옥타클로로디벤조-p-다이옥신

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.

Irradiation experiments (254 nm) were performed to decrease high polychlorinated dibenzo-p-dioxins/furans surface contaminations after a malfunction of a capacitor filled with a technique PCB formulation. Destruction efficiencies > 89% were achieved.

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

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

SRP: The scientific literature for the use of contact lenses in industry is conflicting. The benefit or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.

0.43 [mg/m3]

4.7 [mg/m3]

28 [mg/m3]

Breast milk from 9 women exposed to a PCB fire in Canada contained a mean octachlorodibenzo-p-dioxin concn of 193.44 ng/kg (fat basis) while the mean concn in milk from 16 control women was 131.70 ng/kg(1). Analysis of 30 human milk samples from Germany found levels of 0.185-1.217 (avg 0.530) ppb(2). Analysis of blood samples from a total of 300 humans in Vietnam, Germany and the US found levels of 0.087-1.655 ppb (lipid)(3). The following concns (ppb lipid) were found in human milk from various countries(3): Vietnam: 0.078-0.292; Cambodia: 0.059; Thailand: 0.068; Germany: 0.185; US: 0.233; Siberia: 0.0502(3). Autopsies of two humans from the US general population detected the following octachlorodibenzo-p-dioxin concns (ppb whole wt basis)(4): adipose tissue: 0.428-0.695; liver: 0.224-0.350; muscle: 0.076- 0.171; and kidney: 0.031-0.039(4). Based upon various monitoring studies, the background level of octachlorodibenzo-p-dioxin in human adipose tissue ranges from 0.050-1.500 ppb(5). Human adipose tissue obtained during autopsies in 5 Canadian municipalities had an avg concn of 1.0367 ng/g(6). An octachlorodibenzo-p-dioxin concn of 0.690 ppb was detected in the adipose tissue of a person exposed during a PCB transformer fire in Binghamton, NY(7); the concn in the adipose tissue of 4 control people was 0.428-0.695 ppb(7). Analysis of whole blood samples from 10 persons with no declared exposure found octachlorodibenzo-p-dioxin levels of 439-889 ng/kg fat basis(8). Results of the National Human Adipose Tissue Survey (NHATS) for fiscal year 1982 reported an octachlorodibenzo-p-dioxin concn range of 64-1250 ng/kg and a mean concn of 560 ng/kg(9).

Blood samples from several locations contained octachlorodibenzo-p-dioxin at mean concns as follows (location, concn in parts per trillion lipid wt): Baikalsk, Russia, 57 (whole, n=8); St. Petersburg, Russia, 89 (whole, n=60); North Vietnam, 132.3 (whole, n=82); South Vietnam, 696.4 (whole, n=383); Germany, 610.3 (whole, n=102); USA pooled, 1174 (plasma, n=100); Guam 748.6 (whole, n=10)(1). The concn of octachlorodibenzo-p-dioxin in individuals from Sweden with no, normal and high fish consumption were 357, 458, and 473 pg/g lipid, respectively(2). Whole blood from German mothers (collected in 1989) contained octachlorodibenzo-p-dioxin at a mean concn of 610 pg/g lipid (range, 145-1524 pg/g lipid)(3). Serum samples collected in 1993 from 11 donor with no known exposure to dioxins in Madrid, Spain contained octachlorodibenzo-p-dioxin at an avg concn of 397.03 (range 117.05-690) pg/g fat wt(4). Plasma samples from 20 non-occupationally exposed individuals living in Tarrogona, Spain contain octachlorodibenzo-p-dioxin at a mean concn of 640.5 pg I-TEQ/g lipid (n=20; range, 137.0-993.0 pg I-TEQ/g lipid)(5). Blood samples from 50 normal Japanese women volunteers (approx 20 yo) collected between June 1993-1994 was found to contain octachlorodibenzo-p-dioxin at an avg concn of 310 (range, 110-1000) pg/g lipid wt(6). Adipose, spleen, and kidney tissue samples from 50 normal Japanese women volunteers (approx 20 yo) collected between June 1993-1994 was found to contain octachlorodibenzo-p-dioxin at an avg concns of 2,500 (range, 170-16000) pg/g lipid wt; 1,100 (range, 170-5,400) pg/g lipid wt; and 690 (range, 120-3,500) pg/g lipid wt, respectively(6). The mean concn of octachlorodibenzo-p-dioxin in 8 normal subjects from Japan collected in 1989 was 2,000 pg/g lipid (range, 160-13,000 pg/g lipid)(7). Human blood from individuals living in Germany were as follows (period, concn in pg/g lipid)(8): 1989, 625 (n=228); 1991, 446 (n=95); 1992, 462 (n=157); 1993, 340 (n=17); 1994, 231.0 (n=74); 1995, 293 (n=69); 1996, 257 (n=95); 1997/98, 320 (n=9); 1989-1998, 441 (n=744).

