1,2,3,4,6,7,8,9-八氯二苯并-对-二恶英 | 3268-87-9

• 分子结构分类: 有机化合物 - 有机杂环化合物 - 苯并二恶英
• 中文名称: 1,2,3,4,6,7,8,9-八氯二苯并-对-二恶英
• 中文别名: 1,2,3,4,6,7,8,9-八氯联苯-P-二噁英；八氯二苯并-对-二恶英；1,2,3,4,6,7,8,9-八氯二苯并对二噁英
• 英文名称: 1,2,3,4,6,7,8,9-octachlorodibenzodioxin
• 英文别名: octachlorodibenzo-p-dioxin；octachlorodibenzodioxin；1,2,3,4,6,7,8,9-octachlorodibenzo-p-dioxin
• CAS: 3268-87-9
• 化学式: C₁₂Cl₈O₂
• 分子量: 459.755
• InChiKey: FOIBFBMSLDGNHL-UHFFFAOYSA-N

物化性质

• 物理描述：
  Octachlorodibenzo-p-dioxin appears as colorless crystals or white crystalline solid. (NTP, 1992)
• 颜色/状态：
  Colorless crystals or needles from trichlorobenzene
• 沸点：
  510.0 °C
• 熔点：
  330.0 °C
• 溶解度：
  In water, 4.00X10-7 mg/l @ 20 °C
• 蒸汽压力：
  8.25X10-13 mm Hg @ 25 °C
• 稳定性/保质期：

  Extremely stable, even on heating to 700 °C.

• 分解：
  When heated to decomposition it emits toxic fumes of /hydrogen chloride/.
• 保留指数：
  3150

计算性质

• 辛醇/水分配系数(LogP)：
  8.1
• 重原子数：
  22
• 可旋转键数：
  0
• 环数：
  3.0
• sp3杂化的碳原子比例：
  0.0
• 拓扑面积：
  18.5
• 氢给体数：
  0
• 氢受体数：
  2

ADMET

代谢

CDDs通过口服、吸入和皮肤接触途径被吸收。CDDs通过血清脂质和脂蛋白在血浆中携带，主要分布到肝脏和脂肪组织。CDDs通过微粒体单加氧酶系统非常缓慢地代谢为极性代谢物，这些代谢物可以与葡萄糖醛酸和谷胱甘肽结合。它们可能通过诱导I相和II相酶来增加自己的代谢速率。CDDs的主要排泄途径是胆汁和粪便，尽管也有少量通过尿液和哺乳排出。

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)

来源:Toxin and Toxin Target Database (T3DB)

毒理性

• 毒性总结

CDDs通过结合芳基烃受体并随后改变某些基因的转录来产生其毒性作用。对Ah受体的亲和力取决于特定CDD的结构。基因表达的改变可能是由于Ah受体及其异二聚体形成伙伴芳基烃受体核移位子与基因调控元件的直接相互作用，或者启动磷酸化/去磷酸化级联反应，随后激活其他转录因子。受影响的基因包括几个癌基因、生长因子、受体、激素和药物代谢酶。这些基因的转录/翻译改变被认为是CDDs大多数毒性作用的原因。

CDDs cause their toxic effects by binding to the aryl hydrocarbon receptor and subsequently altering the trascription 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

整体评估：其他多氯二苯并-对-二噁英对人类致癌性不可分类（第3组）。/多氯二苯并-对-二噁英/

Overall evaluation: 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)

来源:Toxin and Toxin Target Database (T3DB)

毒理性

• 健康影响

暴露于大量氯代二苯并二噁烷（CDDs）会引起氯痤疮，这是一种严重的皮肤疾病，其症状类似于粉刺，主要发生在面部和上半身。CDDs还可能引起肝损伤，并导致长期的葡萄糖代谢改变和激素水平的微妙变化。此外，研究表明CDDs可能会破坏内分泌系统，削弱免疫系统，以及造成生殖损害和出生缺陷、中枢和周围神经系统病理变化、甲状腺疾病、子宫内膜异位症和糖尿病。(L177, L178)

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)

来源:Toxin and Toxin Target Database (T3DB)

毒理性

• 暴露途径

口服（L177）；吸入（L177）；皮肤（L177）

Oral (L177) ; inhalation(L177) ; dermal (L177)

来源:Toxin and Toxin Target Database (T3DB)

吸收、分配和排泄

在2周内，喂食22.7（±）微克或120.7（±2.9）微克八氯二苯并-p-二恶英的雄性Wistar大鼠，在其肝脏中保留了约1-2%的给定剂量。心脏、肾脏、脾脏、肺、骨骼肌、睾丸和尿液中没有检测到八氯二苯并-p-二恶英的 levels，但在高剂量组的脂肪组织中发现了少量。粪便分别含有低剂量和高剂量的61%和37%。与胆管插管的雄性Wistar大鼠（400克）单次口服58微克八氯二苯并-p-二恶英后24-72小时内胆汁中的八氯二苯并-p-二恶英量相比，粪便中存在大量八氯二苯并-p-二恶英，这表明粪便中的二恶英主要是未被吸收的八氯二苯并-p-二恶英。

