1,2,3,6,7,8-헥사클로로-p-다이옥신

log Kow = 8.21 /Estimated/

7.8

545 to 547 °F (NTP, 1992)

285-286 °C

285 °C

1,2,3,6,7,8-hexachlorodibenzo-p-dioxin is a fluffy white solid. (NTP, 1992)

White solid; [CAMEO] White crystals; [MSDSonline]

Extremely stable, even on heating to 700 °C. /Chlorodibenzo-para-dioxins/

Solutions of this compound may be sensitive to light. Solutions of this chemical in water, DMSO, 95% ethanol or acetone should be stable for 24 hours when protected from light.

Danger

H301 (100%): Toxic if swallowed [Danger Acute toxicity, oral]

P264, P264+P265, P270, P273, P280, P301+P316, P305+P351+P338, P321, P330, P337+P317, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 39 reports by companies from 1 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: Ingestion, inhalation and skin contact to this class of compounds has caused chloracne which is characterized by comedones, keratin cysts, pustules, papules and abscesses. This may clear in a few months or persist for up to 15 years. Symptoms may occur weeks or months after initial exposure. Exposure to a related compound has caused endocrine, immunologic, hematologic, gastrointestinal and neuropsychiatric effects. Other symptoms include a burning sensation in the eyes, nose and throat; headache, dizziness, nausea, vomiting, arthralgias, extreme fatigue, insomnia, loss of libido, irritability, nervousness, high levels of cholesterol, hyperlipoproteinaemia, porphyria cutanea tarda, hepatic dysfunction, hyperpigmentation, hirsuitism, disorders of the cardiovascular, urinary, respiratory and pancreatic systems; disorders of fat and carbohydrate metabolism, emotional disorders, difficulties with muscular and mental coordination, blurred vision and loss of taste and smell. Itching, swelling and redness of the face may occur just prior to the appearance of chloracne. Other symptoms include muscular weakness, loss of appetite and weight, sleep disturbances, orthostatic hypotension, abdominal pain and liver impairment. It may also cause liver and kidney damage and personality changes.

Ingestion, inhalation and skin contact to this class of compounds has caused chloracne and liver injury; [CAMEO] Polychlorodibenzodioxins have caused chloracne in humans; Produced acnegenic response in rabbit ear bioassay; Teratogenic in rats at doses maternally toxic; Hexachlorodibenzo-p-dioxin mixtures have induced carcinomas, adenomas and non-neoplastic lesions in experimental animals by ingestion and external application; 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);

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 p.262 (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.

DHEW/NCI; Bioassay of a Mixture of 1,2,3,6,7-Hexachlorodibenzo-p-dioxin and 1,2,3,7,8,9-Hexachlorodibenzo-p-dioxin (Gavage) for Possible Carcinogenicity (1980) Technical Rpt Series No. 198 DHEW Pub No. (NIH) 80-1754

DHEW/NCI; Bioassay of a Mixture of 1,2,3,6,7-Hexachlorodibenzo-p-dioxin and 1,2,3,7,8,9-Hexachlorodibenzo-p-dioxin (Dermal Study) for Possible Carcinogenicity (1980) Technical Rpt Series No. 202 DHEW Pub No. (NIH) 80-17584

1,2,3,6,7,8-HEXACHLORODIBENZO-P-DIOXIN is the type of compound that is extremely stable, even on heating to 1292 °F. Solutions of this compound may be sensitive to light. Solutions of this type of compound in methanol are degraded by exposure to summer sunlight or irradiation with an ultraviolet lamp (300 nm). (NTP, 1992)

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.

0.0013 [mg/m3]

0.014 [mg/m3]

0.085 [mg/m3]

Samples of human milk collected in the Netherlands contained 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin concns ranging from 0.17 to 4.2 ng/kg(1). All thirteen samples of human adipose tissue from cancer patients in Japan contained 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin with levels ranging from 26-220 ng/kg(2). They were sampled as part of the general population because they were dead to obtain monitoring levels for the Japanese population. Levels of 6.2 to 13 parts per trillion (fat wt basis) were detected in human milk from West Germany(3). Samples of adipose tissue from 35 individuals not known to have had specific exposure to 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin who died in St. Louis contained 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin levels of 28-436 ng/kg fat(4). The avg concn (about 120 parts per trillion lipid basis) of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin in the adipose tissue of persons in Missouri exposed to elevated soil levels of 2,3,7,8-tetrachlorodibenzo-p-dioxin was only slightly higher than in a control group of 7 persons(5). All 53 samples of human milk collected from North Rhine-Westphalia, Germany (formally West Germany) tested positive with a mean value of 33 ng/kg, and a range of <1-40 ng/kg, calculated on a fat basis(6). Between 1994 to early 1995, the avg concn of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin in adipose tissue was 21 pg/g lipid (n=18; range, 4-54.7 pg/g lipid) for males and 18 pg/g lipid (n=14; range, 0.9-54 pg/g lipid) samples taken from residents of western Kyungnam, Korea(7).

