1,2,3,7,8,9-헥사클로로디벤조-P-다이옥신

469 to 471 °F (NTP, 1992)

243-244 °C

1,2,3,7,8,9-hexachlorodibenzo-p-dioxin is a light pink crystalline solid. (NTP, 1992)

Light pink solid; [CAMEO] Orange powder; [MSDSonline]

/Toxic equivalency factors (TEF), indicate the toxicity of a compound relative to 2,3,7,8-tetrachlorodibenzo-p-dioxin, which itself has been assigned a TEF of 1.0. Concentration data for polychlorinated dibenzo-p-dioxins are frequently reported in units of toxic equivalency which are equal to the measured concentration of substance multiplied by its TEF./ The TEF for 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin is 0.1.

Warning

H302 (97.4%): Harmful if swallowed [Warning Acute toxicity, oral]

P264, P270, P273, P301+P317, P330, P391, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 39 reports by companies from 2 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Hazard Traits - Bioaccumulation; Carcinogenicity; Dermatotoxicity; Endocrine Toxicity; Environmental Persistence; Environmental tox; Hematotoxicity; Hepatotoxicity and Digestive System Toxicity; Reproductive Toxicity; Respiratory Toxicity

Regulation (EC) No 178/2002 (amended)

SYMPTOMS: Symptoms of exposure to this compound may include burning sensations in the eyes, nose and throat, headache, dizziness, nausea, vomiting, itching, redness and swelling of the face, chloracne, painful joints, fatigue, insomnia, loss of libido, irritability, nervousness, emotional disorders, loss of mental and muscular coordination, blurred vision, loss of taste and smell, irritation of the mucous membranes, loss of appetite and weight, sleep disturbances, low blood pressure, abdominal pain and liver dysfunction.

Can cause chloracne and liver injury; [CAMEO] Polychlorodibenzodioxins have caused chloracne in humans; Oral LD50 (rat) = 1.8 (male) and 0.8 (female) mg/kg bw (31% 1,2,3,6,7,8- and 67% 1,2,3,7,8,9-hexachlorodibenzo-p-dioxins); [HSDB] No evidence of carcinogenicity in mice with dermal application, but carcinogenic effects, including hepatocellular carcinomas, observed in gavage study with rats and mice (mixture of 1,2,3,6,7,8- and 1,2,3,7,8,9-hexachlorodibenzo-p-dioxins); [NTP] IARC classification is for polychlorinated dibenzo-para-dioxins other than 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD);

Olson JR et al; Chemosphere 18 (1/6): 371-81 (1989). A review of the toxicological and pharmacokinetic literature on chlorinated dibenzo-p-dioxins and dibenzofurans was presented to evaluate the accuracy and currency of established toxicity equivalence factors.

Skene SA et al; Hum Toxicol 8 (3): 173-204 (1989). Polychlorinated Dibenzo-p-Dioxins and Polychlorinated Dibenzofurans: The Risk to Human Health. A Review.

WHO; Environ Health Criteria 88: Polychlorinated Dibenzo-para-dioxins and Dibenzofurans (1989)

NRCC; Polychlorinated Dibenzo-p-dioxins: Limitations to the Current Analytical Techniques, Publication NRCC No 18576 (1981). A technical review and assessment of the methodology for the analysis of polychlorinated dibenzo-p-dioxins in a variety of substrates. Analytical methodology was evaluated and safety procedures were suggested.

For more Special Reports (Complete) data for 1,2,3,7,8,9-HEXACHLORODIBENZO-p-DIOXIN (6 total), please visit the HSDB record page.

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.

SMALL SPILLS AND LEAKAGE: If you spill this chemical, FIRST REMOVE ALL SOURCES OF IGNITION, then dampen the solid spill material with toluene, then transfer the dampened material to a suitable container. Use absorbent paper dampened with toluene to pick up any remaining material. Your contaminated clothing and absorbent paper should be sealed in a vapor-tight plastic bag for eventual disposal. Solvent-wash all contaminated surfaces with toluene followed by washing with a soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned.

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal, aquatic, and plant life; and conformance with environmental and public health regulations.