Adipose tissue from 17 subjects who died in Madrid, Spain from natural causes contained octachlorodibenzo-p-dioxin at concns ranging from 91-2847.5 pg/g fat wt (mean, 1318.1 pg/g fat wt)(1). Finnish human tissue samples (n=3) taken post-mortem exams in Helsinki contained octachlorodibenzo-p-dioxin at concns as follows (tissue, concn range in pg/g fresh wt)(2): testis, <5-9; liver, 230-700; adipose, 300-350. Placenta and fetus samples were collected in Binghamton, NY between 1984-1985; placenta (pool of 14 samples) had 282.1 ng/kg lipid of octachlorodibenzo-p-dioxin while fetus (8-14 week old, pool of 10) had 98.8 ng/kg lipid of octachlorodibenzo-p-dioxin(3). Tissue and fluid specimens were collected in 1995/96 from mothers from upstate New York; samples were analyzed for octachlorodibenzo-p-dioxin as follows (tissue/fluid sample, concn in pg/g lipid)(4): adipose tissue, 214; predelivery blood, 374; placenta, 103; cord blood, 96; postpartum blood, 226; breast milk, 104. Levels of octachlorodibenzo-p-dioxin in adipose tissue samples from 15 autopsied subjects who lived in Tarragona, Spain (sampled between 1989-1999) ranged from 83.0 to 1,200 ng I-TEQ/kg fat (mean 472.53 ng I-TEQ/kg)(5). Levels of octachlorodibenzo-p-dioxin in adipose tissues from subjects living in Paris, France between Jan to May 1999 ranged from 0.01-0.09 pg I-TEQ/g lipid(6). The avg concn of octachlorodibenzo-p-dioxin in the blood of workers potentially exposed to dioxins in Finland between 1989-1990 were as follows (group, concn in pg/g lipid)(7): bleaching plant, 689 (n=14; range, 285-1471); paper mill, 625 (n=20; range, 288-1198); controls, 804 (range, 369-1745).

The concn of octachlorodibenzo-p-dioxin in human milk samples were determined for several locations around the world as follows (all ng/kg fat wt): USA Tennesse , 234; South Africa (Black), 196; South Africa (White), 254; Karachi, Pakistan, 180; Binh Long, Vietnam, 146; Vung Tau, Vietnam, 181; Tay Ninh, Vietnam, 415; Song Be province, 79.6(1). In a German study, a decrease in the concn of octachlorodibenzo-p-dioxin was found with the number of breast feeding periods(2); for example, the mean concn of octachlorodibenzo-p-dioxin in the first, sixth, and twelfth week of breast feeding was 292 (n=34), 252 (n=23), and 187 (n=6) pg/g fat, respectively(2). For human milk samples collected in 1985/86 at 3-geographic regions of Norway, the avg concn of octachlorodibenzo-p-dioxin ranged from 149.9 to 156.0 pg/g fat basis(3). Breast milk of Intuit women and women from southern Quebec had concns of octachlorodibenzo-p-dioxin of 292.3 (n=40) and 131.7 (n=96) ng/kg fat wt, respectively, for samples collected between 1989-1990(4). 526 human milk samples collected between 1986 and 1991 from mothers living in North Rhine-Westphalia, Germany contain octachlorodibenzo-p-dioxin at an avg concn of 1.4 pg/g fat (range, 0.2-14.0 pg/g fat)(5). Breast milk from Auckland (urban, n=20) and Christchurch (rural, n=17) sampled between Oct 1987 and May 1988 had avg concns of octachlorodibenzo-p-dioxin of 9.0 and 5.5 ng/kg in whole milk, respectively, and 220 and 200 ng/kg in milk fat, respectively(6). 26 human milk samples collected in late 1993-1994 from several locations in Japan contained octachlorodibenzo-p-dioxin at a mean concn of 4.9 pg/g whole milk (range, 1.4 to 14 pg/g whole milk)(7). Octachlorodibenzo-p-dioxin avg levels in human milk from Paris, France and Madrid, Spain were 290.0 (n=15) and 234.0 (n=13) pg/g fat wt collected in 1990(8). Thirty individual human milk samples from 5 main towns in Jordan contain octachlorodibenzo-p-dioxin at concns ranging from 29.0 to 147 ng/kg fat in 1994(9). Human milk samples taken from mothers living on the Kola Peninsula (Russia), a highly contaminated industrialized region, were analyzed for chemical contaminants(10); in human milk samples from the cities of Murmansk, Monchegorsk, and Tromso in April 1993, the concn of octachlorodibenzo-p-dioxin was 49.94 (n=15), 84.95 (n=15), and 106.48 ng/kg milk fat, respectively(10).

