1746-01-6 Usage
Uses
2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN has no known uses except for its application in research. It is an unintended byproduct of chemical manufacturing and combustion processes. There is no commercial manufacture of 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN. The limited production of 2,3,7,8-TCDD for research purposes involves condensation of polychlorophenol or, for this 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.
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.
Check Digit Verification of cas no
The CAS Registry Mumber 1746-01-6 includes 7 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 4 digits, 1,7,4 and 6 respectively; the second part has 2 digits, 0 and 1 respectively.
Calculate Digit Verification of CAS Registry Number 1746-01:
(6*1)+(5*7)+(4*4)+(3*6)+(2*0)+(1*1)=76
76 % 10 = 6
So 1746-01-6 is a valid CAS Registry Number.
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
1746-01-6Relevant academic research and scientific papers
Karademir, Aykan,Bakoglu, Mithat,Taspinar, Fatih,Ayberk, Savas
, p. 1201 - 1207 (2004)
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.
Molina,Diaz-Ferrero,Coll,Marti,Broto-Puig,Comellas,Rodriguez-Larena
, p. 1173 - 1178 (2000)
The evolution of polychlorinated dibenzo-p-dioxins (PCDD) and polychlorinated dibenzofurans (PCDF) in sewage sludge-amended soils used in the restoration of degraded lands, like quarries, has been studied. Two experiments were performed: one in the lab, under controlled conditions, and another in a quarry. Two different doses of sewage sludge were applied in both experiments (with two types of application in the quarry experiment) and the evolution of the amended soils were compared with that of the respective control soils (without addition of sewage sludge). The samples were analyzed with a previously validated method by HRGC-HRMS after the extraction and the necessary clean-up steps. The results reveal that polluted sewage sludge increases PCDD/F concentration in soils and that these compounds are persistent in the matrix after long periods of time. (C) 2000 Elsevier Science Ltd. The evolution of polychlorinated dibenzo-p-dioxins (PCDD) and polychlorinated dibenzofurans (PCDF) in sewage sludge-amended soils used in the restoration of degraded lands, like quarries, has been studied. Two experiments were performed: one in the lab, under controlled conditions, and another in a quarry. Two different doses of sewage sludge were applied in both experiments (with two types of application in the quarry experiment) and the evolution of the amended soils were compared with that of the respective control soils (without addition of sewage sludge). The samples were analyzed with a previously validated method by HRGC-HRMS after the extraction and the necessary clean-up steps. The results reveal that polluted sewage sludge increases PCDD/F concentration in soils and that these compounds are persistent in the matrix after long periods of time. Laboratory and field experiments were conducted in Spain to examine the evolution of PCDDs and PCDFs in sewage-sludge-amended soils. The PCDD/F concentrations were measured in the original sewage sludge and in soil samples over time. Results from the laboratory showed that the PCDD/F concentration in amended soils was related directly to the sewage-sludge dose applied. After 1 yr, however, no evolution of PCDD/Fs was observed in any sample. In the field, high dispersion was observed, which did not allow establishment of a concentration trend over time. (from Eighteenth Symp on Halogenated Environ Organic Pollutants-Dioxin '98, Stockholm, Sweden (Aug 17-21, 98)).
Buser,Rappe
, p. 2257 - 2262 (1980)
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.
Wunderli, Samuel,Zennegg, Markus,Dolezal, Ivan Samuel,Gujer, Erika,Moser, Urs,Wolfensberger, Max,Hasler, Philip,Noger, Dominik,Studer, Christoph,Karlaganis, Georg
, p. 641 - 649 (2000)
PCDD/PCDF were determined in solid samples from wood combustion. The samples included grate ashes, bottom ashes, furnace ashes as well as fly and cyclone ashes. The solid waste samples were classified into bottom and fly ash from native wood and bottom and fly ash from waste wood. For each of the four classes concentration distribution patterns from individual congeners, the sums of PCDD/PCDF and the international toxicity equivalents (I-TEQ) values are given. The I-TEQ levels of fly ash from waste wood burning can be approximately up to two thousand times higher than the values from fly ashes of natural wood. The I-TEQ levels in bottom ashes from waste wood combustion systems are as low as the corresponding ashes from the combustion of native wood. Grate ash samples from waste wood combustion systems with low carbon burnout show high levels of PCDD/PCDF.
