1,2,3,7,8,9-hexachlorodibenzo-p-dioxin is a light pink crystalline solid. (NTP, 1992)
蒸汽压力：
4.88X10-11 mm Hg @ 25 °C
稳定性/保质期：
This compound is stable under normal laboratory conditions. Solutions may be sensitive to light. Solutions of this chemical in water, DMSO, 95% ethanol or acetone should be stable for 24 hours under normal lab conditions.
Little is known about the metabolism of these compounds in mammalian systems. The half-life of some of these compounds in humans can be measured not in hours, days, weeks, or months, but in years. /Polychlorodibenzodioxins/
CDDs are absorbed through oral, inhalation, and dermal routes of exposure. CDDs are carried in the plasma by serum lipids and lipoproteins, distributing mainly to the liver and adipose tissue. CDDs are very slowly metabolized by the microsomal monooxygenase system to polar metabolites that can undergo conjugation with glucuronic acid and glutathione. They may increase the rate of their own metabolism by inducing both phase I and phase II enzymes. The major routes of excretion of CDDs are the bile and the faeces, though smaller amounts are excreted in the urine and via lactation. (L177)
CDDs cause their toxic effects by binding to the aryl hydrocarbon receptor and subsequently altering the transcription of certain genes. The affinity for the Ah receptor depends on the structure of the specific CDD. The change in gene expression may result from the direct interaction of the Ah receptor and its heterodimer-forming partner, the aryl hydrocarbon receptor nuclear translocator, with gene regulatory elements or the initiation of a phosphorylation/dephosphorylation cascade that subsequently activates other transcription factors. The affected genes include several oncogenes, growth factors, receptors, hormones, and drug-metabolizing enzymes. The change in transcription/translation of these genes is believed to be the cause of most of the toxic effects of CDDs. (L177)
来源:Toxin and Toxin Target Database (T3DB)
毒理性
致癌性证据
分类：B2；可能的人类致癌物。分类依据：小鼠和大鼠经灌胃引起的肝脏肿瘤。人类致癌性数据：无。
CLASSIFICATION: B2; probable human carcinogen. BASIS FOR CLASSIFICATION: Hepatic tumors in mice and rats by gavage. HUMAN CARCINOGENICITY DATA: None.
Evaluation: There is limited evidence in experimental animals for the carcinogenicity of a mixture of 1,2,3,6,7,8- and 1,2,3,7,8,9-hexachlorodibenzo-para-dioxins. Other polychlorinated dibenzo-para-dioxins are not classifiable as to their carcinogenicity to humans (Group 3). /Polychlorinated dibenzo-para-dioxins/
来源:Hazardous Substances Data Bank (HSDB)
毒理性
致癌物分类
3, 其对人类致癌性无法分类。
3, not classifiable as to its carcinogenicity to humans. (L135)
Exposure to large amounts of CDDs causes chloracne, a severe skin disease with acne-like lesions that occur mainly on the face and upper body. CDDs may also cause liver damage and induce long-term alterations in glucose metabolism and subtle changes in hormonal levels. In addition, studies have shown that CDDs may disrupt the endocrine system and weaken the immune system, as well as cause reproductive damage and birth defects, central and peripheral nervous system pathology, thyroid disorders, endometriosis, and diabetes. (L177, L178)
The polychlorinated dibenzo-p-dioxins and the polychlorinated dibenzofurans are predominantly stored in fat, but they are also excreted in milk and pass the placenta. They also appear in the blood and vital organs at lower concentrations. /Polychlorinated dibenzo-p-dioxins/
...The role of dietary fiber or Chlorella in the fecal excretion of PCDDs and PCDFs in rats /was investigated/. Rice bran fibers enhanced the fecal excretion of PCDDs form 0.6 to 2.3 and of PCDFs from 0.5- to 10.4 fold above that of rats on a control diet. Chlorella is a unicellular green algae sold as a health food or health supplement. Chlorella in the diet of rats also enhanced the fecal excretion of PCDDs from 0.8 to 5.6 and PCDFs from 0.9- to 11.1-fold above that of rats on a control diet. Dietary fiber, chlorophyll, and /or lipid in the Chlorella may be factors responsible for the enhanced fecal excretion of PCDDs and PCDFs observed in this study. Thus, fiber and/or Chlorella may be other dietary factors capable of increasing the fecal excretion of PCDDs and PCDFs. /Polychlorinated dibenzo-p-dioxins and dibenzofurans/