Autopsies of two humans from the general population detected the following concns of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin (in parts per trillion) in various tissue: abdominal fat, 61-64; subcutaneous fat, 60-61; liver, 6.5-48; muscle, 5.8-7.9; kidney, 2.5-4.0(1). 1,2,3,6,7,8-Hexachlorodibenzo-p-dioxin concns of 35-48 ng/kg (lipid basis) were detected in two human milk samples collected in 1986 from Binghamton, NY(2). Forty-six samples of adipose tissue collected from the general population in Canada in 1976 contained a mean 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin concn of 87 parts per trillion wet wt basis(3). In the fall of 1993, the mean concns of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin in the serum of Great Lakes sport fish consumers were measured as follows (all parts per trillion lipid wt)(4): all lakes, 134 (n=31; range, 71.9-190); Lake Michigan, 120 (n=11; range, 88.7-228); Lake Huron, 142 (n=11; range, 88.7-228); Lake Eire, 115 (n=11; range, 85.1-150); comparison group, 70.8 (range 24.8-160). In 1994-1996, the breast milk of primaparas and muliparas Japanese women from western Japan contained 29 pg/g lipid (n=51) and 19 pg/g lipid (n=44), respectively(5). Between the years 1993-1994, the mean concn of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin in the blood of 50 normal women (age approx 20 years old) was 30 pg/g lipid (range, 13-75 pg/g lipid)(6). Pooled samples of breast milk from 15 mothers living in the Tarragona area (southern Catalonia, Spain) contained 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin at an avg concn of 27.88 pg/g fat (range, 15.10-38.00 pg/g fat) sampled in 1996(7). Human milk from Swedish women contained 42, 27, 20, 27, and 21 pg/g lipids sampled in the years 1972, 1990, 1991, 1992, and 1997, respectively(8). In 1992, a pooled sample of breast milk from 40 mothers (ages 15-38 years old, most primiparae) living in the urban area of Rio de Janeiro, Brazil contained 21 pg/g milk fat of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin(9). The concn of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin in human fat samples from volunteers in Coimbatore, southern India, was 20 pg/g fat wt (range, 8.2-48 pg/g fat wt) for males and 22 pg/g fat wt (range, 9.0-38 pg/g fat wt) for females(10).

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)

LD50 Oncorhynchus mykiss (Rainbow trout, newly fertilized eggs) injection 1.427 ug/L 7 days post-exposure (95% CI: 0.996-2.822) /Conditions of bioassay not specified/

EC50 Oryzias latipes (Japanese medaka, embryos) 7-ethoxyresorufin O-deethylase induction 6.4 ng/L/72 hr /Conditions of bioassay not specified/

EC50 Oryzias latipes (Japanese medaka, embryos) abnormal growth 0.200 ug/L (95% CI: 0.075-0.530) 3 days post-hatch, static

EC50 Oryzias latipes (Japanese medaka, embryos) decreased hatch 29.5 ng/L/72 hr /Conditions of bioassay not specified/

ED50 Cyprinus carpio (Carp) ip injection, increased enzyme activity in the liver 0.500 mmol/kg 2 wk post-exposure /Conditions of bioassay not specified/

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 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin is expected to be immobile in soil(SRC). Volatilization of 1,2,3,6,7,8-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). 1,2,3,6,7,8-Hexachlorodibenzo-p-dioxin is not expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 3.6X10-11 mm Hg(4). No biodegradation was reported for 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin in a sludge-amended soil field study(5); however, in an anologous study, a half-life of approx 20 years was reported(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 1,2,3,6,7,8-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 in the water column(SRC). The estimated volatilization half-life from a model pond is 410 days if adsorption is considered(5). According to a classification scheme(6), a BCF of 87,100 for guppies(7), suggests bioconcentration in aquatic organisms is very high(SRC). Based on field studies in soil, 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin is not expected to biodegrade(8) or will biodegrade slowly with a half-life of 20 years(9).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin, which has a vapor pressure of 3.6X10-11 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely in the particulate phase in the ambient atmosphere(SRC). Particulate-phase 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin may be removed from the air by wet and dry deposition(SRC).