0.0013 [mg/m3]

0.014 [mg/m3]

0.085 [mg/m3]

The mean concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in human milk samples collected from the city of Berlin, Germany (formerly West Germany) was 11 parts per trillion (range, 7.7 to 16 parts per trillion) on a wet wt basis(1). In Binghamton, NY and Germany (formerly West Germany), the concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in human milk was 6.2 (n=42) and 6.3 (n=185) parts per trillion, respectively(2). Human milk samples were collected from 96 volunteer women from Quebec, Canada between December 1988 and February 1989; the mean concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in these samples was 6.4 pg/g milk fat(3). The mean concn in human milk from different regions of Germany of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin was as follows (all pg/g fat wt)(4): Berlin (n=53), 9.4; Weiden (n=14), 9.6; Rheinfelden (n=11), 11; Recklinghausen (n=10), 8.3; Flensburg (n=6), 8.3; Rastatt (n=12), 6.7; Berlin (n=112; range, 2.0-20 pg/g fat wt), 9. Between the years 1986-1991, the mean concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in human milk from North Rhine Westphalia, Germany was 6.4 pg/g fat wt (range, 5.8-1.3 pg/g fat wt)(5). The concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in human milk taken in 1986 from 2 mothers living southern Japan was 4.1 and 7.1 pg/g lipid(6). The concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in human milk taken in 1984 from 3 mothers living India was 6.8, 3.8, and 4.1 pg/g lipid(6). The concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in human milk taken in 1986 from 2 mothers living Binghamton, New York was 11 and 13 pg/g lipid(6).

From the cities of Murmank and Monchegorsk (both in Russia), the concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in human milk was 1.99 and 1.81 ng/kg milk fat, respectively(1). A pooled human milk sample from healthy native Swedish mothers living in the Stockholm region contained 10,6,5,7 pg/g fat wt of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in the years 1972, 1990, 1991, and 1992, respectively(2). The mean concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in a pooled sample of breast milk from mothers (age 25-35 y.o.) living in Tarrogona, Spain (Catalonia) was 4.55 pg/g fat wt (range, 2.26-7.53 pg/g fat wt)(3). In 1992, a pooled sample of breast milk from 40 mothers (age 15-38 y.o.) Living in the urban area of Rio de Janeiro County, Brazil contained 4.4 pg/g milk fat of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin(4). The concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in 38 women from urban (cites of Auckland and Christchurch) and rural (towns of Northland and N. Caterbury) locations was determined(5); in milk fat, rural and urban mothers had 6.3 (n=17) and 5.6 (n=20) ng/kg fat, respectively(5); in whole breast milk, rural and urban mothers had 0.2 (n=20) and 0.2 (n=17) ng/kg fat, respectively(5).

The mean concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in 13 human adipose tissue samples from Japan, sampled in 1985, was 12 pg/g wet wt (range, 4-44 pg/g pg/g wet wt)(1). In 1989, tissues samples taken from the Japanese general population contained 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin at mean levels as follows (all pg/g lipid)(2): adipose tissue, 17 (range, 2.1-62); brain samples, 0.71 (range, 0.22-1.1); spleen, 10 (range, 3.0-22); muscle, 17 (range, 1.9-42); kidney, 10 (1.4-37); lung, 17 (range, 10-31); liver, 33 (range, 4.5-72). Between the years 1990-1991, the mean concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin was 17 pg/g lipid (N=40; range, 6.0-39 pg/g lipid) in the adipose tissue of British Columbia residents who had elective abdominal surgery(3). 1,2,3,7,8,9-Hexachlorodibenzo-p-dioxin was found in blood from the general population of Germany at a mean concn of 7.39 pg/g lipid basis (N=744) during the period from 1989 to 1998(4). The concn of 1,2,3,7,8,9-Hexachlorodibenzo-p-dioxin in the serum of Great lakes sport fishermen was as follows (all in parts per trillion): all lakes, 7.0 (range, not detected-22.8); Lake Michigan, 8.7 (range, not detected-22.8); Lake Huron, 6.5 (range, not detected-16.1); Lake Erie, 5.8 (range, not detected-13); comparison group, 9.4 (range, not detected-25.8)(5). For the years 1995-1996, the mean concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin was determined in blood and tissue samples from 5 women living in upstate New York(6); concns in adipose tissue (3.1 pg/g lipid); pre-delivery blood (4.2 pg/g lipid); placenta (2.6 pg/g lipid); cord blood (1.8 pg/g lipid); post-partum blood (4.1 pg/g lipid); and breast milk (3.5 pg/g lipid) were determined(6).