Male Wistar rats fed 22.7 (+ or -) ug or 120.7 (+ or - 2.9) ug octachlorodibenzo-p-dioxin over a 2 wk period were found to retain about 1-2% of the given dose in the liver. The heart, kidneys, spleen, lung, skeletal muscle, testes, and urine contained no detectable levels of octachlorodibenzo-p-dioxin, but minor amounts were found in the adipose tissue of the high dose group. Feces contained 61% and 37%, respectively, of the low and high doses given. The presence of a large quantity of octachlorodibenzo-p- dioxin in the feces compared to that in the bile 24-72 hr after a single oral dose of 58 ug octachlorodibenzo-p-dioxin to bile-cannulated male Wistar rats (400 g) indicated that the dioxin present in the feces was mainly unabsorbed octachlorodibenzo-p-dioxin.

来源:Hazardous Substances Data Bank (HSDB)

吸收、分配和排泄

在雄性Sprague Dawley大鼠连续21天每天服用含有12.6皮克(35)S-巯基-七氯代二苯并-p-二恶英的100微克八氯代二苯并-p-二恶英后，放射性主要在粪便和尿液中回收，摄入放射性剂量的百分比分别为93 (+或- 6)% 和5.2 (+或- 0.8)%。高粪便排泄表明吸收不良。在放射性体内负荷中，有50%包含在肝脏中。微粒体部分含有肝脏放射性的96.3 (+或- 8.2)%。

After 21 daily doses of 100 ug octachlorodibenzo-p-dioxin containing 12.6 picograms (35)S-thio-heptachlorodibenzo-p-dioxin to male Sprague Dawley rats, the radioactivity was mainly recovered in the feces and urine, the percentages of the ingested radioactive dose being 93 (+ or - 6) and 5.2 (+ or - 0.8)% respectively. The high fecal excretion suggests poor absorption. Of the radioactive body burden, 50% was contained in the liver. The microsomal fraction contained 96.3 (+ or - 8.2)% of the hepatic radioactivity.

来源:Hazardous Substances Data Bank (HSDB)

吸收、分配和排泄

八氯二苯并-p-二噁英的处置在雄性Fischer 344大鼠中进行研究，以便更好地评估慢性环境暴露于八氯二苯并-p-二噁英的重要性。大鼠通过静脉注射50微克/千克八氯二苯并-p-二噁英，口服50、500或5000微克/千克，并在个体代谢笼中饲养3天。另外一些通过静脉注射处理的大鼠被饲养长达56天，以跟踪消除八氯二苯并-p-二噁英衍生的放射性，并确定终末组织分布。无论是通过哪种暴露途径，粪便都是消除的主要途径，尿液中几乎没有放射性出现。在500至5000微克/千克的剂量下，胃肠道吸收是非线性的，从未超过给药剂量的10%。肝脏是主要的储存库，其次是脂肪组织和皮肤。在组织、胆汁或排泄物中没有检测到八氯二苯并-p-二噁英的代谢物。八氯二苯并-p-二噁英从整个身体中消除的半衰期在3到5个月之间。重复口服暴露导致组织中线性积累八氯二苯并-p-二噁英。因此，尽管八氯二苯并-p-二噁英吸收不良，但在低剂量、重复暴露的情况下，它可以在肝脏和脂肪组织中积累和浓缩。

...The disposition of (14)C-octachlorodibenzo-p-dioxin was studied in male Fischer 344 rats in order to better assess the significance of chronic environmental exposure to octachlorodibenzo-p-dioxin. Rats were treated with 50 ug octachlorodibenzo-p-dioxin/kg iv, and 50, 500, or 5,000 ug/kg orally and held in individual metabolism cages for 3 days. Additional rats treated iv were held up to 56 days to follow elimination of octachlorodibenzo-p-dioxin derived radioactivity and to determine terminal tissue distribution. Feces was the major route of elimination after both routes of exposure with little radioactivity ever appearing in the urine. GI absorption was nonlinear between 500 and 5,000 ug/kg, never exceeding 10% of the administered dose. Liver was the major depot, followed by adipose tissue and skin. No metabolites of octachlorodibenzo-p-dioxin were detected in tissues, bile, or excreta. The whole body half-life for the elimination of octachlorodibenzo-p-dioxin was between 3 and 5 months. Repeated oral exposure resulted in linear accumulation of octachlorodibenzop-dioxin in the tissues. Thus, octachlorodibenzo-p-dioxin while poorly absorbed, can accumulate upon low-dose, repeated exposure and concentrate in the liver and adipose tissue.