1,2,3,6,7,8-Hexachlorodibenzo-p-dioxin levels of 8.1 and 5.7 ng/kg (wet basis) were detected in chicken and eggs, respectively, purchased from markets in Matsuyama, Japan in 1986(1); levels in vegetables, oil, rice, wheat, fish, beef, and pork were below detection limits(1). A sample of pork fat was found to contain a 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin concn of 123 ng/kg(2). Meat collected at a local market in Mettupalayan, India contained 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin at concns as follows (all pg/g fat wt)(3): chicken (0.8); lamb (4.2); goat (3.0). Food samples collected in 1995 from Binghamton, NY; Atlanta, GA; Chicago, IL; San Diego, CA; Louisville, KY contained 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin at concns as follows (all pg/g wet wt): beef, 6.5; pork, 1.7; hot dog/bologna, 3.6; fresh fish, 2.6; butter 10.0; cheese, 3.1; ice cream, 2.8(4). The concn of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin was measured in cooked and uncooked meat samples taken from Binghamton, NY supermarkets in 1996(5). Hamburger, uncooked and cooked, contained mean concns of 304.8 pg/kg wet wt (range, 294.8-314.9 pg/kg wet wt) and 293.2 pg/kg wet wt (range, 270.9-314.4 pg/kg wet wt) of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin, respectively, with a net concn change of -3.8% with cooking(5). Bacon, uncooked and cooked, contained mean concns of 87.7 pg/kg wet wt (range,<56.6-152.2 pg/kg wet wt) and 139.0 pg/kg wet wt (range, <62.1-282.1 pg/kg wet wt) of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin, respectively, with a net concn change of +58.5% with cooking(5). Catfish, uncooked and cooked, contained mean concns of 235.4 pg/kg wet wt (range, 207.6-269.5 pg/kg wet wt) and 140.6 pg/kg wet wt (range, 106.5-162.6 pg/kg wet wt) of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin, respectively, with a net concn change of -40.3% with cooking(5).

The concn of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin in US fast foods are as follows (all pg/g wet wt): McDonald's Big Mac, 2.2; Pizza Hut Personal Pan pizza, 1.5; Haagan Daz Ice Cream, 2.8(1). In three butter samples from Spain, 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin detected at mean concns of 0.61 pg/g fat wt (n=3; range, not quantified to 0.94 pg/g fat wt), 0.94 pg/g fat wt (n=3; range, not quantified to 1.33 pg/g fat wt), and ranging from not quantified to 0.32 pg/g fat wt (not quantified = 3X detection limit)(2). The concn of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin in 9 butter samples from Australia ranged from 0.02 to 0.27 pg/g fat(3). The mean concns of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin in food sampled in Germany between the years 1993-1996 were as follows(4): butter, 0.36 pg/g fat (n=222; range, 0.00-1.10 pg/g fat); eggs, 1.70 pg/g fat (n=218; range, 0.09-35.13 pg/g fat); meat, 0.42 pg/g fat (n=107; range, 0.04-5.42 pg/g fat); fish, 3.81 (n=138; range, 0.00-100.59). Samples of food of animal origin from Germany (formerly West Germany) had levels of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin as follows (all ng/kg fat basis)(10): cheese, 0.8 (n=10; range, 0.4-1.2); beef, 0.7 (n=5; range, 1.3-6.0); veal, 5.3 (n=4; range, 3.3-8.0); pork, <0.5 (n=3); sheep, 3.0 (n=2; range, 2.3-3.7); chicken, 1.8 (n=2; 1.7-1.8); canned meat, 3.2 (n=2; range, 0.9-7.4); lard, 0.3 (n=4; range, <0.5-0.6).