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 classification scheme(1), an estimated Koc value of 420,000(SRC), determined from a structure estimation method(2), indicates that 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin is expected to be immobile in soil(SRC). Volatilization of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin from moist soil surfaces is expected to be an important fate process(SRC) given an estimated Henry's Law constant of 1.9X10-6 atm-cu m/mole(SRC), using a fragment constant estimation method(3). However, adsorption to soil is expected to attenuate volatilization(SRC). 1,2,3,7,8,9-Hexachlorodibenzo-p-dioxin is not expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 4.88X10-11 mm Hg(4). No biodegradation was reported for 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in a sludge-amended soil field study(5). A half-life of approx 20 years was reported for 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in a sludge-amended soil field study(6).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 420,000(SRC), determined from a structure estimation method(2), indicates that 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is expected(3) based upon an estimated Henry's Law constant of 1.9X10-6 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). Using this Henry's Law constant and an estimation method(3), volatilization half-lives for a model river and model lake are 2 and 28 days, respectively(SRC). However, volatilization from water surfaces is expected to be attenuated by adsorption to suspended solids and sediment(SRC). The estimated volatilization half-life from a model pond is 65 years if adsorption is considered(5). According to a classification scheme(6), BCF values of 30,200 and 85,000 for guppies(7,8) suggest that bioconcentration in aquatic organisms is very high(SRC). Based on field studies in soil(9,10), 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin is not expected to biodegrade in water(SRC).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin, which has a vapor pressure of 4.88X10-11 mm Hg at 25 °C(2) is expected to exist solely in the particulate phase in the ambient atmosphere(SRC). Particulate-phase 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin may be removed from the air by wet and dry deposition(SRC).

The concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in chicken and egg food items purchased at Matsryama, Japan were 2.7 and 1.8 pg/g wet wt, respectively(1). Samples of food of animal origin from Germany (formerly West Germany) had levels of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin as follows (all ng/kg fat basis)(2): cheese, 0.5 (n=10); beef, 2.0 (n=3); veal, 1.8 (n=4); sheep, 0.7 (n=2); chicken, 0.6 (n=2); canned meat, 1.2 (n=2). Food samples collected in 1995 from Binghamton, NY; Atlanta, GA; Chicago, IL; San Diego, CA; Louisville, KY contained 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin at concns as follows(3): beef, 0.14 pg/g wet wt; fresh fish, 0.20 pg/g wet wt; butter 0.39 pg/g wet wt. The concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin was measured in cooked and uncooked meat samples(4). Hamburger, uncooked and cooked, contained mean concns of 72.4 pg/kg wet wt (range, 66.9-79.0 pg/kg wet wt) and 65.1 pg/kg wet wt (range, 56.8-70.2 pg/kg wet wt) of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin, respectively, with a net concn change of -10% with cooking(4). Bacon, uncooked and cooked, contained mean concns of 9.4 pg/kg wet wt (range, not detected-<56.6 pg/kg wet wt) and 18.9 pg/kg wet wt (range, not detected-56.8 pg/kg wet wt) of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin, respectively, with a net concn change of +101% with cooking(4). Catfish, uncooked and cooked, contained mean concns of 254.6 pg/kg wet wt (range, 226.4-303.7 pg/kg wet wt) and 156.8 pg/kg wet wt (range, 139.7-173.6 pg/kg wet wt) of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin, respectively, with a net concn change of -38.4% with cooking(4).

The mean concns of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in food sampled in Germany between the years 1993-1996 were as follows(1): butter, 0.15 pg/g fat (n=222; range, 0.00-0.57 pg/g fat); eggs, 0.82 pg/g fat (n=218; range, 0.00-15.65 pg/g fat); meat, 0.20 pg/g fat (n=107; range, 0.03-1.94 pg/g fat); fish, 1.09 (n=138; range, 0.00-24.39). The concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in butter samples from Australia ranged from <0.02 to 0.15 pg/g fat(2). In two butter samples from Spain, 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin detected at mean concns of 0.25 and 0.34 pg/g fat wt(3).