来源:Hazardous Substances Data Bank (HSDB)

吸收、分配和排泄

对人类母乳中二苯并-p-二恶英含量的研究进行了调查。共获得168份母乳样本，这些样本来自哺乳期的母亲。其中79份样本来自第一次哺乳的母亲，74份来自第二次哺乳的母亲，还有15份样本来自第三次或第四次哺乳的母亲。从单个母亲那里获得的母乳样本，在分娩后1、5、10至13周以及52至60周进行采集，并分析了二苯并-p-二恶英的含量。在所有样本中均发现了具有2,3,7,8-氯取代的二苯并-p-二恶英。八氯二苯并-p-二恶英的平均含量为每万亿195份。随着哺乳儿童数量的增加，样本中的二苯并-p-二恶英含量降低。单个母亲的母乳中二苯并-p-二恶英的含量在分娩后52周降至约30至40%的初始值。最大幅度的降低通常发生在分娩后1至5周。得出的结论是，哺乳期母亲母乳中的二苯并-p-二恶英残留物从第一个孩子到第二个孩子以及分娩后随着时间的推移而减少。哺乳可以被视为母亲的一种排泄过程。

A study of dibenzo-p-dioxins concn in human milk was conducted. A total of 168 milk samples were obtained from mothers who breast fed their children. Seventy nine samples were obtained from mothers nursing their first child, 74 from mothers nursing their second child, and 15 samples were collected from mothers nursing their third or fourth child. Milk samples were obtained from a single mother 1, 5, 10 to 13, and 52 to 60 wk after delivery and analyzed for dibenzo-p-dioxins. Dibenzo-p-dioxins with 2,3,7,8-chlorine substitution were found in all samples. The mean concn of dibenzo-p-dioxins was 195 parts per trillion for octachlorodibenzo-p-dioxin. The dibenzo-p-dioxin concn in the samples decreased with increasing number of children who were breast fed. The concn of dibenzo-p-dioxins in the breast milk from the single mother decreased to about 30 to 40% of their initial value 52 wk after delivery. The largest decreases generally occurred 1 to 5 wk after delivery. It was concluded that dibenzo-p-dioxins residues in human milk from mothers who nurse their infants decrease from the first to the second child and with time after delivery. Lactation can be regarded as an excretory process for the mother.

来源:Hazardous Substances Data Bank (HSDB)

安全信息

• 海关编码：
  2932999099
• 危险类别：
  6.1(a)
• 危险品运输编号：
  UN 2811

反应信息

• 作为反应物：
  描述：

  1,2,3,4,6,7,8,9-八氯二苯并-对-二恶英 在 Fe/Pd-SWy-2 作用下， 以 丙醇 、 水 为溶剂， 生成 二苯并对二噁英
  参考文献：
  名称：

  SYNTHESIS OF CLAY-TEMPLATED SUBNANO-SIZED ZERO VALENT IRON (ZVI) PARTICLES, CLAYS CONTAINING SAME, AND USE OF BOTH IN CONTAMINANT TREATMENTS

  摘要：

  提供一种黏土，其中包括具有负电荷位点的2:1 铝硅酸盐黏土，该2:1 铝硅酸盐黏土含有分布在黏土表面上的次纳米级零价铁（ZVI）颗粒。在一个实施例中，至少一些或所有颗粒的横截面为五（5）埃或更小。还描述了合成方法以及新型黏土和黏土模板的次纳米尺度 ZVI 颗粒本身。这种新型产品在各种治理应用中很有用，包括用于还原和脱氯反应。

  公开号：

  US20110130575A1
• 作为产物：
  描述：

  硫丙磷 在 氯 作用下， 以 solid matrix 为溶剂， 反应 1.0h， 以80%的产率得到1,2,3,4,6,7,8,9-八氯二苯并-对-二恶英
  参考文献：
  名称：

  Microchlorination procedure for the synthesis of higher chlorinated dibenzo-p-dioxins from [13C]-2,3,7,8-tetrachlorodibenzo-p-dioxin

  摘要：

  DOI：

  10.1021/ac00240a013

文献信息

• On Dioxin Formation in Iron Ore Sintering
  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

  铁矿石烧结是“二恶英”，多氯二苯并对二恶英和二苯并呋喃（PCDD / Fs）的重要来源。本文报道了尝试确定造成PCDD / F形成的材料，条件和机理的尝试（i）通过研究矿石的显着特性（即关于模型有机物的氧化，冷凝和氯化），以及（ii）使用现实生活的材料在微观尺度上模拟工业过程。采用实验设计原理（DOE）。铁矿石的反应性差异很大。褐铁矿/针铁矿“软”矿石是一种非常活泼的氧化催化剂（例如，用于苯和苯酚），该特性可用于清除粗烧结工艺废气，而赤铁矿/磁铁矿“硬”矿石则不是。后者，但是强烈促进苯酚缩合为二苯并呋喃。新建的实验室级微型烧结设备可以部分或整体令人满意地模仿大规模过程。用实际的进料混合物获得的结果表明，在烧结床中二恶英的形成水平足以说明在现实生活中观察到的大部分产出。通过添加约8 ppm（wt）的氯化物作为NaCl，PCDD / F的产量增加了一倍，但是在氯的施用比例与C2Cl4相同的情况
• Peroxidase-catalyzed in vitro formation of polychlorinated dibenzo-p-dioxins and dibenzofurans from chlorophenols
  作者：Jürgen Wittsiepe、Yvonne Kullmann、Petra Schrey、Fidelis Selenka、Michael Wilhelm

  DOI：10.1016/s0378-4274(99)00066-1

  日期：1999.6

  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