1,2,3,6,7,8-Hexachlorodibenzo-p-dioxin

390.9 g/mol

390.86

B94L7A4G3D

2811

DTXSID0023824

18.5 Ų

log Kow = 8.21 /Estimated/

285-286 °C

This compound should be stored at ambient temperatures and protected from light.

3.60e-11 mmHg|3.6X10-11 mm Hg at 25 °C /extrapolated/

Henry's Law constant = 1.9X10-6 atm-cu m/mole @ 25 °C /Estimated/

/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 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin is 0.1.

Insoluble in water.

Ethers

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)

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.

Solutions of this type of compound in methanol are degraded by exposure to summer sunlight or irradiation with an ultraviolet lamp (300 nm).

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

Flash point data for this compound are not available; however, it is probably combustible. (NTP, 1992)

|Danger|H301 (100%): Toxic if swallowed [Danger Acute toxicity, oral]|P264, P270, P273, P280, P301+P310, P305+P351+P338, P321, P330, P337+P313, P405, and P501|Aggregated GHS information provided by 38 companies from 1 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Excerpt from ERG Guide 154 [Substances - Toxic and/or Corrosive (Non-Combustible)]: As an immediate precautionary measure, isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids. SPILL: Increase, in the downwind direction, as necessary, the isolation distance shown above. FIRE: If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. (ERG, 2016)

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. STORAGE PRECAUTIONS: This compound should be stored at ambient temperatures and protected from light. Allow only your most experienced personnel access to this aliquot. (NTP, 1992)

MINIMUM PROTECTIVE CLOTHING: If Tyvek-type disposable protective clothing is not worn during handling of this chemical, wear disposable Tyvek-type sleeves taped to your gloves. RECOMMENDED RESPIRATOR: Where the neat test chemical is weighed and diluted, wear a NIOSH-approved half face respirator equipped with a combination filter cartridge, i.e. organic vapor/acid gas/HEPA (specific for organic vapors, HCl, acid gas, SO2 and a high efficiency particulate filter). (NTP, 1992)

Fires involving this material can be controlled with a dry chemical, carbon dioxide or Halon extinguisher.

...Dioxins may be formed during the combustion of PCBs in fires and explosions. /Dioxins/

The concn of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin (plus the 1,2,3,4,7,8-isomer) detected on the fly ash from a municipal incinerator was 50.54 ug/kg(1). A 1,2,3,6,7,8- hexachlorodibenzo-p-dioxin concn of 1,440 ppb was detected in oil leachates from a waste dump site in Germany which had been receiving waste oils and liquid chemical wastes(2). Levels of 3.7 to 40 ng/cu m were monitored in stack effluents from a municipal solid waste incinerator in Sweden in 1985(3). Soot from a PCB transformer fire in Binghamton, NY contained a 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin concn of 0.6 ppm(4). 1,2,3,6,7,8-Hexachlorodibenzo-p-dioxin was detected in gasoline and diesel engine exhaust particles and suspended particulate matter at concns ranging from 1.36 to <3.8 pg/g (n=3) and 4.59 to <17.3 pg/g (n=3), respectively(5). The concn of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin in emission gas from 2 Japanese crematories was 2.6 ng/normal cu/m and 0.62-2.6 ng/normal cu m, respectively(6).|1,2,3,6,7,8-Hexachlorodibenzo-p-dioxin was emitted from municipal and industrial waste incinerators (located in northeast Spain) at mean values ranging from 0.46-8.72 ng/normal cu m and 43.63-60.19 ng/normal cu m, respectively(1), while the concn of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin in ambient air at these locations ranged from 0.020-0.155 pg/normal cu m(1). Emissions of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin from a municipal waste incinerator in the northeast of Spain were 1.57 ng/normal cu m(2). Paper mill effluent and highly contaminated leachate from a landfill contained 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin at concns of 270 and 169.1 pg/L, respectively(2).

