1,2,3,7,8,9-Hexachlorodibenzo-p-dioxin

390.86100

390.86

CV865M3P15

2811

DTXSID6023781

2932999060

18.46000

7.50500

1.777g/cm3

243-244 °C

478ºC at 760mmHg

182.9ºC

1.666

This compound should be stored under refrigeration at 5 °C and protected from light.

7.72E-09mmHg at 25°C

/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.

Insoluble in water.

Ethers

1,2,3,7,8,9-HEXACHLORODIBENZO-P-DIOXIN is stable under normal laboratory conditions. Solutions may be sensitive to light. Methanol solutions are degraded on exposure to sunlight or ultraviolet irradiation. (NTP, 1992)

I

6.1(a)

UN 2811

This compound is stable under normal laboratory conditions. Solutions may be sensitive to light. Solutions of this chemical in water, DMSO, 95% ethanol or acetone should be stable for 24 hours under normal lab conditions.

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.

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.

Flash point data for this chemical are not available. It is probably combustible. (NTP, 1992)

|Warning|H302 (100%): Harmful if swallowed [Warning Acute toxicity, oral]|P264, P270, P273, P301+P312, P330, P391, 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 under refrigeration at 41° F 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). RECOMMENDED GLOVE MATERIALS: It is recommended that you wear two dissimilar glove types when working with this chemical. (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/

1,2,3,7,8,9-Hexachlorodibenzo-p-dioxin was emitted from municipal and industrial waste incinerators at emissions ranging from 0.69-7.06 ng/normal cu m (n=4) and 18.47-156.06 pg/normal cu m (n=2), respectively(1). Emissions of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin from an incinerator in northeast Spain were 6.44 ng/normal cu m(2). Paper mill effluent contained 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin at a concn of 351.1 pg/L(2). Highly contaminated leachate from a landfill contained 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin at a concn of 270 pg/L(2). Emissions of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in the flue gas from a hazardous waste incinerator in Biebesheim, Germany was 0.024 ng/normal cu m in September 1992(3). In Bayreath, Germany, samples of household water contained concns of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin ranging from 0.56-3.6 pg/L (n=3) in 1991 and 0.45-1.3 pg/L (n=5) in 1992(4). The concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in vehicle exhaust particles ranged from <1.8 to 0.63 pg/g for gasoline engines and <1.5 to <17.3 pg/g for diesel engines(5).

SOIL: In a rural district in the western part of Germany, the mean concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin was determined in the following in soils (all ng/kg dry matter)(1): plowland, 2.0 (n=14; range 1.6-2.4); grassland, 1.7 (n=7); deciduous forests, 19.1 (n=9; range 3.6-82.0); and coniferous forests, 16.2 (n=11; range 5.3-54.3). Archived soil samples collected from the same plot in southeast England between the period 1846-1986 range from 160 to 520 pg/kg(2). Soil samples collected in the surroundings of chemical waste incinerator (CWI) in Madrid, Spain contained 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin at concns ranging from not detected to 4.50 pg/g (detection limit, 0.02-0.51 pg/g)(3). The concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in soil samples collected in the vicinity of a municipal solid waste incinerator (MSWI) in Tarrogona, Spain ranged from 0.35-0.70 ng/kg dry wt in 1996 and 0.51-0.96 ng/kg dry wt in 1997(4). The concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in soil from an old landfill near Marka (north of Amman), Jordan, which was used for more than 35 years, ranged from <10 to 567 ng/kg dry wt(5). The concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in soil and soil near roadways sampled at Stockholm, Sweden ranged from <1.6-11 pg TEQ/g (n=4) and 5.0-16.6 pg TEQ/g (n=4), respectively(6).|SEDIMENT: In Sweden, the concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in sediments 3 and 10 kilometers from a pulp and paper mill were 2.7 and 2.5 pg/g dry wt, respectively(1). The concn of 1,2,3,7,8,9-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(2); between the years 1865-1918, it was not detected; 1951-1957, 0.54 ng/kg dry wt; 1957-1963, 0.53 ng/kg dry wt; 1963-1968, 2.64 ng/kg dry wt; 1968-1972, 1.93 ng/kg dry wt; 1972-1977, 3.75 ng/kg dry wt; 1977-1981, 5.59 ng/kg dry wt; 1981-1985, 11.06 ng/kg dry wt; 1991-1993, 6.68 ng/kg dry wt(2). At 24 sites from the Venice lagoon, Italy, the concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin ranged from <0.003 to 0.184 ug/kg(3). The concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in stormwater sediment (collected in sediment traps) from Bayreath, Germany ranged from 4.2-19 ng/kg(4); the concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in other sediments also from this urban location were as follows (all ng/kg): industry runoff, 1.7; household runoff, 2.4; runoff, 2.0; runoff basin sediments, 4.0(4).

