2052
T3D2048
1,3-Dichlorodibenzo-p-dioxin
1,3-Dichlorodibenzo-p-dioxin is one of 75 chlorinated dibenzo-p-dioxin (CDD) congeners. CDDs are a class of manufactured chemicals that consist of dioxin skeletel structures with chlorine substituents. They are also persistent organic pollutants (POPs), thus their production is regulated in most areas. Dioxins occur as by-products from the manufacture of organochlorides, the bleaching of paper, chlorination by waste and drinking water treatment plants, municipal solid waste and industrial incinerators, and natural sources such as volcanoes and forest fires. (L177, L178)
50585-39-2
39727
C12H6Cl2O2
251.974480
Colorless solid.
Oral (L177) ; inhalation(L177) ; dermal (L177)
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)
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)
3, not classifiable as to its carcinogenicity to humans. (L135)
Dioxins occur as by-products from the manufacture of organochlorides, the bleaching of paper, chlorination by waste and drinking water treatment plants, municipal solid waste and industrial incinerators, and natural sources such as volcanoes and forest fires. (L177, L178)
Acute Oral: 0.0002 ug/kg/day (L134)
Intermediate Oral: 0.00002 ug/kg/day (L134)
Chronic Oral: 0.000001 ug/kg/day (L134)
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)
In addition to chloracne, CDD exposure causes skin rashes, discoloration, and excessive body hair. (L177)
Treatment of CDD exposure may include washing the area of contact, GI decontamination, administering an IV, or forced alkaline diuresis. (L346)
2009-06-24T17:37:18Z
2014-12-24T20:25:07Z
CPD-925
1,3-Dichlorodibenzo-p-dioxin
true
ClC1=CC(Cl)=C2OC3=CC=CC=C3OC2=C1
C12H6Cl2O2
InChI=1S/C12H6Cl2O2/c13-7-5-8(14)12-11(6-7)15-9-3-1-2-4-10(9)16-12/h1-6H
InChIKey=AZYJYMAKTBXNSX-UHFFFAOYSA-N
253.081
251.97448485
Exogenous
Solid
36324