In general, absorption is vehicle-dependent and congener-specific. Passage across the intestinal wall is predominantly limited by molecular size and solubility. These parameters are most significant for hepta- and octachlorinated congeners, which exhibit decreased absorption in mammals. The predominant CDD carriers in human plasma are serum lipids and lipoproteins, but chlorine substitution plays a role in the distribution in these fractions. For most mammalian species, the liver and adipose tissue are the major storage sites of CDDs; in some species, skin and adrenals also can act as primary deposition sites. 2,3,7,8-Substituted CDDs are the predominant congeners retained in tissues and body fluids. Tissue deposition is congener-specific and depends on the dose, the route of administration, and age. CDDs are very slowly metabolized by the microsomal monooxygenase system to polar metabolites that can undergo conjugation with glucuronic acid and glutathione. The major routes of excretion of CDDs are the bile and the feces; smaller amounts are excreted via the urine. In mammalian species, lactation is an effective way of eliminating CDDs from the liver and other extrahepatic tissues. /Chlorinated dibenzo-p-dioxins/
来源:Hazardous Substances Data Bank (HSDB)
吸收、分配和排泄
大多数实验性组织分布和消除数据是在暴露于单一同类物后获得的，而实际环境中对TCDD及其相关化合物的暴露则是由多种同类物组成的复杂混合物。研究了雄性和雌性绒猴的肝脏和脂肪组织中各种PCDDs和PCDFs的持久性。动物单次皮下暴露于一定量的PCDD/PCDF混合物（总剂量为27,800 ng/kg体重），其中包含120 ng TCDD/kg体重。使用现在有些过时的国际TCDD毒性当量（I-TE）因子，总给药剂量相当于464 ng I-TE/kg体重。在暴露后1、6、16或28周测量了肝脏和脂肪组织中特定同类物的浓度。所有2,3,7,8-取代的PCDDS和PCDFs在绒猴的脂肪组织中普遍比肝脏中更持久。通常，脂肪组织中的持久性大约是肝脏的1.3-2.0倍，除了1,2,3,4,7,8-/1,2,3,4,7,9-六CDF、七CDF和OCDF，这些在脂肪组织中的持久性是肝脏的三倍多。对于后者和OCDD，半衰期值有显著差异，这可能是由于特别持久的同类物吸收延迟和不完全，以及相对较短（28周）的调查期。在暴露后一周，与2,3,7,8-取代的同类物相比，非2,3,7,8-取代的PCDDs和PCDFs在肝脏和脂肪组织中的含量相对较少；然而，非2,3,7,8-取代的化合物在暴露混合物中占有相当大的百分比。在本研究中，通过气相色谱/质谱法无法在肝脏中检测到任何非2,3,7,8-取代的TCDDs、五氯二苯并对二恶英、TCDFs或五氯二苯并呋喃。一些六氯和七氯同类物在脂肪组织和肝脏中被检测到，但在一周后，肝脏中的总量仅占给药剂量的5%以上的情况是1,2,4,6,8,9-六CDF。在大鼠暴露于一定量的PCDDs和PCDFs的复杂混合物后，也得到了类似的结果。大鼠的额外短期研究提供了证据，表明在暴露后一周测量的非2,3,7,8-取代同类物的低组织浓度是由于快速消除，因为在大约13到14小时后，这些同类物在肝脏中的检测水平更高。这些在猴子和大鼠中的结果与人类组织样本和牛奶的分析数据相兼容，其中非2,3,7,8-取代的同类物也没有显示出与2,3,7,8-取代的同类物相比有显著浓度。/多氯二苯并-p-二恶英和二苯并呋喃/
Most experimental tissue distribution and elimination data are obtained after exposure to a single congener, while real-world exposure to TCDD and related compounds occurs as a complex mixture of congeners. ...The persistence of various PCDDs and PCDFs in hepatic and adipose tissue of male and female marmoset monkeys /was examined/. Animals received a single subcutaneous exposure to a defined PCDD/PCDF mixture (total dose of 27,800 ng/kg bw), which contained 120 ng TCDD/kg bw. Using the now somewhat dated I-TE (internation TCDD toxic equivalence) factors, the total administered dose corresponded to 464 ng I-TE/kg bw. The concentrations of specific congeners in liver and adipose tissue were measured at 1, 6, 16, or 28 weeks after exposure... . All 2,3,7,8-substituted PCDDS and PCDFs were consistently more persistent in the adipose tissue of marmoset monkeys. In general, the persistence in adipose tissue was from about 1.3-2.0 fold greater than that in liver, with the exception of 1,2,3,4,7,8-/1,2,3,4,7,9-hexaCDF, heptaCDFs, and OCDF, which were more than threefold more persistent in adipose tissue. For the latter congeners and OCDD, there was marked variance in half-life values, which may be due to delayed and incomplete absorption of the exceptionally persistent congeners and the relatively short (28 weeks) period of investigation. ...One week after exposure..., the non-2,3,7,8-substituted PCDDs and PCDFs were present in liver and adipose tissue in relatively minor quantities compared with 2,3,7,8-substituted