The mean concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in human milk samples collected from the city of Berlin, Germany (formerly West Germany) was 11 parts per trillion (range, 7.7 to 16 parts per trillion) on a wet wt basis(1). In Binghamton, NY and Germany (formerly West Germany), the concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in human milk was 6.2 (n=42) and 6.3 (n=185) parts per trillion, respectively(2). Human milk samples were collected from 96 volunteer women from Quebec, Canada between December 1988 and February 1989; the mean concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in these samples was 6.4 pg/g milk fat(3). The mean concn in human milk from different regions of Germany of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin was as follows (all pg/g fat wt)(4): Berlin (n=53), 9.4; Weiden (n=14), 9.6; Rheinfelden (n=11), 11; Recklinghausen (n=10), 8.3; Flensburg (n=6), 8.3; Rastatt (n=12), 6.7; Berlin (n=112; range, 2.0-20 pg/g fat wt), 9. Between the years 1986-1991, the mean concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in human milk from North Rhine Westphalia, Germany was 6.4 pg/g fat wt (range, 5.8-1.3 pg/g fat wt)(5). From the cities of Murmank and Monchegorsk (both in Russia), the concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in human milk was 1.99 and 1.81 ng/kg milk fat, respectively(6). A pooled human milk sample from healthy native Swedish mothers living in the Stockholm region contained 10,6,5,7 pg/g fat wt of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in the years 1972, 1990, 1991, and 1992, respectively(7). The mean concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in a pooled sample of breast milk from mothers (age 25-35 years old) living in Tarrogona, Spain (Catalonia) was 4.55 pg/g fat wt (range, 2.26-7.53 pg/g fat wt)(8). In 1992, a pooled sample of breast milk from 40 mothers (age 15-38 years old) Living in the urban area of Rio de Janeiro County, Brazil contained 4.4 pg/g milk fat of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin(9).

The mean concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in milk sampled in Germany between the years 1993-1996 was 0.18 pg/g fat (n=538; range, 0.00-0.82 pg/g fat)(1). Between the years 1992-1994, milk collect at farms with elevated dioxin concns in the Bolsover area of Derbyshire (United Kingdom) contained concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin ranging from 0.02-0.66 ng/kg(2). Cow's milk samples collected in 1995 from farms located in Asturias (northern Spain) and Toledo (Spain) contained 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin at concns ranging from 0.25-1.04 pg/g fat wt(3). These farms were located near potential emission sources and control areas(3). Pasteurized milk purchased at retail outlets in Spain contained 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin at a mean concn of 0.46 pg/g fat wt (n=23)(3).

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)

For the residents of Madrid, Spain in April 1995, the daily intake of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin was determined to be 30.28 pg/person/day(1). The mean daily intake of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in a breast fed infant was 29.3 pg TEQ/day (6.4 pg TEQ/day/kg body wt) after 4 weeks; 24.4 pg TEQ/day (5.1 pg TEQ/day/kg body wt) after 8 weeks; and 19.6 pg TEQ/day (3.2 pg TEQ/day/kg body wt) after 12 weeks(2).

/FIELD STUDIES/ The activity of cytochromes P4501A and P4502B have been related to contaminant concentration in polar bears (Ursus maritimus). Studying liver samples of 16 adult male polar bears (from legally controlled hunts by Inuits in the Canadian artic) ... workers found that CYP1A protein content correlated strongly with the concentration of PCBs, polychlorinated dibenzodioxins (PCDDS) and polychlorinated dibenzofurans (PCDFs) in the liver ... . /Polychlorinated dibenzodioxins/

The concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in Sable Island, Newfoundland, Canada, grey seal tissues (sampled in February 1995) were as follows(1): maternal blubber, 1.56 pg/g lipid (n=1); maternal milk, 0.53, 0.32 pg/g lipid (n=2); and maternal blood, 200 pg/g lipid (n=1). Osprey muscle tissue sampled in Sweden contained 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin at a concn of 0.6 parts per trillion fresh wt(2). Oysters and mussels sampled from southern coastal areas of South Korea between 1995-97 contained 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin at a concns of <0.02-0.091 and 0.032 pg/g wet wt, respectively(3).

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)

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/

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/

Found in emissions from waste incineration, PCB's, automobiles (using leaded gas), and improper waste disposal of some chlorinated compounds; Not commercially produced; [HSDB] Hexachlorodibenzo-p-dioxins (HCDD): Found as impurities in polychlorinated phenols and chlorophenol derivative herbicides (i.e. 2,4-D); [NTP]

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)