic solutions were 4, 8, and 16 h, respectively (Botré et al., 1978). TCDD photodegrades rapidly in alcoholic solutions by reductive dechlorination. In water, however, the reaction was very slow (Crosby et al., 1973). In an earlier study, Crosby et al. (1971) reported a photolytic halflife of 14 d when TCDD in distilled water was exposed to sunlight. The major photodegradative pathway of TCDD involves a replacement of the chlorine atom by a hydrogen atom. The proposed degradative pathway is TCDD to 2,7,8-trichlorodibenzo[b,e][1,4]dioxin to 2,7-dichlorodibenzo- [b,e][1,4]dioxin to 2-chlorodibenzo[b,e][1,4]dioxin to dibenzo[b,e][1,4]dioxin to 2-hydroxydiphenyl ether, which undergoes polymerization (Makino et al., 1992). Chemical/Physical. TCDD was dehalogenated by a solution of poly(ethylene glycol), potassium carbonate, and sodium peroxide. After 2 h at 85 °C, >99.9% of the applied TCDD decomposed. Chemical intermediates identified include tri-, di-, and chloro[b,e]dibenzo[1,4]dioxin, dibenzodioxin, hydrogen, carbon monoxide, methane, ethylene, and acetylene (Tundo et al., 1985). TCDD will not hydrolyze to any reasonable extent (Kollig, 1993).

Metabolism

Absorption. TCDD is retained in all tissues. The highest retention is in fat and liver. Penetration values into human skin are low. For example, a dose of 6.5 ng/cm2 in acetone gave a rate of 5 g/cm2/h. Transfer to the fetus has been observed (43). Absorption rates after single dose in the diet were 50 to 70–90% (44–48). Rates in rats were lower (50–60%) when administered in the diet for more than 6 weeks (49), compared with a single-dose absorption rate of 70% (46). Distribution. The major storage sites are liver and adipose tissue. The skin can act as an important storage site, and high concentrations can also be found in the adrenals (1). After one day of exposure for rats, mice, hamsters and guinea pigs, 25–70% of the dose was stored in the liver (41). Excretion. Excretion is mostly fecal. Breast milk can be a route of elimination. Whole body half-lives were from 17 to 31 days in rat studies (46–52). Mice had lower halflives (53,54). Female rhesus monkeys with four years of dietary exposure had a longer half-life (391 days) (55,56). These half-lives are very fast considering human half-lives of 5.8–11.3 years (cited earlier).

Solubility in organics

Acetone (110 mg/L), benzene (570 mg/L), chlorobenzene (720 mg/L) chloroform (370 mg/L), o-dichlorobenzene (1,400 mg/L), methanol (10 mg/L) and octanol (48–50 mg/L) (Crummett and Stehl, 1973; Arthur and Frea, 1989); benzene (570 mg/L), tetrachloroethene (680 mg/L), lard oil (40 mg/L), hexane (280 mg/L) (quoted, Keith and Walters, 1992).

Solubility in water

Acetone (110 mg/L), benzene (570 mg/L), chlorobenzene (720 mg/L) chloroform (370 mg/L), o-dichlorobenzene (1,400 mg/L), methanol (10 mg/L) and octanol (48–50 mg/L) (Crummett and Stehl, 1973; Arthur and Frea, 1989); benzene (570 mg/L), tetrachloroethene (680 mg/L), lard oil (40 mg/L), hexane (280 mg/L) (quoted, Keith and Walters, 1992).

Toxicity evaluation

Mortality Mortality occurs after several days to weeks of exposure. Toxic effects observed in all animal species are progressive loss of body weight, reduced intake of food, atrophy of the thymus, gastrointestinal hemorrhage, and delayed lethality (17,18). Skin Skin effects are exhibited by humans and non human primates and are not modeled by laboratory animals, although some experimentation has been performed with hairless mice. Cachexia All mammalian species show body weight loss and reduced intake of food. Studies by Pohjanvirta and Tuomisto (19) indicated that TCDD may suppress the formation of hunger-related signals. A serotonergic mechanism was proposed because of increased levels of tryptophan and its metabolites, serotonin and 5-hydroxyindoleacetic acid, in blood and brain. Endocrine effects A variety of hormone systems are involved with exposure to TCDD, specifically, sex steroids, corticosteroids, and thyroid hormones. A target organ for TCDD is the pituitary gland where normal feedback mechanisms are disrupted (20). Immunological Effects Immunological effects are observed in mammals but are probably without relevance for humans.

