1,2,3,4,6-Pentachlorodibenzo-p-dioxin

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 82,000(SRC), determined from a log Kow of 6.50(2) and a regression-derived equation(3), indicates that pentachlorodibenzo-p-dioxin is expected to be immobile in soil(SRC). Volatilization of pentachlorodibenzo-p-dioxin from moist soil surfaces is expected to be an important fate process(SRC) given an estimated Henry's Law constant of 2.2X10-6 atm-cu m/mole(SRC), derived from its vapor pressure, 5.6X10-10 mm Hg(4), and water solubility, 1.2X10-4 mg/l(5). However, adsorption to soil is expected to attenuate volatilization(SRC). Pentachlorodibenzo-p-dioxin is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(4). Pentachlorodibenzo-p-dioxin is susceptible to direct photolysis based on a half-life of 7.6 hr in n-hexadecane solution for 1,2,3,7,8-pentachlorodibenzo-p-dioxin(6). Therefore, some photodegradation may occur on surfaces exposed to sunlight(SRC), although the relative importance of surface photodegradation is unknown(SRC). Biodegradation of pentachlorodibenzo-p-dioxin in soil is expected to be very slow(SRC). 100 percent of pentachlorodibenzo-p-dioxin (as 1,2,3,7,8-pentachlorodibenzo-p-dioxin) applied to a sandy loam soil, at pH 8.1, remained in the soil after a 15 month period(7).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 82,000(SRC), determined from a log Kow of 6.50(2) and a regression-derived equation(3), indicates that pentachlorodibenzo-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 2.2X10-6 atm-cu m/mole(SRC), derived from its vapor pressure, 5.60X10-10 mm Hg(4), and water solubility, 1.20X10-4 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 21 and 236 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 52 years if adsorption is considered(6). According to a classification scheme(7), BCF values of 810(8) and 1,434(9) are high and very high, respectively(SRC). Pentachlorodibenzo-p-dioxin in water is susceptible to direct photolysis in sunlight(9); however, adsorption to sediment and suspended solids may minimize any importance of aquatic photodegradation(SRC). Based on a soil field study(10), biodegradation of pentachlorodibenzo-p-dioxin in water is expected to be very slow(SRC). 100 percent of pentachlorodibenzo-p-dioxin (as 1,2,3,7,8-pentachlorodibenzo-p-dioxin) applied to a sandy loam soil, at pH 8.1, remained in the soil after a 15 month period(10).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), pentachlorodibenzo-p-dioxin, which has a vapor pressure of 5.60X10-10 mm Hg at 25 °C(2), is expected to exist solely in the particulate phase in the ambient atmosphere(SRC). However, monitoring data suggest that pentachlorodibenzo-p-dioxin will also exist in the vapor-phase in the ambient atmosphere(3). Vapor-phase pentachlorodibenzo-p-dioxin is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 28 days(SRC), calculated from its rate constant of 5.8X10-13 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(4). Particulate-phase pentachlorodibenzo-p-dioxin may be removed from the air by wet and dry deposition(SRC). Particle-bound pentachlorodibenzo-p-dioxin is removed from the atmosphere in rain and has been identified in precipitation samples(5,6). Dry deposition also has been observed(6). Photodegradation of pentachlorodibenzo-p-dioxin bound to fly ash is not an important atmospheric removal mechanism(7).

The concn of pentachlorodibenzo-p-dioxin averaged 28, 1,509, 164, and 186 parts per trillion in apple, chicken, egg, and sugar samples, respectively, purchased during the period of October 1985-March 1986 in Akita city, Japan(1). In the same study, the concn ranged from <10-208 parts per trillion in cereals, 16-204 parts per trillion in beans, and 13-38 parts per trillion in vegetables(1). Pentachlorodibenzo-p-dioxin median concns were 38 pg/g in egg, 246 pg/g in chicken liver and 198 pg/g in chicken fat in samples taken from Oroville, CA in 1988 following a fire at a wood treatment plant(2). The concn of pentachlorodibenzo-p-dioxin in vegetable, chicken, and egg samples collected in Japan during June of 1986 were 0.1, 1.3, and 0.9 pg/g, respectively(3). Pentachlorodibenzo-p-dioxin was found at concns < 2 ng/kg dm in apples and pears from trees in Rheinfelden, Germany(4).

The average concn of pentachlorodibenzo-p-dioxin in milk samples purchased during the period of October 1985-March 1986 in Akita city, Japan was 121 parts per trillion(1).

1,2,3,7,8-Pentachlorodibenzo-p-dioxin has been detected in human milk; avg levels in human milk fat are <30 parts per trillion(1). In 1989, the avg pentachlorodibenzo-p-dioxin concn in human milk samples taken from 100 nursing mothers from Stockholm, Sweden was approximately 10 pg/g fat(2). The concn of pentachlorodibenzo-p-dioxin in breast milk samples was measured in mothers from Kazakstan in 1994(location, concn in pg/g fat): rural, 14.60 (n=7); Almaty, 2.39 (n=5); Aralsk, 1.91 (n=6); Atyrau, 3.97 (n=6); Shymkent, 2.43 (n=5); Qyzyl-Orda, 1.38(n=5)(3).

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)

/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/

1,2,3,7,8-Pentachlorodibenzo-p-dioxin concns ranged 4.6-104 pg/g in snapping turtles taken from the upper St. Lawrence river in 1984 and 1985(1). The concn of pentachlorodibenzo-p-dioxin in sea slug, sea urchin, starfish, mussel, and snail taken from Hiraiso, Japan was 0.59, 3.40, 2.40, 8.6, and 0.53 pg/g wet wt, respectively(2). Between 1990-91, pentachlorodibenzo-p-dioxin was found in nonviable eggs of the endangered Mississippi sandhill crane (Jackson County, Mississippi) at concns ranging from not detected (detection limit = 1 pg/g) to 216 pg/g wet wt (n=10)(3).