Samples of human milk collected in the Netherlands contained 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin concns ranging from 0.17 to 5.2 ng/kg(1). Levels detected in human milk from Germany (formerly West Germany) were 6.2-13 parts per trillion (fat wt basis), respectively(2). 1,2,3,6,7,8-Hexachlorodibenzo-p-dioxin concns of 35-48 ng/kg (lipid basis) were detected in two human milk samples collected in 1986 from Binghamton, NY(3). All 53 samples of human milk collected from North Rhine-Westphalia, Germany tested positive with a mean value of 33 ng/kg, and a range of <1-40 ng kg, calculated on a fat basis(4). In 1994-1996, the breast milk of primaparas and muliparas Japanese women from western Japan contained 29 pg/g lipid (n=51) and 19 pg/g lipid (n=44), respectively(5). Pooled samples of breast milk from 15 mothers living in the Tarragona area (southern Catalonia, Spain) contained 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin at an avg concn of 27.88 pg/g fat (range, 15.10-38.00 pg/g fat) sampled in 1996(6). Human milk from Swedish women contained 42, 27, 20, 27, and 21 pg/g lipids sampled in the years 1972, 1990, 1991, 1992, and 1997, respectively(7). In 1992, a pooled sample of breast milk from 40 mothers (ages 15-38 y.o. most of which were primiparae) living in the urban area of Rio de Janeiro, Brazil contained 21 pg/g milk fat of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin(8).

Levels detected in cow's milk from Germany (formerly West Germany) was 0.3-0.73 parts per trillion (fat wt basis)(1). 1,2,3,6,7,8-Hexachlorodibenzo-p-dioxin levels of 0.068-0.29 ng/kg were detected in six samples of cow's milk from Switzerland(2); levels were higher in samples collected in the vicinity of incinerators(2). Samples of cow's milk from North Rhine-Westphalia Germany contained 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin at a concn of 4.0 parts per trillion fat basis (range, 0.05-10.0 parts per trillion fat basis)(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)

1,2,3,6,7,8-Hexachlorodibenzo-p-dioxin /was calculated/ to be about 3.5 yr. The estimation was based on the analysis of fat tissue biopsies collected with an interval of 28 months from one 14 year old girl who for a period of about 2-3 years had been exposed to technical pentachlorophenol.

/In a/... study of 48 workers at a German pesticide facility, elimination half times were estimated for several CDD congeners. The estimated half-/life was/... 13.1 years for 1,2,3,6,7,8-HxCDD... .

In rats, primary hydroxylation of dibenzo-p-dioxins takes place exclusively at 2, 3, 7, or 8 position.

The metabolism of seven polychlorodibenzofuran isomers were studied in female Sprague Dawley rats. Bile samples were taken from surgically implanted bile duct cannulas over a period of 3 to 7 days, beginning 2 hr after dosing with the appropriate polychlorodibenzofuran isomer. Doses were administered either intravenously or by oral gavage. Metabolites were isolated from bile and analyzed as hydroxylated cmpd by GS/MS. The tetrachlorodibenzofuran isomers underwent rapid biotransformation. No ring opened products were seen, and both isomers were metabolized to hydroxylated tetrachlorodibenzofurans and trichlorodibenzofurans, and dihydroxy-trichlorodibenzofurans. The metabolites of the pentachlorodibenzofuran isomers showed quantitative differences in distribution; 1,2,3,4,8-pentachlorodibenzofuran metabolized primarily to hydroxy-pentachlorodibenzofurans, 1,2,3,7,8-pentachlorodibenzofuran resulted in dihydroxy-pentachlorodibenzofurans, and 2,3,4,7,8-pentachlorodibenzofuran metabolites were varied and resulted from ether bond cleavage. Neither 1,2,3,6,7,8-hexachlorodibenzofuran nor 1,2,3,4,6,7,8-heptachlorodibenzofuran resulted in discernible metabolite concn. It was concluded that polychlorodibenzofuran metabolism in rat liver is primarily due to oxidation, or hydrolytic or reductive dechlorination, that ether bond cleavage is a relatively unimportant metabolic mechanism, that chlorine substitution patterns affect metabolism, and that metabolism of polychlorodibenzofurans decreases with more than two chlorines in each ring.

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)

In the period 1980 to 1982, 19 cormorants (Phalacrocorax carbo), 3 herons (Ardea cinerea), and 1 great crested grebe (Podiceps crisatus) were collected in The Netherlands. The livers of these fish-eating birds were analyzed for polychlorinated dibenzo-p-dioxins and dibenzofurans. Only congeners with a 2,3,7,8-chlorine substitution pattern were found in the livers. The major component was 2,3,4,7,8-pentachlorodibenzofuran and 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin, 2,3,7,8-tetrachlorodibenzo-p-dioxin, 1,2,3,7,8-pentachloridibenzo-p-dioxin were also present. Six pooled samples of the eel Anquilla anquilla showed the same congeneric pattern of chemicals as found in these bird species. In the eel, 2,3,4,7,8-pentachlorobenzofuran and 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin were generally present in the 1-5 ng/kg range. Since the eel is the cormorant's major food, this indicates strong bioaccumulation for both congeners in the liver of the cormorant.