SOIL: Soils from three rural areas of Europe contained 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin levels below 2 ng/kg while two soils from industrialized areas contained levels of 19-64 ng/kg(1). In a rural district in the western part of Germany, the mean concn of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin was determined in the following in soils (all ng/kg dry matter)(2): plowland, 1.5 (n=14; range, 1.1-1.8); grassland, 1.9 (n=7; range, 1.4-2.9); deciduous forests, 12.4 (n=9; range, 3.1-49.4); and coniferous forests, 11.1 (n=11; range, 3.7-28.8). The concn of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin ranged from 0.25 to 0.54 ng/kg dry matter in soil samples collected 4-6 km from the stack of a municipal solid waste incinerator located near Tarragona, Spain(3).|SEDIMENT: Hexachlorodibenzo-p-dioxins have been detected in sediments from Lake Lugano, Switzerland, Lake Siskiwit (Michigan) and the Danube River Southwest Germany(1). 1,2,3,6,7,8-Hexachlorodibenzo-p-dioxin concns of 2.0-48 ng/kg were identified in sediments collected from the archipelago of Stockholm, Sweden(2). The concn of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin in sediments of Grober Arbersee (near Bayerisch-Eisenstein in the Bavarian Forest, southeast Germany) increased between the approx years 1951 to 1993(3); between the years 1865-1918, it was not detected; 1951-1957, 0.89 ng/kg dry wt; 1957-1963, 1.07 ng/kg dry wt; 1963-1968, 2.11 ng/kg dry wt; 1968-1972, 1.88 ng/kg dry wt; 1972-1977, 4.57 ng/kg dry wt; 1977-1981, 4.40 ng/kg dry wt; 1981-1985, 9.63 ng/kg dry wt; 1991-1993, 7.61 ng/kg dry wt(3). Sediments from the Venice (Italy) lagoon contained 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin at concns ranging from 0.08 to 3.35 pg/g dry wt(4). At 18 sites in the Venice lagoon (Italy), the concn of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin in surficial sediments ranged from <0.002 to 0.208 ug/kg(5). In 1998, the concn of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin in sediments from the upper Detroit and Rouge rivers ranged from 0.72-51.6 (n=6) and 28.3-43.1 (n=4) pg/g dry wt, respectively(6).

URBAN/SUBURBAN: 1,2,3,6,7,8-Hexachlorodibenzo-p-dioxin has been detected in urban dust collected in Washington, DC(1). Air samples collected in Hamburg, Germany contained 0.23-2.2 pg/cu m(2). Air particulates collected at various locations in Sweden contained 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin levels of 0.004-0.046 pg/cu m(2). Between 1991-1995, the concn of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin typically ranged from 10-170 fg/cu m in the urban air of London and Manchester in the United Kingdom(3). In 1987, ambient air samples from Ohio contained 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin at concns ranging from not detected to 78 fg/cu m(4). Between 1998-1999, the concn of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin was 11.93 fg/cu m at Seoul (an urban site) and 48.75 fg/cu m at Incheon (an industrial site), both cities in South Korea(5). The concn of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin in the ambient air from North-Rhine-Westphalia, Germany ranged from 42 to 90 fg I-TEQ/cu m (or 420 to 900 fg/cu m using TEF of 0.1) in 1987-88, 11 to 38 fg I-TEQ/cu m (or 110 to 380 fg/cu m using TEF of 0.1) in 1991-92, and 20 to 51 fg I-TEQ/cu m (or 200 to 510 fg/cu m using TEF of 0.1) in 1993-1994(6).|INDOOR: The indoor air of kindergarten classrooms in Germany with pentachlorophenol (PCP)-treated wood interior structures had levels of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin ranging from 1.34 to 2.70 pg/cu m(1).

1,2,3,6,7,8-Hexachlorodibenzo-p-dioxin has been identified in commercial sample of pentachlorophenol and its sodium salt(1); the avg concentrations of hexachlorodibenzo-p-dioxin in technical pentachlorophenol from 4 manufacturers was determined to 1.3-33.6 ppm(2). Maximum 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin levels of 2.1 and 5.1 ug/kg have been detected in motor oils and refined waste oils(3). The following concentrations (in parts per trillion) were detected in various types of paper: newsprint, 1.2; laboratory filter paper, 3.2; cosmetic tissue, 12; recycled scrap paper, 48(4). The concn of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin in 19 contemporary sewage sludges from Catalonia, Spain ranged from 2.5 to 360 pg/g dry wt in the years 1994 to 1998, while 24 archived sewage samples (years 1979 to 1987) ranged from 26 to 55,000 pg/g dry wt(5). Undigested sewage sludge from Sachsen-Anbalt, Germany contained 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin at a concn of 272 ng/kg dry wt(6). The concn of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin in municipal waste incinerator fly ash and slag were 2.24 and 0.18 ng/g at a facility in the northeast of Spain(7).