Incompatibilities

Decomposes in ultraviolet (UV) light.

InChI:InChI=1/C12H4Cl4O2/c13-5-1-9-10(2-6(5)14)18-12-4-8(16)7(15)3-11(12)17-9/h1-4H

Upstream product

• 262-12-4 dioxin 
• 39227-28-6 1,2,3,4,7,8-hexachlorodibenzodioxin 
• 133-06-2 captan 
• 108-90-7 chlorobenzene 
• 9004-34-6 cellulose 
• 1878-66-6 4-chlorophenylacetic Acid 
• 120-83-2 2,4-dichlorophenol 
• 127-18-4 1,1,2,2-tetrachloroethylene 
• 95-95-4 2,4,5-trichlorophenol 
• 67-66-3 chloroform 
• 7553-56-2 iodine 
• 7782-50-5 chlorine 

Downstream Products

• 262-12-4 dioxin 
• 19408-74-3 1,2,3,6,7,8-hexachlorodibenzodioxin 
• 35822-46-9 HpCDD 1234678 
• 3268-87-9 1,2,3,4,6,7,8,9-octachlorodibenzodioxin 
• 18268-81-0 4,5-dichloro-1,2-benzoquinone 
• 33857-28-2 2,3,7-trichlorodibenzodioxin 
• 33857-26-0 2,7-dichloro-dibenzo[1,4]dioxine 
• 933-75-5 2,3,6-trichlorophenol 
• 100-52-7 benzaldehyde 
• 615-13-4 2-indanone 
• 88-06-2 2,4,6-Trichlorophenol 

Relevant articles and documents

Removal of PCDD/Fs from Flue Gas by a Fixed-Bed Activated Carbon Filter in a Hazardous Waste Incinerator

The adsorption of polychlorinated dibenzodioxins and dibenzofurans (PCDD/Fs) by activated carbon (AC) was examined in a fixed-bed AC unit in a hazardous waste incinerator (IZAYDAS) in Turkey. Results showed that the removal efficiencies of PCDD/Fs decrease as the chlorination level increases, which was explained by the difference in gas/particle partitioning of the compounds. Since dioxins are tightly adsorbed by activated carbon, other flue gas constituents showed no clear effect on the dioxin removal. Adsorption kinetics indicated that the adsorption of volatile congeners and homologues fits well with Henry's law, possibly due to the higher gaseous fractions, while the correlation was lower for lowly volatile ones. PCDD/F congeners and homologues had a concentration value up to which no adsorption occurred, which could be attributed to the insufficient contact times at the low concentrations.

High-resolution gas chromatography of the 22 tetrachlorodibenzo-p-dioxin isomers

The 22 tetrachlorodibenzo-p-dioxins (TCDDs) were synthesized in microgram quantities by a simple pyrolysis procedure from different potassium chlorophenates. The separation of these TCDD isomers was studied on high-resolution glass capillary columns with different stationary phases (Silar 10c, OV-17, OV-101) and by use of mass spectrometric detection. Conditions were found that allowed the unambiguous assignment of many of these isomers, including the very toxic 2378-TCDD. The determination of the various TCDD isomers is illustrated in the analysis of samples from known contaminated areas in Seveso, Italy, and in eastern Missouri, and the method is also applied to the analysis of fish from the Tittabawassee River in Michigan and fly ash samples from municipal incinerators in Switzerland.