URBAN/SUBURBAN: Outdoor air samples were taken a total 127 days between May, 1985 and March, 1986 from North Rhine-Westphalia, Germany; the concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in these samples ranged from 0.02 to 0.12 pg/cu m(1). In 1987, ambient air samples from Ohio contained 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin at concns ranging from not detected to 64 fg/cu m(2). In the atmosphere of Bloomington, IN in 1986, the vapor and particulate phase concns of 1,2,3,7,8,9/1,2,3,4,6,7-hexachlorodibenzo-p-dioxin were determined to be 1.3 and 8.9 fg/cu m(3). During the Fall/Winter of 1987-88, the concn of 1,2,3,7,8,9-hexachlorodibenzo- p-dioxin averaged 0.075 pg/cu m in the Bridgeport, CT metropolitan area(4). At several locations around Southern California during the period 1987-1989, the concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin averaged between 0.18 to 0.29 pg/cu m(5). The concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in the ambient air of northeast Spain (Catalonia) ranged from 0.020 to 0.210 pg/normal cu m(6). Between 1991-1995, the concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin typically ranged from 30-200 fg/cu m in the urban air of London and Manchester in the United Kingdom(7). The concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in the ambient air from North-Rhine-Westfalia, Germany ranged from 35 to 78 fg I-TEQ/cu m (or 350 to 780 fg/cu m using TEF of 0.1) in 1987-88 and 17 to 42 fg I-TEQ/cu m (or 170 to 420 fg/cu m using TEF of 0.1) in 1993-1994(8). Between 1998-1999, the concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin was 19.70 fg/cu m at Seoul (an urban site) and 59.53 fg/cu m at Incheon (an industrial site), both cities in South Korea(9).|INDOOR: The indoor air of kindergarten classrooms in Germany with PCP-treated wood interior structures had levels of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin ranging from 0.15 to 0.26 pg/cu m(1).|RURAL/REMOTE: At central McMurdo, Antartica, 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin was detected in one air sample at a concn of 0.04 pg/cu m at Dec 28-30, 1992(1).|SOURCE DOMINATED: At sampling sites near a municipal waste incinerator (MWI) in Dayton, OH, the concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin was 0.91 pg/cu m in the year 1988(1). The concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin was 16 ng/g and 110 pg/cu m in dust and air, respectively, sampled over a 6-day period from a municipal incineration plant from Europe (location unspecified)(2).

The concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in flue dust from steel producing plants in Germany ranged 4.28-554 ng/kg (n=4)(1). Fly ash and slag from an incinerator in northeast Spain contained 3.24 and 0.55 ng/g of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin, respectively(2). The concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in biosludge from a Kraft paper mill in Finland ranged from not detected (detection limit unspecified) to 5 pg/g dry wt(3). Municipal wastewater sludge from Finland contained 3.3 pg/g dry wt of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin(3). Sewage sludge samples collected from 4 locations around Stockholm, Sweden between May-August 1989 contained 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin at concns ranging from <1.0 to 1.7 pg/g organic wt(4).

LD50 Rat (male) oral 1.8 mg/kg body wt /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 body wt /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 body wt /Mixture of 31% 1,2,3,6,7,8- and 67% 1,2,3,7,8,9-hexachlorobenzo-p-dioxins/|LD50 Mouse (female) oral 0.5 mg/kg body wt /Mixture of 31% 1,2,3,6,7,8- and 67% 1,2,3,7,8,9-hexachlorobenzo-p-dioxins/|LD50 Guinea pig oral 60-100 ug/kg

/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/

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 of alveolar/bronchiolar 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 incidence 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 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin when compared with the untreated controls. In female mice, the incidences of frbrosarcomas of the skin were significantly higher (p= 0.044) in animals administered mixture of 1,2,3,6,7,8- and 1,2,3,7,8,9-hexachlorodibenzo-p-dioxins (both with and without pretreatment with DMBA) than in the untreated control group; however, when the incidences were compared with those of the vehicle controls (relative risk= 3.037) the results were not significant.

1,2,3,7,8,9-Hexachlorodibenzo-p-dioxin is neither produced or used in the USA. 1,2,3,7,8,9-Hexachlorodibenzo-p-dioxin is currently released to the environment primarily through emissions from the incineration of municipal and chemical wastes, in exhaust from automobiles using leaded gasoline, with PCB emissions, and from the improper disposal of certain chlorinated chemical wastes(1).

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).