LD50 Rat (male) oral 1.8 mg/kg bw /Mixture of 31% 1,2,3,6,7,8- and 67% 1,2,3,7,8,9-hexachlorodibenzo-p-dioxins/|LD50 Rat (female) oral 0.8 mg/kg bw /Mixture of 31% 1,2,3,6,7,8- and 67% 1,2,3,7,8,9-hexachlorodibenzo-p-dioxins/|LD50 Mouse (male) oral 0.75 mg/kg bw /Mixture of 31% 1,2,3,6,7,8- and 67% 1,2,3,7,8,9-hexachlorobenzo-p-dioxins/|LD50 Mouse (female) 0.5 mg/kg bw /Mixture of 31% 1,2,3,6,7,8- and 67% 1,2,3,7,8,9-hexachlorobenzo-p-dioxins/|LD50 Guinea pig oral 70 ug/kg

/FIELD STUDIES/ Studying liver samples of 16 adult male polar bears /(Ursus maritimus)/ ...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/

Groups of 50 male and 50 female Osborne-Mendel rats were administered via gavage doses of 1.25, 2.5, or 5 ug/kg/wk of a mixture of 1,2,3,6,7,8- and 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in corn oil/acetone (9:1) 2 days/week for 104 weeks. A dose-related depression in mean body weight gain was noted with no adverse effect on survival. In female rats, an increase in the incidence of hepatocellular carcinomas or adenomas (neoplastic nodules) was noted. Nonneoplastic liver and lung lesions were also noted. /Hexachlorodibenzo-p-dioxin mixture/|Groups of 50 male B6C3F1 mice were administered via gavage doses of 1.25, 2.5, or 5 ug/kg/wk and groups of 50 female mice were administered 2.5, 5, or 10 ug/kg/wk of a mixture of 1,2,3,6,7,8- and 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in corn oil/acetone (9:1) 2 days/week for 104 weeks. No adverse effect on survival was noted for either sex. In male and female mice, an increase in the incidence of hepatocellular carcinomas or adenomas was noted. Nonneoplastic liver and lung lesions were also noted. /Hexachlorodibenzo-p-dioxin mixture/|A mixture of 1,2,3,6,7,8- and 1,2,3,7,8,9-hexachlorodibenzo-p-dioxins ... (0.01 ug) suspended in 0.1 ml acetone was applied to the backs of 30 /Swiss Webster/ mice of each sex 3 days per week for 104 weeks. During the first 16 weeks, doses were 0.005 ug mixture of 1,2,3,6,7,8- and 1,2,3,7,8,9-hexachlorodibenzo-p-dioxins per application. An additional 30 mice of each sex were pretreated with one application of 50 ug 7,12-dimethylbenz(a)anthracene (DMBA) in 0.1 ml acetone 1 week before the inititation of the mixture of 1,2,3,6,7,8- and 1,2,3,7,8,9-hexachlorodibenzo-p-dioxins applications. As vehicle controls, 45 mice of each sex received 0.1 ml of acetone three times per week. Thirty animals of each sex served as untreated controls. ... Mean body weights of untreated controls were higher than those of the test and vehicle control groups. In male mice, the incidence ronchiolar carcinomas in the group administered only mixture of 1,2,3,6,7,8- and 1,2,3,7,8,9-hexachlorodibenzo-p-dioxins was significantly higher (p= 0.045) than that in the vehicle control group; however, the idence was not significantly higher when compared with untreated controls. In male mice, the incidence of lymphomas or leukemias was significantly lower (p= 0.011) in the group administered only mixture of 1,2,3,6,7,8- and when compared with the untreated were significantly higher (p= 0.044) in animals administered mixtures of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxins (both with and p; however, when the incidences were compared with those of the vehicle risk= 3.037) the results were not significant.