Yang, Hee-Chul,Kim, Joon-Hyung
, p. 421 - 428 (2004)
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.
Buekens,Stieglitz,Hell,Huang,Segers
, p. 729 - 735 (2001)
In thermal metallurgical processes such as iron ore sintering and metal smelting operations, large flows of off-gases are generated. Mainly due to residue recycling in such processes, chlorine and volatile organics are always present in the feed. As a consequence of de novo formation, the off-gases from such processes typically contain dioxins in the range 0.3-30 ng I-TEQ/Nm3. So far there are only very few studies about the mechanisms of dioxin formation and destruction in these metallurgical processes. In an European Union (EU) research project Minimization of dioxins in thermal industrial processes: mechanisms, monitoring and abatement (MINIDIP) , integrated iron and steel plant has been selected as one of the industrial sectors for further investigation. A large number of particulate samples (feed, belt siftings, electrofilter) were collected from the iron ore sintering installations from various steel plants and analyzed for their organochlorocompound contents. Measurable amounts of PCDD/F, PCBz, PCB were found for all samples. The various parameters influencing their de novo synthesis activity were also evaluated in laboratory experiments, and such activity was found to be moderate for samples from the ore sinter belt, but extremely high for some ESP dusts. Fine dust is active in a wide range of temperatures starting at 200°C and declining above 450°C; the optimal temperature for de novo synthesis was found to be around 350°C; some inhibitors, such as triethanolamine, may reduce de novo activity by 50%, and lowering the O2 concentration in the gas stream leads to a much lower amount of PCDD/F formation. On the basis of their relative mass, typical operating conditions and specific activity of the different samples, the regions in the sintering plant where de novo synthesis may take place were tentatively established.
Wittsiepe, Juergen,Kullmann, Yvonne,Schrey, Petra,Selenka, Fidelis,Wilhelm, Michael
, p. 191 - 200 (1999)
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.
Pekarek,Grabic,Marklund,Puncochar,Ullrich
, p. 777 - 782 (2001)
The effect of oxygen-nitrogen atmosphere (N2 + 10%O2, N2 + 1%O2 and 99.999% N2) on the formation of PCB, PCDD and PCDF by the de novo synthetic reactions in the system consisting of extracted fly ash
Kim, Sam-Cwan,Jeon, Sung-Hwan,Jung, Il-Rok,Kim, Ki-Heon,Kwon, Myung-Hee,Kim, Jae-Hyung,Yi, Jun-Heung,Kim, Seung-Jin,You, Jae-Cheon,Jung, Dong-Hee
, p. 701 - 707 (2001)
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
Hatanaka, Takeshi,Kitajima, Akio,Takeuchi, Masao
, p. 73 - 79 (2004)
Combustion experiments in a laboratory-scale fluidized-bed reactor were performed to elucidate the role of copper chloride in formation of polychlorinated dibenzo-p-dioxins (PCDDs) and dibenzofurans (PCDFs) during model waste incineration. The amounts of PCDDs and PCDFs formed, the homologue profiles, and the isomer distributions were measured in the flue gas from incineration of model wastes containing various levels of copper. A correlation was found between the Cu content of the waste and the proportion of each congener. An increase in copper enhanced the formation of certain congeners, showing that copper acts as a catalyst for formation of PCDDs and PCDFs. An increase in the copper content of the waste decreased the CO concentration in the flue gas and reduced the formation of PCDDs and PCDFs during incineration. This indicates that copper also works as an oxidation catalyst to promote combustion, leading to lower concentrations of products of incomplete combustion. It is indispensable to consider both roles of the catalyst, i.e., enhancement and suppression, in the formation of PCDDs and PCDFs during waste incineration, which are estimated separately from the isomer distributions and the amounts of PCDDs and PCDFs formed.
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