1,2,3,7,8,9-Hexachlorodibenzo-p-dioxin is expected to exist solely in the particulate phase in the ambient atmosphere(SRC). Accordingly, photooxidation is not expected to be important(SRC). 1,2,3,7,8,9-Hexachlorodibenzo-p-dioxin is not expected to undergo hydrolysis in the environment due to the lack of hydrolyzable functional groups(1).

8.32e+03|The lipid based BCF value for 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in guppies (Poecilia reticulata) was calculated to be 30,200(1). In a second study, a BCF value of 85,000 was measured for guppies(2). In the presence of sediment, the BCF for guppies was slightly lower at 22,000(3). The avg biota-sediment accumulation factor for guppies was determined to be 0.008(6). According to a classification scheme(4), these BCF values suggest the potential for bioconcentration in aquatic organisms is very high(SRC).

Using a structure estimation method based on molecular connectivity indices(1), the Koc for 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin can be estimated to be 420,000(SRC). According to a classification scheme(2), this estimated Koc value suggests that 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin is expected to be immobile in soil(SRC).

The Henry's Law constant for 1,2,3,7,8,9-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 1,2,3,7,8,9-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). 1,2,3,7,8,9-Hexachlorodibenzo-p-dioxin's Henry's Law constant indicates that volatilization from moist soil surfaces may occur(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 65 years if adsorption is considered(3). 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).

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).

Occupational exposure to 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin may occur through inhalation and dermal contact with this compound at workplaces where 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin is produced or used(SRC). The concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in the blood of magnesium production workers from Porsgrunn, Norway was 7.3 pg/g lipid (n=9; range, 3.3-14 pg/g lipid) while the concn in a control group was 4.2 pg/g lipid (n=9; range, 2.1-5.9 pg/g lipid)(1). The concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in the blood of chimney sweeps from Bavaria, Germany was 5.79 pg/g blood fat (n=227; range, 2.01-15.97 blood fat) while the concn in a control group was 4.77 blood fat (n=60; range, 0.96-15.31 pg/g lipid)(2). The mean concn of 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin in the serum of workers exposed to dioxin was 13 parts per trillion (n=151; range, 3-39 parts per trillion) while the mean concn of the referent (unexposed group) was 13 parts per trillion (n=49; range, 3.6-33 parts per trillion)(3). Monitoring data indicate that the general population may be exposed to 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin via inhalation of ambient air, and ingestion of food containing 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin(SRC).

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).

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/

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/

19.95 Days|/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/... 4.9 years for 1,2,3,7,8,9-HxCDD... . /1,2,3,7,8,9-Hexachlorodibenzo-p-dioxin/

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. ACUTE/CHRONIC HAZARDS: This chemical is extremely hazardous. Ingestion of small quantities can cause toxic effects. It can 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. When heated to decomposition it emits very toxic fumes. (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)

Persons with recent exposure to polychlorodibenzodioxins ... should have the chemicals removed from their skin as quickly as possible to prevent additional absorption of the compounds. Exposed person should be asked for an exposure history, including onset of exposure, duration of exposure, and type of exposure. Physical examinations, including a thorough examination of the skin, should be given. Routine blood and liver laboratory tests should be carried out. In most situations, however, evidence of exposure and disease relatable to the exposure will be lacking. Because chloracne is the only human effect documented thus far, no other specific abnormality can be considered pathognomonic for exposure. /Polychlorodibenzodioxins/|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/ Other less consistently reported effects from dioxin exposure in humans include /asthenia/, headaches, and pain in the extremities, peripheral neuropathy, ulcers, altered liver function, enzyme induction, altered lipid metabolism, and abnormal urinary porphyrin patterns. Immune system dysfunction and altered T-cell subsets have been reported by some investigators but have not been found by others. /Polychlorodibenzodioxins/|/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 hepatic porphyria in mice. A serum sample taken after the consumption 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).|/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/|For more Human Toxicity Excerpts (Complete) data for 1,2,3,7,8,9-HEXACHLORODIBENZO-p-DIOXIN (7 total), please visit the HSDB record page.

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

Thermal or chemical degradation of chlorophenols can produce ... /Polychlorodibenzoparadioxins/

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.|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.|EPA Method 8280A, The Analysis of Polychlorinated Dibenzo-p-Dioxins and Polychlorinated Dibenzofurans by High Resolution Gas Chromatography/Low Resolution Mass Spectrometry; Analyte: 1,2,3,7,8,9-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.|Method: EPA-EAD 1613, Tetra-through Octa-Chlorinated Dioxins and Furans by Isotope Dilution High Resolution Gas Chromatography/High Resolution Mass Spectrometry; Analyte: 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin; Matrix: water, soil, sediment, sludge, tissue, and other sample matrices; Detection Level: 50 picogram/l.