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/

Human adipose tissue samples obtained during autopsies in 5 Canadian municipalities within the Great Lakes basin were analyzed for polychlorinated dibenzodioxins and dibenzofurans using GC-high resolution-MS. The mean congener values for male and female donors in each municipality are comparable with previously reported data. No significant differences in congener levels between male and female and between municipalities were detected. A positive correlation between congener level and age was observed for several congeners as well as for the total congener concn expressed as its 2,3,7,8-tetrachlorodibenzodioxin toxic equivalent.

The tissue distribution of 2,3,7,8-chlorine substituted dibenzo-p-dioxins was conducted in 11 patients who died of cancer. The concn of octachlorodibenzo-p-dioxin was the highest in each organ and tissue and heptachlorodibenzo-p-dioxin was also found at relatively high levels, second only to octachlorodibenzo-p-dioxin. The levels of 1,2,3,7,8-pentachlorodibenzo-p-dioxin and 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin in the spleen were the highest, respectively. 2,3,7,8-Tetrachlorodibenzo-p-dioxin was also detected and its concentration was the highest in the gonad (0.8-3.2 pg/g-range). From the 2,3,7,8-tetrachlorodibenzodioxin toxic equivalent calculations, the highest equivalent value was obtained from a 54 yr old female who died of cancerous goiter. This individual had the highest concentration of 2,3,7,8-substituted penta- and hexachlorodibenzo-p-dioxins among the 11 patients.

For more Absorption, Distribution and Excretion (Complete) data for 1,2,3,6,7,8-HEXACHLORODIBENZO-P-DIOXIN (8 total), please visit the HSDB record page.

Found in emissions from waste incineration and PCB transformer fires and as impurity in chlorinated pesticides and pentachlorophenol; Not commercially produced; [HSDB] Hexachlorodibenzo-p-dioxins (HCDD): Found as impurities in polychlorinated phenols and chlorophenol derivative herbicides (i.e. 2,4-D); [NTP]

NOT USED COMMERCIALLY IN THE USA

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)

MORE TOXIC MEMBERS OF THE SERIES OF CHLORINATED DERIV OF DIBENZODIOXIN, WHICH CAN RANGE FROM MONO- TO OCTA-SUBSTITUTED HAVE AT LEAST 3 BUT NO MORE THAN 7 HALOGENS /SRP: IN THE 2,3,7,8-POSITIONS/. /POLYCHLORINATED DIBENZODIOXINS/

PENTACHLOROPHENOL MAY CONTAIN 9-27 MG/KG MIXED ISOMERS OF HEXACHLORODIBENZO-PARA-DIOXIN ... . /HEXACHLORODIBENZO-PARA-DIOXIN/

One of the 21 tetrachlorophenol samples /that were analyzed/ contained ... 29 mg/kg ... /of/ hexachlorodibenzo-p-dioxin. ... Analysis /of 8 commercial pentachlorophenols/ ... showed /that/ hexachlorodibenzo-p-dioxins ... ranged from 0.03 to 38 mg/kg; they were present in all of the 8 pentachlorophenol samples. /Hexachlorodibenzo-p-dioxins/

/Samples analyzed by mass fragmentography/ were found to contain ... 6 mg/kg of hexachlorodibenzo-p-dioxins /in commercial 2,3,4,6-tetrachlorophenol (TCP) and/ 9 mg/kg hexachlorodibenzo-p-dioxins /in technical pentachlorophenol (PCP)/. The positional isomers of the dioxins were not identified. /Hexachlorodibenzo-p-dioxins/

Hexachlorodibenzo-p-dioxins were found in both technical and analytical grades of commercial pentachlorophenol, as determined by gas chromatography coupled with several detection methods. When an electron capture detector was used, the technical grade product was found to contain 42 mg/kg ... and the analytical grade product had 0.03 mg/kg /of hexachlorodibenzo-p-dioxins/. /Hexachlorodibenzo-p-dioxins/