Levels of octachlorodibenzo-p-dioxin in pooled samples of breast milk collected in 1996 from mothers living in the Tarrogona area, Spain ranged from 53.00 to 234.00 pg/g fat (mean, 145.67 pg/g fat)(1). Human milk samples were collected from mother's living in Helsinki (urban) and Kuopio (rural), Finland; samples collected between 1992-1994 were found to contain octachlorodibenzo-p-dioxin at mean concns of 230 (n=20; range, 58.0-349) and 126 (n=64; range, 62.7-310) pg/g fat, respectively(2). A pooled sample of human milk (40 mothers) from Rio de Janeiro, Brazil in 1992 contained 420 pg octachlorodibenzo-p-dioxin per g milk fat(3). The concn of octachlorodibenzo-p-dioxin in Swedish mother's milk was determined as follows (year, concn in TEQ pg/g lipid where TEF=0.0001): 1972, 0.06; 1976, 0.04; 1980, 0.03; 1984/85, 0.02; 1988/89, 0.03; 1990, 0.03; 1991, 0.02; 1992, 0.02; 1997, 0.01(4).

Exposure to large amounts of CDDs causes chloracne, a severe skin disease with acne-like lesions that occur mainly on the face and upper body. CDDs may also cause liver damage and induce long-term alterations in glucose metabolism and subtle changes in hormonal levels. In addition, studies have shown that CDDs may disrupt the endocrine system and weaken the immune system, as well as cause reproductive damage and birth defects, central and peripheral nervous system pathology, thyroid disorders, endometriosis, and diabetes. (L177, L178)

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 690,000(SRC), determined from a log Kow of 8.20(2) and a regression-derived equation(3), indicates that octachlorodibenzo-p-dioxin is expected to be immobile in soil(SRC). Volatilization of octachlorodibenzo-p-dioxin from moist soil surfaces is expected to be an important fate process(SRC) given an estimated Henry's Law constant of 6.7X10-6 atm-cu m/mole(SRC), derived from its vapor pressure, 8.25X10-13 mm Hg(4), and water solubility, 4.00X10-7 mg/L(5). However, volatilization from moist soil surfaces is expected to be attenuated by adsorption to soil(SRC). Octachlorodibenzo-p-dioxin is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(4). Based on an aerobic digestion study in water(6), octachlorodibenzo-p-dioxin is not expected to degrade in soil under aerobic conditions(SRC). Using sewage sludge highly impacted by polychlorinated dibenzodioxins/dibenzofurans (PCDD/Fs), no increase or decrease in octachlorodibenzo-p-dioxin (in sludge) was observed under completely aerobic conditions after 100 days of sludge digestion at 20 °C(6). Under semi-aerobic conditions, a 2-fold increase octachlorodibenzo-p-dioxin in the sludge occurred(6). Under anaerobic conditions, a 20% loss of octachlorodibenzo-p-dioxin in sludge occurred as a result of mineralization(6).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 690,000(SRC), determined from a log Kow of 8.20(2) and a regression-derived equation(3), indicates that octachlorodibenzo-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 6.7X10-6 atm-cu m/mole(SRC), derived from its vapor pressure, 8.25X10-13 mm Hg(4), and water solubility, 4.00X10-7 mg/L(5). Using this Henry's Law constant and an estimation method(3), volatilization half-lives for a model river and model lake are 8 and 93 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 65 years if adsorption is considered(6). According to a classification scheme(7), BCF values of 8,500 in rainbow trout and 22,300 in fathead minnow(8), suggests bioconcentration in aquatic organisms is very high(SRC). Octachlorodibenzo-p-dioxin is not expected to degrade in water under aerobic conditions(SRC). Using sewage sludge highly impacted by polychlorinated dibenzodioxins/dibenzofurans (PCDD/Fs), no increase or decrease in octachlorodibenzo-p-dioxin (in sludge) was observed under completely aerobic conditions after 100 days of sludge digestion at 20 °C(9). Under semi-aerobic conditions, a 2-fold increase octachlorodibenzo-p-dioxin in the sludge occurred(9). Under anaerobic conditions, a 20% loss of octachlorodibenzo-p-dioxin in sludge occurred as a result of mineralization(9).