Characteristics of dioxins and metals emission from radwaste plasma arc melter system

This study investigated the emission characteristics of PCDD/Fs and the partitioning of three heavy metals (Cd, Hg and Pb) and two radioactive metal surrogates (Co and Cs) in a radwaste plasma arc melter system. Typical mixtures of low-level radioactive wastes were simulated as the trial burn surrogate wastes. The emission of PCDD/Fs and the partitioning of the metals were strongly influenced by the feed waste stream and melter operating temperature, respectively. The emissions of PCDD/Fs, cadmium and lead were greatly enhanced when the polyvinyl chloride was included in the feed waste stream. Most of the nonvolatile cobalt partitioned into the glass. A significant quantity of cesium, cadmium and lead was vaporized during the highest melter temperature test. A lower melter temperature resulted in more cesium, cadmium and lead species remaining in the glass. The results of this study suggest that wet scrubbing as well as a low-temperature two-step fine filtration, or both of them together could not effectively capture the gas-phase or fine particle phase PCDD/Fs and mercury species. In order to effectively treat low-level radioactive waste streams, the tested high-temperature melter should include an adsorption system, which could collect the gas-phase PCDD/Fs and mercury species.

Peroxidase-catalyzed in vitro formation of polychlorinated dibenzo-p-dioxins and dibenzofurans from chlorophenols

Chlorophenols (CP) are transformed in vitro to polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/F) by a peroxidase-catalyzed oxidation. This is shown for 2,4,5-tri-, 2,3,4,6-tetra- and pentachlorophenol with plant horseradish peroxidase and with myeloperoxidase recovered from human leukocytes, each in the presence of hydrogen peroxide. The yield, the reaction and the PCDD/F-pattern found are dependent on the CP. The amounts of PCDD/F formed within 4 or 24 h are in the μmol/mol-range for all substrates and both peroxidases. The experiments suggest that biochemical formation of PCDD/F from precursors such as CPs can take place in the human body and that this metabolic pathway may lead to a higher inner exposure to PCDD/F than up to now assumed based on intake data for PCDD/F. Copyright (C) 1999 Elsevier Science Ireland Ltd.

Formation and emission status of PCDDS/PCDFS in municipal solid waste incinerators in korea

This study was carried out to examine the formation and the emission status of polychlorinated dibenzo-p-dioxins/ polychlorinated dibenzofurans (PCDDs/PCDFs) in the flue gases of commercial-scale municipal solid waste (MSW) incinerators, and thus to provi

Reactions of dibenzofuran and 1,2,3,4,7,8-hexachlorodibenzo-p-dioxin on municipal waste incinerator fly ash

Dibenzofuran (DF) on fly ash can be converted to polychlorinated dibenzofurans (PCDF)in a N2/O2/HCl atmosphere, yielding especially 2,3,7,8- substituted congeners. This is consistent with an electrophilic aromatic substitution mechanism. 1,2,3,4,7,8-Hexa-chlorodibenzo-p-dioxin (1,2,3,4,7,8- H6CDD) on fly ash can be chlorinated by HCl both in N2 and O2 atmospheres. Dechlorination and decomposition reactions are not important under these conditions, and isomerization reactions do not take place either. 1,2,3,4,7,8-H6CDD dechlorinates or decomposes on fly ash when no HCl is present. Only a limited number of dechlorination products are formed. Chlorination and dechlorination are separate processes, not occurring simultaneously.

Formation of dioxins in the catalytic combustion of chlorobenzene and a micropollutant-like mixture on Pt/γ-Al2O3

Catalytic combustion over a 2 wt % Pt/γ-Al2O3 catalyst of chlorobenzene (PhCl) and of a micropollutant-like mixture representative for a primary combustion offgas has been investigated. Typical conditions were 1000-1500 ppm of organics in the inflow, contact times ～0.3 s, 16% O2 in nitrogen at ～1 bar, and temperature range 200-550 °C. PhCl reacts considerably slower than when processing Cl-free compounds such as heptane. At intermediate temperatures-and incomplete conversion-byproducts are formed, especially polychlorobenzenes (PhCl x). These are accompanied by polychlorinated dibenzo-p-dioxins (PCDDs) and dibenzofurans (PCDFs) at levels of about 10-6 relative to PhClx. Additional HCl-made by co-reacting PhCl with tert-butylchloride-leads to much higher levels of PhClx and PCDD/Fs. Using the micropollutant-like mixture, the total chlorine input is reduced almost 20-fold, but it nevertheless leads to a 30-fold higher PCDD/F output. This is ascribed to reaction of the small amounts of (chloro)phenols in the mixture. The congener/isomer patterns of the PCDD/Fs for the mixture and with PhCl per se are quite comparable with those found in emissions from incinerators. As carbon is not present nor formed on the catalyst surface, de-novo formation therefrom cannot be involved. Rather condensation of phenolic entities or like precursors must have occurred. Consequences and options to ensure safe application are briefly discussed as well.

