2,3,7,8-테트라클로로디벤조-P-디옥신

log Kow = 6.8

6.8/7.02

Colorless needles

Colorless to white, crystalline solid

Colorless liquid

Needles

less than 1 mg/mL at 77 °F (NTP, 1992)

In water, 2X10-4 mg/L at 25 °C

1.4 g/L in ortho-dichlorobenzene; 0.72 g/L in chlorobenzene; 0.57 g/L in benzene; 0.37 g/L in chloroform; 0.11 g/L in acetone; 0.05 g/L in n-octanol; 0.01 g/L in methanol; 0.04 g/L in lard oil

Solubility in water: none

0.00000002%

Decomposes at 932 °F (NTP, 1992)

Decomposes

Decomposes

/2,3,7,8-Tetrachlorodibenzo-p-dioxin/ begins to decompose at 500 °C and virtually complete decomposition occurs within 21 seconds at a temp of 800 °C.

When heated to decomposition it emits toxic fumes of /hydrogen chloride/.

UV light (decomposes)

750-800 °C. Decomposes under the influence of UV light. This produces chlorine.

563 °F (NTP, 1992)

305 °C

305-306 °C

295 °C

581 °F

6.4e-10 mmHg at 68 °F ; 0.0000000014 mmHg at 77 °F (NTP, 1992)

1.50X10-9 mm Hg at 25 °C

Vapor pressure at 25 °C: negligible

(77 °F): 0.000002 mmHg

2,3,7,8-tetrachlorodibenzo-p-dioxin (tcdd) appears as white crystals or tan crystalline powder. (NTP, 1992)

Colorless to white, crystalline solid; [NIOSH]

COLOURLESS-TO-WHITE NEEDLE-LIKE CRYSTALS.

Colorless to white, crystalline solid. [Note: Exposure may occur through contact at previously contaminated worksites.]

Changed chemically when exposed in isooctane or n-octanol to UV light.

Tetrachlorodibenzo-p-dioxin is stable under ordinary conditions of storage.

2,3,7,8-TCDD is considered relatively stable toward heat, acids, and alkalies.

TCDD can undergo slow photochemical and bacterial degradation. It is degraded... when exposed to UVR. It is stable in water, DMSO, 95% ethanol, and acetone.

2336

2348；2350；2348；2350；2353；2386；2386；2386；2385；2385；2386

Danger

H300 (100%): Fatal if swallowed [Danger Acute toxicity, oral]；H319 (97.4%): Causes serious eye irritation [Warning Serious eye damage/eye irritation]；H400 (97.4%): Very toxic to aquatic life [Warning Hazardous to the aquatic environment, acute hazard]；H410 (100%): Very toxic to aquatic life with long lasting effects [Warning Hazardous to the aquatic environment, long-term hazard]

P264, P264+P265, P270, P273, P280, P301+P316, P305+P351+P338, P321, P330, P337+P317, P391, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 39 reports by companies from 2 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.；Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown. For more detailed information, please visit ECHA C&L website.

Hazard Traits - Bioaccumulation; Carcinogenicity; Dermatotoxicity; Developmental Toxicity; Endocrine Toxicity; Environmental Persistence; Hematotoxicity; Hepatotoxicity and Digestive System Toxicity; Reproductive Toxicity; Respiratory Toxicity；Authoritative List - CA MCLs; CA TACs; CWA 303(c); CWA 303(d); IARC Carcinogens - 1; NTP RoC - known; OEHHA RELs; OSPAR Priority Action Part A; Prop 65; WA PBTs；Report - regardless of intended function of ingredient in the product

Regulation (EC) No 178/2002 (amended)

The New Jersey Worker and Community Right to Know Act requires public and private employers to provide information about hazardous substances at their workplaces. (N.J.S.A. 34:5A-1 et. seq.)

Literature sources indicate that this chemical is nonflammable. (NTP, 1992)

Gives off irritating or toxic fumes (or gases) in a fire.

Excerpt from NIOSH Pocket Guide for 2,3,7,8-Tetrachloro-dibenzo-p-dioxin:；Exposure Routes: Inhalation, skin absorption, ingestion, skin and/or eye contact；Symptoms: Irritation eyes; allergic dermatitis, chloracne; porphyria; gastrointestinal disturbance; possible reproductive, teratogenic effects; In Animals: liver, kidney damage; hemorrhage; [potential occupational carcinogen]；Target Organs: Eyes, skin, liver, kidneys, reproductive system；Cancer Site: [in animals: tumors at many sites] (NIOSH, 2024)

2,3,7,8-Tetrachlorodibenzo-p-dioxin .