Analysis of food composites from market baskets collected by the Swedish EPA in 1989 found octachlorodibenzo-p-dioxin concns of 1.0-2.1 ng/kg(1); raw and fried Baltic herring had levels of 0.34-7.2 ng/kg(1). Various infant formulas were found to contain levels of 0.021-0.036 ppb octachlorodibenzo-p-dioxin(2). A market basket survey of Japanese foods found the following levels (in ng/kg wet basis)(3): vegetables: <0.3; oil: 4.4; rice & wheat: <1.3, fish: <5.0; beef: <4.5; pork: 11.9; chicken: <4.0; and eggs: <4.0(3). The following concns (in ng/kg) were detected in various foods collected between 1979-1984 as part of US Food and Drug Administration's Total Diet Study(4): bacon: 160; chicken: 29-252; eggs: 80-1610; pork chops: 27-53; beef liver: 133-3830(4). Levels of octachlorodibenzo-p-dioxin in food of animal origin were determined for sample collected from North Rhine-Westphalia, Germany as follows (sample, concn in parts per trillion fat basis)(5): cheese, 10.5 (n=10); butter, 11.6 (n=5); beef, 5.4 (n=3); veal, 22.3 (n=4); pork, 8.2 (n=3); sheep, 19.3 (n=2); chicken, 16.5 (n=2); canned meat, 53.0 (n=2); lard, 16.0 (n=4). Levels of octachlorodibenzo-p-dioxin in food samples (n=1414) purchased between 1993-1996 in North Rhine-Westphalia, Germany were as follows (sample, concn in pg/g fat)(6): milk, 1.82 (n=538; range, 0.09-13.46); butter, 1.37 (n=222; range, 0.75-4.76); eggs, 72.27 (n=218; range, 2.33-1923.56); meat, 11.13 (n=107; range, 1.11-212.88); fish, 20.53 (n=138; range, 2.01-425.82). The concn of octachlorodibenzo-p-dioxin in butter samples from Spanish supermarkets ranged from 1.35 to 26.6 pg/g fat wt(7). Fast food samples collected from Binghamton, NY; Atlanta, GA; Chicago, IL; San Diego, CA; Louisville, KY contained octachlorodibenzo-p-dioxin at concns as follows (all pg/g wet wt): McDonald's Big Mac, 1.59; Pizza Hut Personal Pan Pizza, 4.04; Kentucky Fried Chicken's Original Recipe, 2.55(8). 100 specimens of meat, dairy products, fish, vegetables, and fruit from Binghamton, NY, Louisville, KY, Atlanta, GA, Chicago, IL, San Diego, CA contained octachlorodibenzo-p-dioxin at concns as follows (all pg/g wet wt): ocean fish, 0.45; beef, 4.29; chicken, 1.07; pork, 8.00; hot dog/bologna, 25.70; eggs, 33.10; fresh fish, 5.88; butter, 59.2(9). Seafood samples from southern Mississippi collected in April and May 1994 contained octachlorodibenzo-p-dioxin at avg concns as follows (all pg/g fat wt): oyster, 537 (n=3); blue crab body, 320 (n=3); blue crab claw, 303 (n=3); crawfish head, 73 (n=2); crawfish tail, 225 (n=2); crawfish farm-raised, 800 (n=3); mullet fillet, 20.4 (n=2); Spanish mackerel, 76(10).