Catalytic NOx reduction with simultaneous dioxin and furan oxidation.

The engineering, construction, performance and running costs of a catalytic flue gas cleaning component in the low dust area of a municipal waste incinerator is discussed. For this purpose, the case study of a Flemish incineration plant is presented, covering the history, the design procedure of the catalyst, relevant process data and the financial aspects. A reliable PCDD/F-destruction by means of oxidation by the catalyst to typical values of 0.001 ng TEQ/Nm3 has been demonstrated. At the same time, NOx- and CO-emissions are reduced by 90% and 20% to about 50 mg/Nm3 and below 10 mg/Nm3, respectively.

Polychlorinated dibenzo-p-dioxin/polychlorinated dibenzofuran releases into the atmosphere from the use of secondary fuels in cement kilns during clinker formation

The aim of this study was to evaluate the influence of using waste materials, such as tires or meat meal, as a secondary fuel during clinker production on the polychlorinated dibenzo-p-dioxin (PCDD)/polychlorinated dibenzofuran (PCDF) emission levels to the atmosphere. For this purpose, three different cement plants in Spain were chosen to conduct the project in different sampling episodes. Different materials were separately evaluated in each plant: the first plant included the addition of meat meal in the kiln, the second plant used rejected tires, and the third plant used a mixture of both. In all cases, PCDD/F emission values remained below the limit established by the European Union Directive of 0.1 ng I-TEQ/Nm3, with values ranging from 0.001 to 0.042 ng I-TEQ/Nm3. The major contribution to total TEQ in the majority of cases came from 2,3,7,8-tetrachlorodibenzofuran owing to its relatively higher levels and 2,3,4,7,8-pentachlorodibenzofuran because of its TEF of 0.5. The remaining 15 toxic congeners collectively provided only a minor contribution to TEQ. Furthermore, no marked differences were found compared with reported data obtained from Spanish cement kiln plants using conventional fuel. This fact indicates that the addition of used tires or meat meals had no effect on PCDD/ PCDF emission levels.

Emission factors and importance of PCDD/Fs, PCBs, PCNs, PAHs and PM 10 from the domestic burning of coal and wood in the U.K.

This paper presents emission factors (EFs) derived for a range of persistent organic pollutants (POPs) when coal and wood were subject to controlled burning experiments, designed to simulate domestic burning for space heating. A wide range of POPs were emitted, with emissions from coal being higher than those from wood. Highest EFs were obtained for particulate matter, PM10, (～ 10 g/kg fuel) and polycyclic aromatic hydrocarbons (～ 100 mg/ kg fuel for ΣPAHs). For chlorinated compounds, EFs were highest for polychlorinated biphenyls (PCBs), with polychlorinated naphthalenes (PCNs), dibenzo-p-dioxins (PCDDs) and dibenzofurans (PCDFs) being less abundant. EFs were on the order of 1000 ng/kg fuel for ΣPCBs, 100s ng/ kg fuel for ΣPCNs and 100 ng/kg fuel for ΣPCDD/Fs. The study confirmed that mono- to trichlorinated dibenzofurans, Cl1,2,3DFs, were strong indicators of low temperature combustion processes, such as the domestic burning of coal and wood. It is concluded that numerous PCB and PCN congeners are routinely formed during the combustion of solid fuels. However, their combined emissions from the domestic burning of coal and wood would contribute only a few percent to annual U.K. emission estimates. Emissions of PAHs and PM 10 were major contributors to U.K. national emission inventories. Major emissions were found from the domestic burning for Cl1,2,3DFs, while the contribution of PCDD/F-ΣTEQ to total U.K. emissions was minor.