1,2,3,6,7,8-Hexachlorodibenzo-p-dioxin occurs as a contaminant in the pesticide 2,4,5-T and in the wood preservative pentachlorophenol(1-3); therefore, environmental applications of these compounds may release 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin to the environment(SRC). 1,2,3,6,7,8-Hexachlorodibenzo-p-dioxin is also released to the environment in stack effluents and fly ash emissions from municipal waste incineration(4,5). Leachates from waste dump sites receiving waste oils and liquid chemical wastes may release the compound to soil and groundwater(6). Releases of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin have occurred in soot emissions from accidental transformer fires involving PCBs and chlorinated hydrocarbons(7).

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).

The rate constant for the vapor-phase reaction of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin with photochemically-produced hydroxyl radicals has been estimated as 0.31X10-12 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 51 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). 1,2,3,6,7,8-Hexachlorodibenzo-p-dioxin is not expected to undergo hydrolysis in the environment due to the lack of hydrolyzable functional groups(2). 1,2,3,6,7,8-Hexachlorodibenzo-p-dioxin will undergo direct photolysis in sunlight(3).

8.51e+03|The BCF value for 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin in guppies was calculated to be 87,096 using contaminated food (concn in food ranged from 32 to 753 ug/kg lipid wt for 73 polychlorinated dibenzo-p-dioxins) and 80-day exposure period (1). According to a classification scheme(2), this BCF suggests bioconcentration in aquatic organisms is very high(SRC). Carp exposed to fly ash from a municipal incinerator readily bioaccumulated 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin during a continuous flow exposure study(3); concn in the carp increased from not detectable at time zero to 47 ng/kg after 30 days to 105 ng/kg after 60 days of exposure(3).

Using a structure estimation method based on molecular connectivity indices(1), the Koc for 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin can be estimated to be 420,000(SRC). According to a classification scheme(2), this estimated Koc value suggests that 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin is expected to be immobile in soil(SRC).

The Henry's Law constant for 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin is estimated as 1.9X10-6 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin is expected to volatilize from water surfaces(2). Based on this Henry's Law constant, the volatilization half-life from a model river (1 m deep, flowing 1 m/sec, wind velocity of 3 m/sec)(2) is estimated as 2 days(SRC). The volatilization half-life from a model lake (1 m deep, flowing 0.05 m/sec, wind velocity of 0.5 m/sec)(2) is estimated as 28 days(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(3). 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).

SURFACE WATER: In a perchlorophenol (PCP) contaminated stream (Puareng) near Lake Rotorua, North Island, New Zealand; the concn of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin was measured as 4.1 pg/L during a sampling in May 1993(1).

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).

Occupational exposure may occur through inhalation and dermal contact to fire fighters and cleanup workers involved with PCB transformer fires(1,2), to workers involved with incineration operations(3), and to workers handling chlorinated pesticides, pentachlorophenol, or other compounds which may contain small impurities of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin(SRC). Cleanup workers inside an office building in Binghamton, NY were exposed to 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin levels of 0.6-1.2 ppm in surface dusts and soot during cleanup operations after a PCB transformer fire in February, 1981(1,2). Cable incineration workers and electricians from Sweden, who were potentially exposed to dioxins, had blood plasma concns of 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin ranging from 24-54 pg/g lipid while a control group had blood plasma concns ranging from 29-46 pg/g lipid(3). Monitoring data indicate that the general population may be exposed to 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin via inhalation of ambient air(4) and ingestion of food containing 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin(5).

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).

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.

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.

