2,7-디클로로디벤조-P-디옥신

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)

TERRESTRIAL FATE: Based on a soil TLC study using five different soils types, 2,7-dichlorodibenzo-p-dioxin is expected to be immobile in soil(1). If applied indirectly to soils, it is not expected to move any further into the soil profile, although it may be subject to runoff or wind erosion transport(1). A single biodegradation study using two soil types has shown that about 5% of initial concns of 2,7-dichlorodibenzo-p-dioxin are metabolized to CO2 over a ten week incubation period(2). No data are currently available to suggest that dichlorodibenzo-p-dioxin is abiotically degraded within soil systems. Photodecomposition on soil surfaces is not important(3).

AQUATIC FATE: 2,7-Dichlorodibenzo-p-dioxin has been found to be immobile in soil mobility studies(1) which suggests that partitioning from the water column to sediment and suspended material may be significant. In the presence of significant adsorption, volatilization may not be important. The volatilization half-life from a model environmental pond, which considers the effect of adsorption, can be estimated to be about 30 years(2,SRC); if parameters are introduced into the pond model to exclude adsorption effects, the volatilization half-life is reduced to 15.2 days(SRC). Photodegradation may have some importance in surface waters exposed to sunlight; 2,7-dichlorodibenzo-p-dioxin in methanol solution has been shown to decompose within several hours when exposed to sunlight(3). Based upon a predicted log Kow of 5.75(4), significant bioconcentration in aquatic organisms may occur. Aquatic hydrolysis is not expected to be important. Insufficient data are available to predict the importance of biodegradation in water. (SRC)

ATMOSPHERIC FATE: Based upon a predicted vapor pressure of 1.125X10-6 mm Hg at 25 °C(1), 2,7-dichlorodibenzo-p-dioxin may exist in both the vapor and particulate phases in the ambient atmosphere(2,SRC). When associated with fly ash releases, dichlorodibenzodioxin can be expected to be very tightly adsorbed to particulates based on experimental examination of monochloro and other chlorinated dibenzo-p-dioxins(3). Vapor-phase 2,7-dichlorodibenzo-p-dioxin is degraded relatively rapidly in the atmosphere by reaction with photochemically produced hydroxyl radicals; the half-life for this reaction has been estimated to be about 1.6 days in average air(4). The vapor phase may also be susceptible to direct photolysis. Particulate phase dibenzo-p-dioxin is susceptible to physical removal from air by both wet and dry deposition processes. (SRC)

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)

The following link will take the user to the National Toxicology Program (NTP) Test Agent Search Results page, which tabulates all of the "Standard Toxicology & Carcinogenesis Studies", "Developmental Studies", and "Genetic Toxicity Studies" performed with this chemical. Clicking on the "Testing Status" link will take the user to the status (i.e., in review, in progress, in preparation, on test, completed, etc.) and results of all the studies that the NTP has done on this chemical. [http://ntp-apps.niehs.nih.gov/ntp_tox/index.cfm?fuseaction=ntpsearch.searchresults&searchterm=33857-26-0]

Using soil thin layer chromatography, 2,7-dichlorodibenzo-p-dioxin was found to be immobile (Rf values of 0.0) in five different types of soil(1); if applied to soils, it is not expected to move any farther into the soil profile, although it may be subject to runoff or wind erosion transport(1).

The most prominent acute manifestation of toxicity that has been shown in humans is chloracne, an acne-like condition that takes months or years to disappear. Clinically, this skin lesion is characterized by hyperplasia and hyperkeratosis of the interfollicular epidermis, hyperkeratosis of the sebaceous follicles, and the squamous metaplasia of the sebaceous glands that form cysts and keratinaceous comedones in a typical distribution. Data are not yet available to determine the amount, route, or duration of exposure that is necessary to cause chloracne. /Polychlorodibenzodioxins/

Other less consistency reported effects from dioxin exposure in humans include aesthenia, headaches, and pain in the extremities, peripheral neuropathy, ulcers, altered liver function, enzyme induction, altered lipid metabolism, and abnormal urinary porphyrin patterns. Immune system dysfunction and altered T-cell subsets have been reported by some investigators but have not been found by others. /Polychlorodibenzodioxins/