Analysis of cow's milk from various areas in Germany detected octachlorodibenzo-p-dioxin levels at or below 0.01 ng/kg fat basis(1). The following concns (ppb lipid) were found in human milk from various countries(2): Vietnam: 0.078-0.292; Cambodia: 0.059; Thailand: 0.068; Germany: 0.185; US: 0.233; Siberia: 0.0502(2). Cow's milk from NY had a reported level of 0.015 ppb(3). An analysis of various commercially available cow's milk in Sweden found levels of 1.0-7.8 ng/kg fat(4). Cow's milk (whole) collected from England and Wales, United Kingdom in 1989 contained octachlorodibenzo-p-dioxin at concns ranging from 0.256 to 0.322 ng/kg(5). In the Derbyshire, United Kingdom; whole milk samples were collected from affected farms (located near industrialized area) and non-affected farms and analyzed for chemical contaminants such as octachlorodibenzo-p-dioxin(6). The mean concn of octachlorodibenzo-p-dioxin in whole milk samples from non-affected farms between 1991-1993 was 0.47 (range, 0.12-2.9) ng/kg(6). The mean concn of octachlorodibenzo-p-dioxin in whole milk samples from affected farms between 1990-1991 ranged from 0.41-2.2 ng/kg (n=7) while between 1992-1994, the concn of octachlorodibenzo-p-dioxin ranged from 0.05-0.42 ng/kg (n=10)(6).

The concn of octachlorodibenzo-p-dioxin in human milk samples were determined for several locations around the world as follows (all ng/kg fat wt): USA Tennessee , 234; South Africa (Black), 196; South Africa (White), 254; Karachi, Pakistan, 180; Binh Long, Vietnam, 146; Vung Tau, Vietnam, 181; Tay Ninh, Vietnam, 415; Song Be province, 79.6(1). In a German study, a decrease in the concn of octachlorodibenzo-p-dioxin was found with the number of breast feeding periods(2); for example, the mean concn of octachlorodibenzo-p-dioxin in the first, sixth, and twelfth week of breast feeding was 292 (n=34), 252 (n=23), and 187 (n=6) pg/g fat, respectively(2). For human milk samples collected in 1985/86 at 3-geographic regions of Norway, the avg concn of octachlorodibenzo-p-dioxin ranged from 149.9 to 156.0 pg/g fat basis(3). Breast milk of Intuit women and women from southern Quebec had concns of octachlorodibenzo-p-dioxin of 292.3 (n=40) and 131.7 (n=96) ng/kg fat wt, respectively, for samples collected between 1989-1990(4). 526 human milk samples collected between 1986 and 1991 from mothers living in North Rhine-Westphalia, Germany contain octachlorodibenzo-p-dioxin at an avg concn of 1.4 pg/g fat (range, 0.2-14.0 pg/g fat)(5). Breast milk from Auckland (urban, n=20) and Christchurch (rural, n=17) sampled between Oct 1987 and May 1988 had avg concns of octachlorodibenzo-p-dioxin of 9.0 and 5.5 ng/kg in whole milk, respectively, and 220 and 200 ng/kg in milk fat, respectively(6). 26 human milk samples collected in late 1993-1994 from several locations in Japan contained octachlorodibenzo-p-dioxin at a mean concn of 4.9 pg/g whole milk (range, 1.4 to 14 pg/g whole milk)(7). Octachlorodibenzo-p-dioxin avg levels in human milk from Paris, France and Madrid, Spain were 290.0 (n=15) and 234.0 (n=13) pg/g fat wt collected in 1990(8). Thirty individual human milk samples from 5 main towns in Jordan contain octachlorodibenzo-p-dioxin at concns ranging from 29.0 to 147 ng/kg fat in 1994(9). Human milk samples taken from mothers living on the Kola Peninsula (Russia), a highly contaminated industrialized region, were analyzed for chemical contaminants(10); in human milk samples from the cities of Murmansk, Monchegorsk, and Tromso in April 1993, the concn of octachlorodibenzo-p-dioxin was 49.94 (n=15), 84.95 (n=15), and 106.48 ng/kg milk fat, respectively(10).