16.22 Days|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... .

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. ACUTE/CHRONIC HAZARDS: When heated to decomposition this compound may emit very toxic fumes of chloride ion. This compound is extremely toxic. Ingestion of very small quantities can cause toxic effects. It may also be absorbed through the skin. Allow only your most experienced personnel to work with this chemical. All non-essential personnel should leave the laboratory. (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. SKIN: IMMEDIATELY flood affected skin with water while removing and isolating all contaminated clothing. Gently wash all affected skin areas thoroughly with soap and water. IMMEDIATELY call a hospital or poison control center even if no symptoms (such as redness or irritation) develop. IMMEDIATELY transport the victim to a hospital for treatment after washing the affected areas. INHALATION: IMMEDIATELY leave the contaminated area; take deep breaths of fresh air. IMMEDIATELY call a physician and be prepared to transport the victim to a hospital even if no symptoms (such as wheezing, coughing, shortness of breath, or burning in the mouth, throat, or chest) develop. Provide proper respiratory protection to rescuers entering an unknown atmosphere. Whenever possible, Self-Contained Breathing Apparatus (SCBA) should be used; if not available, use a level of protection greater than or equal to that advised under Protective Clothing. INGESTION: If the victim is conscious and not convulsing, give 1 or 2 glasses of water to dilute the chemical and IMMEDIATELY call a hospital or poison control center. Generally, the induction of vomiting is NOT recommended outside of a physician's care due to the risk of aspirating the chemical into the victim's lungs. However, if the victim is conscious and not convulsing and if medical help is not readily available, consider the risk of inducing vomiting because of the high toxicity of the chemical ingested. Ipecac syrup or salt water may be used in such an emergency. IMMEDIATELY transport the victim to a hospital. If the victim is convulsing or unconscious, do not give anything by mouth, ensure that the victim's airway is open and lay the victim on his/her side with the head lower than the body. DO NOT INDUCE VOMITING. IMMEDIATELY transport the victim to a hospital. OTHER: Since this chemical is a known or suspected carcinogen you should contact a physician for advice regarding the possible long term health effects and potential recommendation for medical monitoring. Recommendations from the physician will depend upon the specific compound, its chemical, physical and toxicity properties, the exposure level, length of exposure, and the route of exposure. (NTP, 1992)

Emergency and supportive measures. Treat skin, eye, and respiratory irritation symptomatically. /Dioxins/|Specific drugs and antidotes. There is no specific antidote. /Dioxins/|Decontamination. 1. Inhalation. Remove victims from exposure and give supplemental oxygen if available. 2. Eyes and skin. Remove contaminated clothing and wash affected skin with copious soap and water; irrigate exposed eyes with copious tepid water or saline.Personnel involved in decontamination should wear protective gear appropriate to the suspected level of contamination. 3. Ingestion. a. Prehospital. Administer activated charcoal if available. Ipecac-induced vomiting may be useful for initial treatment at the scene (eg, children at home) if it can be given within a few minutes of exposure. b. Hospital. Administer activated charcoal. Gastric emptying is not necessary if activated charcoalcan be given promptly. /Dioxins/|Enhanced elimination. There is no known role for these procedures. /Dioxins/