congeners; however, non-2,3,7,8-substituted compounds represented a considerable percent of the exposure mixture. In this study, none of the non-2,3,7,8-substituted TCDDs, penta-CDDs, TCDFs, or penta-CDFs could be detected in the liver by gas chromatography/mass spectroscopy. Some of the hexa and hepta congeners were detected in adipose tissue and liver, but after 1 wk, the total amount in the liver was more than 5% of the dose administered only in the case of 1,2,4,6,8,9-hexaCDF. Similar results were obtained in rats after exposure to a defined, complex mixture of PCDDs and PCDFs. Additional short-term studies in rats provide evidence that the low tissue concentration of non-2,3,7,8-substituted congeners, measured 1 wk after exposure, was the result of rapid elimination, since these congeners were detected at higher levels in the liver 13 to 14 hr after exposure. These results in monkeys and rats are compatible with data from analysis of human tissue samples and milk in which the non-2,3,7,8-substituted congeners have also not been shown to be present in significant concentrations compared with the 2,3,7,8-substituted congeners. /Polychlorinated dibenzo-p-dioxins and dibenzofurans/
...A digestive tract mass balance study of six German men (age 41-73 yr) with occupational exposure to PCDDs and PCDFs /was conducted/. Blood lipid levels of the subjects in 1996 ranged from 84-505 pg/g lipid for TCDD and 270-640 pg/g lipid for TEQs, compared with background levels in unexposed persons of 5.2 and 32 pg/g lipid, respectively. The daily quantity of nonmetabolized 2,3,7,8-chlorine substituted PCDDs and PCDFs excreted in the feces exceeded the daily uptake from food, indicating significant clearance across the gastrointestinal tract. The concentration of these compounds in feces was also found to be highly correlated with that in blood, demonstrating that the fecal PCDD and PCDF content was related directly to the body burden of these compounds. No significant clearance (excretion via feces at least fourfold greater than uptake by food) was observed for congeners, including 2,3,7,8-TCDF, 1,2,3,7,8-pentaCDF, 1,2,3,4,7,8,9-heptaCDF, or octaCDF, which were not markedly elevated in the serum lipids. Together, these results support the relationship that fecal excretion is regulated by the lipid-based blood concentration of these compounds. The half-lives in these subjects, due to fecal clearance of nonmetabolized congeners, were estimated from the excretion rate and current body burden and ranged form 10 years for octaCDD (OCDD) to 22 years for TCDD to 33 years for 2,3,4,7,8-penta CDF. Congener-specific half-lives... were also calculated based on the decrease in serum lipid levels of congeners between 1990-1992 and 1996. The fecal clearance of non-metabolized PCDDs and PCDFs contributed on average from 37% (TCDD) to 90% (OCDD) of the total elimination. Thus, fecal clearance plays an important role in the overall elimination of most congeners, with the daily fecal excretion estimated to be equivalent to the amount of TEQ present in about 1.7 g of blood lipids. /Polychlorinated dibenzo-p-dioxins and dibenzofurans/
Formation of Dioxins in the Catalytic Combustion of Chlorobenzene and a Micropollutant-like Mixture on Pt/γ-Al2O3
摘要：
Catalytic combustion over a 2 wt % Pt/gamma-Al2O3 catalyst of chlorobenzene (PhCl) and of a micro pollutant-like mixture representative for a primary combustion offgas has been investigated. Typical conditions were 1000-1500 ppm of organics in the inflow, contact times similar to0.3 s, 16% O-2 in nitrogen at similar to1 bar, and temperature range 200-550 degreesC. 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,). These are accompanied by polychlorinated dibenzo-p-dioxins (PCDDs) and dibenzofurans (PCDFs) at levels of about 10(-6) relative to PhCl,. Additional HCI-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 PCDC/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 there from 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.