CDDs cause their toxic effects by binding to the aryl hydrocarbon receptor and subsequently altering the trascription of certain genes. The affinity for the Ah receptor depends on the structure of the specific CDD. The change in gene expression may result from the direct interaction of the Ah receptor and its heterodimer-forming partner, the aryl hydrocarbon receptor nuclear translocator, with gene regulatory elements or the initiation of a phosphorylation/dephosphorylation cascade that subsequently activates other transcription factors. The affected genes include several oncogenes, growth factors, receptors, hormones, and drug-metabolizing enzymes. The change in transcription/translation of these genes is believed to be the cause of most of the toxic effects of CDDs. (L177)

WATER: Based upon monitoring of Canadian drinking water, the avg daily intake of octachlorodibenzo-p-dioxin has been estimated to be 0.0001 ng/adult/day(1). FOOD: The daily intake of all polychlorinated dibenzodioxin isomers has been estimated to be 0.1397 ng/adult/day, the majority of which is octachlorodibenzo-p-dioxin(1); food contribution comes from most food groups with meat, eggs and dairy products the major contributors(1). Based upon a Japanese market basket survey, the avg daily intake for octachlorodibenzo-p-dioxin has been estimated as 0.690 ng/adult/day(2). Based on food samples collected in Madrid, Spain during April 1995, the avg daily intake of octachlorodibenzo-p-dioxin has been estimated as 16,144.96 pg/person/day(3).

/FIELD STUDIES/ Subchronic or Prechronic Exposure/ ... The effects of /octachlorodibenzo-p-dioxin (OCDD) and octachlorodibenzofuran (OCDF)/ on the early-life stages of zebra fish (Brachydanio rerio) were determined during a flow-through test based on a column generator method. No statistically significant effect of OCDD and OCDF on the survival and hatching time of the eggs was found. Furthermore, no effects on survival, weight, general appearance or behaviour of the larvae were observed at the end of the exposure period of 32 days. GC-MS analysis of test solution samples revealed geometric mean measured concentrations of 32 (OCDD) and 34 ng/l (OCDF), respectively. Concentrations in surviving larvae at the end of the study were 61 (OCDD) and 94 (OCDF) g/kg, respectively. These concentrations in zebra fish larvae were several orders of magnitude higher than concentrations in fish collected from the wild. In a review of the available laboratory fish experiments, we found a lack of biomagnification of OCDD and OCDF.

/FIELD STUDIES/ Recent reports reveal PCDDs and PCDFs in blubber of dugongs from northeastern Australia at concentrations ranging up to 390 pg/g. ... Only congeners with at least 2,3,7,8-chlorination were found in the dugongs, PCDDs predominated over PCDFs, and OCDD was highest. Octa and heptachlorinated compounds predominated over tetra and penta forms. ...The sources and possible effects of PCDDs and PCDFs on dugongs ar unknown. Exposure may be higher in dugongs than in other marine mammals because of feeding close to sediments, relatively higher inputs of OCDDs and hepta-CDDs from adjacent agricultural regions, biotransformation from precursors during hindgut digestion, or unique metabolic degradation capacities. /Polychlorinated dibenzodioxins/

/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/

Not commercially manufactured; May exist as impurity in certain herbicides and fungicides; [HSDB]

Farming (Pesticides) [Category: Industry]

Dioxins occur as by-products from the manufacture of organochlorides, the bleaching of paper, chlorination by waste and drinking water treatment plants, municipal solid waste and industrial incinerators, and natural sources such as volcanoes and forest fires. (L177, L178)

... By heating pentachlorophenol in the presence of an initiator, such as chlorine, bromine, iodine or 2,3,4,4,5,6-hexachloro-2,5-cyclohexadienone. Hexachlorocyclohexadienone, when heated in an atmosphere of carbon dioxide for 30 minutes, also yields octachlorodibenzo-p-dioxin.

Chlorodibenzo-p-dioxins are not manufactured commercially but ... are present as impurities in certain herbicide and fungicide formulations, such as 2,4,5-T and the pentachlorophenols. ... Pentachlorophenol may contain 575-2510 mg/kg octachlorodibenzo-p-dioxin.