/HUMAN EXPOSURE STUDIES/ All members of a Spanish family (father, mother and six children) developed chloracne. The causative agent was found to be the family's stock of olive oil, which had become contaminated with polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans, pentachlorophenol, and hexachlorobenzene. The more highly chlorinated polychlorinated dibenzo-p-dioxins, in particular octachlorodibenzo-p-dioxin, were the predominant congeners in the oil. Three members of the family exhibited either an overt or a sub-clinical disturbance of kidney function. The father also had a chronic respiratory problem. These changes could not be unequivocally attributed to the polychlorinated dibenzo-p-dioxins. Experimental toxicity of the oil was limited to the development of the oil ceased, contained high levels of the polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans. Extrapolation back to ingested dose was used to validate dosage estimates. The use of toxicity equivalence factors provided estimates of cumulative dosage to produce chloracne as 0.13-0.31 ug 2,3,7,8-tetrachlorodibenzodioxin/kg (using EPA toxicity equivalence factors) or 6.7-16 ug 2,3,7,8-tetrachlorodibenzodioxin/kg (using Nordic/NATO toxicity equivalence factors). This is the first incident in which human toxicity is related primarily to ingestion of polychlorinated dibenzo-p-dioxins and for which estimates of dosage can be made.|/HUMAN EXPOSURE STUDIES/ Workers exposed to dioxin had adipose tissue levels with a mean of 246 ppt. Unexposed workers had levels of 86 ppt. Nine workers with a history of exposure to PCDD's and chloracne in 1971 to 1973 had TCDD serum levels of 340 pg per gram blood lipid in 1990.|/HUMAN EXPOSURE STUDIES/ Due to their lipophilicity, /Chlorinated dibenzo-p-dioxins/ (CDDs) can concentrate in human breast milk and can be transferred to infants through nursing. In general, the amount of individual congeners in breast milk decreased as chlorination decreases. Excretion via milk is highest during the first weeks after delivery. Also, the concentration of CDDs in milk is higher in mothers breast-feeding their first child than in those breast-feeding their second child. CDDs transferred to infants through nursing are readily absorbed by the infants. A pharmacokinetic model predicted that the increased body burden in infants that results from breast-feeding does not translate into raised lifetime body burden. /Chlorinated dibenzo-p-dioxins/|/HUMAN EXPOSURE STUDIES/ Two studies of nursing infants suggest that ingestion of breast milk with a higher dioxin-furan TEQ value may alter thyroid function. Both studies had similar exposure groupings and some findings in common: both had significant increases in /thyroid-stimulating hormone (TSH)/ at about 3 months of age with higher TEQs, and in one report, significant increases at about 2 weeks of age and in the cord blood. ...These two developmental studies investigated relatively small numbers of infants with thyroid parameters in the normal range. However, tha:high" group, at about 3 months of age, had increased TSH levels in comparison to the "low" group. Total T4 levels and total T4 to thyroid binding globulin (TBG) ratio were generally elevated in the high infants. /Polychlorinated dibenzo-p-dioxins and dibenzofurans/|For more Human Toxicity Excerpts (Complete) data for 1,2,3,6,7,8-HEXACHLORODIBENZO-P-DIOXIN (8 total), please visit the HSDB record page.

1,2,3,6,7,8-hexachlorodibenzo-p-dioxin

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/

Fat, oil, fatty acid, or lipid is treated with sulfuric acid and extracted with petroleum ether. Extract is purified on an aluminum oxide column, further treated with sulfuric acid, and examined by EC/GC. Peaks with retention times relative to aldrin (Ra) between 8 and 45 indicate presence of chick edema factors (hexa-, hepta-, and octa-chlorodibenzo-p-dioxins). ... Peaks at 8-13 /are due/ to the hexachlorodibenzo-p-dioxin isomers.|Method: EPA-EAD 1613, Tetra-through Octa-Chlorinated Dioxins and Furans by Isotope Dilution High Resolution Gas Chromatography/High Resolution Mass Spectrometry; Analyte: 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin; Matrix: water, soil, sediment, sludge, tissue, and other sample matrices; Detection Level: 50 picogram/l.|EPA Method 8280A, The Analysis of Polychlorinated Dibenzo-p-Dioxins and Polychlorinated Dibenzofurans by High Resolution Gas Chromatography/Low Resolution Mass Spectrometry; Analyte: 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin; Matrix: water, soil, fly ash, and chemical wastes; Quantitation Limit: water: 25 ng/l; soil: 2.5 ug/kg; fly ash: 2.5 ug/kg; and chemical wastes: 25 ug/kg.|Commercial chlorophenols were analyzed for chlorodibenzo-para-dioxins by fractionation on an aluminum oxide column, followed by GC with ECD and confirmation by MS. Di-, tri-, tetra-, penta-, hexa-, hepta- and octachlorodibenzo-para-dioxins were determined, with a detection limit of 20 ug/kg.|High-performance, reverse-phase, partition LC has been investigated as a means of determining chlorodibenzo-para-dioxins in pentachlorophenol. The samples were first subjected to an ion-exchange column cleanup to remove phenoxyphenols. Recoveries of 93-104%, with a relative error of + or - 10%, and a detection limit of 0.2 mg/kg for hexachlorodibenzo-p-dioxin ... was reported.

A method for multicomponent determinations of organochlorine contaminants in human milk is described. The lipophilic gel Lipidex 5000 was used for extraction of lipids and organochlorine cmpds. Further purification and separation was achieved by chromatography on partly deactivated aluminum oxide, Lipidex, silica gel, and active basic and acidic aluminum oxide. 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin was determind by selected-ion monitoring capillary column GC/MS at a resolution of 8000-9000.