作者：Mariusz K. Cieplik、Jose Pastor Carbonell、Christina Muñoz、Sarah Baker、Sophie Krüger、Per Liljelind、Stellan Marklund、Robert Louw
DOI：10.1021/es026292g
日期：2003.8.1
sintering facility could satisfactorily imitate the large-scale process, in part or as a whole. Results obtained with realistic feed mixtures point at dioxin formation in the sinter bed at levels significant enough to explain a major part of the outputs observed in the real-life process. With approximately 8 ppm (wt) of chloride added as NaCl, the PCDD/F output doubled, but with the same proportion of
PCDD/DF formations by the heterogeneous thermal reactions of phenols and their TiO2 photocatalytic degradation by batch-recycle system
作者：Hajime Muto、Koki Saitoh、Hitoshi Funayama
DOI：10.1016/s0045-6535(00)00552-x
日期：2001.10
and dibenzofurans (PCDD/DFs) formation by the thermal reactions of phenols with CuCl2 under oxygen flux were carried out in relation to their formation mechanisms. To evaluate the effect of photocatalytic degradation of titaniumdioxide (TiO2) thin film prepared by the sol-gel method, the photocatalysis of PCDD/DFs in acetonitrile/water solution by batch-recycle system was conducted. For the thermal reaction
Emissions of polychlorinated dibenzo-p-dioxins and dibenzofurans from catalytic and thermal oxidizers burning dilute chlorinated vapors
作者：John R. Hart
DOI：10.1016/j.chemosphere.2003.10.017
日期：2004.3
(ng/dscm)=8.4 exp(-0.0084T degrees C); (2) dioxin/furan production occurs at the combustion catalyst; (3) small variations in temperature cause large changes in the congener distribution of the dioxin and furan isomers; (4) molar TEQ yields from the parent compounds fed to the oxidizers are very small (10(-9)-10(-13)); (5) catalytic and thermal oxidizers may destroy dioxins fed from the ambient air; and (6)
Emission Factors and Importance of PCDD/Fs, PCBs, PCNs, PAHs and PM<sub>10</sub> from the Domestic Burning of Coal and Wood in the U.K.
作者：Robert G. M. Lee、Peter Coleman、Joanne L. Jones、Kevin C. Jones、Rainer Lohmann
DOI：10.1021/es048745i
日期：2005.3.1
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 PM10 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-sigmaTEQ to total U.K.emissions was minor.
本文介绍了当煤和木材经过受控燃烧实验时针对一系列持久性有机污染物（POPs）得出的排放因子（EFs），旨在模拟空间供暖的家庭燃烧。排放了各种各样的持久性有机污染物，煤炭的排放量高于木材的排放量。对于颗粒物，PM10（大约10 g / kg燃料）和多环芳烃（对于sigmaPAHs大约100 mg / kg燃料）获得了最高的EF。对于氯化物，多氯联苯（PCB）的EF最高，而多氯萘（PCN），二苯并-对-二恶英（PCDD）和二苯并呋喃（PCDF）的丰度较低。对于sigmaPCB，EF大约为1000 ng / kg燃料，对于sigmaPCNs大约为100s ng / kg燃料，对于sigmaPCDD / Fs大约为100 ng / kg燃料。该研究证实，一氯化至三氯化二苯并呋喃Cl1,2,3DFs是低温燃烧过程（如煤炭和木材的国内燃烧）的有力指标。结论是，在固体燃料燃烧期间通常形成许多PCB和PC
Polychlorinated Dibenzo-<i>p</i>-dioxin/Polychlorinated Dibenzofuran Releases into the Atmosphere from the Use of Secondary Fuels in Cement Kilns during Clinker Formation
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 polychlorinateddibenzo-p-dioxin (PCDD)/polychlorinateddibenzofuran (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
这项研究的目的是评估在熟料生产过程中使用废料（例如轮胎或肉粉）作为二次燃料对多氯二苯并对二恶英（PCDD）/多氯二苯并呋喃（PCDF）排放水平的影响。大气层。为此，在西班牙选择了三个不同的水泥厂以不同的采样次数进行该项目。每家工厂分别评估了不同的材料：第一家工厂在窑中添加了肉粉，第二家工厂使用了废旧轮胎，第三家工厂使用了两者的混合物。在所有情况下，PCDD / F排放值均保持在欧盟指令规定的0.1 ng I-TEQ / Nm3的限值以下，范围在0.001至0.042 ng I-TEQ / Nm3的范围内。在大多数情况下，对总TEQ的主要贡献来自2,3,7，8-四氯二苯并呋喃的含量较高，而2,3,4,7,8-五氯二苯并呋喃的含量较高，因为其TEF为0.5。其余15种有毒同源物仅对TEQ贡献很小。此外，与使用常规燃料从西班牙水泥窑厂获得的报告数据相比，没有发现显着差异。这一事实表明，添加废轮胎或肉粉对PCDD