Dioxins accumulate in adipose tissue; they are animal carcinogens. Chloracne is the only overt clinical sign of dioxin exposure in humans. Of the 22 isomers of tetra-chlorinated dioxin, 2,3,7,8-TCDD is the one that contaminated the production of 2,4,5-trichlorophenol, Silvex, and 2,4,5-T. In acute animal studies, TCDD is toxic to the liver. Recent studies failed to find an association between TCDD and porphyrin levels; [LaDou, p. 517-20] Causes adverse reproductive effects in animals; No documented evidence of congenital abnormalities in humans; [REPROTOX] There are no firmly established relationships between concentrations (mainly considering TCDD) and health effects in people. Observations following industrial and accidental exposures have suggested that acute exposures resulting in serum concentrations of about 800 pg/g of lipid might be necessary to induce clinical effects such as chloracne, although levels in the thousands of pg/g of lipid do not always produce this effect. [Reference #2, p. 384] IARC classification for 2,3,7,8-Tetrachlorodibenzo-p-dioxin is known and for other isomers is not classifiable; An increased risk for all cancers combined was found in the high-exposure populations studied; [Reference #1] The German MAK Commission classifies TCDD as class 4, defined as: Substances with carcinogenic potential for which genotoxicity plays no or at most a minor role. No significant contribution to human cancer risk is expected, provided the MAK value is observed. [Guide to Occupational Exposure Values, p. xi] Mean levels in exposed workers were 2000 ppt in the US cohort, 1434 ppt in accident workers in the Dutch cohort, and 1008 ppt in the BASF workers (Germany) with chloracne. Levels were up to 2252 ppt in the Boehringer cohort (Germany). These levels are comparable to levels in rats that developed hepatocellular nodules when fed 10 ng/kg bw daily (1500-2000 ppt) and that developed hepatocellular carcinoma when fed 100 ng/kg/bw daily (5,000-10,000 ppt)

WHO; Environ Health Criteria 88: Polychlorinated Dibenzo-para-dioxins and Dibenzofurans p.262 (1989)

Clarke AN et al; A Review of 2,3,7,8-Tetra Chlorinated Dibenzodioxins and Toxicity Equivalencies in Fish in the United States and International Waterways; Hazardous Waste and Hazardous Materials 13 (4): 419-443 (1996).

Clarke AN et al; A Review of Polychlorinated Dibenzofurans and Polychlorinated Dibenzodioxins in Sediments in the United States and International Waterways; Hazardous Waste and Hazardous Materials 11 (2): 253-275 (1994).

Young AL et al; US NTIS AD REP AD-A062, 143: 247 (1978). Use in South Vietnam of Agent Orange, its toxicology, environmental fate and human risk were reviewed, incl nature & quantities, their handling & application. Emphasis was placed on herbicide orange & its assoc contaminant TCDD.

For more Special Reports (Complete) data for 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN (38 total), please visit the HSDB record page.

Listed as a hazardous air pollutant (HAP) generally known or suspected to cause serious health problems. The Clean Air Act, as amended in 1990, directs EPA to set standards requiring major sources to sharply reduce routine emissions of toxic pollutants. EPA is required to establish and phase in specific performance based standards for all air emission sources that emit one or more of the listed pollutants. 2,3,7,8-Tetrachlorodibenzo-p-dioxin is included on this list.

ln November 1953, an uncontrolled decomposition reaction occurred in an enclosed TCP production facilty of BASF at Ludwigshafen, Germany. 2,3,7,8-TCDD was formed during the reaction and contaminated the autoclave section of the building. Employees were exposed to 2,3,7,8-TCDD contamnant during subsequent clean-up and repair activities.

Explosion which produced cloud containing TCDD which settled over Seveso, Italy many weeks passed before public was alerted to dangers, children were already suffering from chloracne and many animals had died. Effects of TCDD on pregnant women & their babies show higher incidence of spontaneous abortion in TCDD exposed mothers. Other findings suggest deleterious effects on peripheral nervous system, as well as liver damage.

A chemical plant failure 13 miles north of Milan, Italy produced a dangerous contamination of inhabited areas. Environmental specimens were sampled & analyzed to assess distribution of tetrachlorodibenzo-p-dioxin in soil surface layer. On basis of contamination maps, 3 zones were established: Zone A, Zone B, & Zone R which enclosed the former 2. This report describes the procedure adopted to assess contamination of soil due to 2,3,7,8-tetrachlorodibenzo-p-dioxin. TCDD concn were seen to vary, ranging from less than 0.75 to approx 20X10+3 ug/m sq. TCDD levels were highest in Zone A, while Zones B & R exhibited lower levels of below 50 & below 5 ug/m sq, respectively.

TCDD was component of products of explosion which took place in 1963 at Philips Duphar 2,4,5-T factory in Netherlands. ... An estimated 30-200 g TCDD were released ... TCDD was identified as product of explosion which occurred in coalite company's 2,4,5-trichlorophenol factory in UK in 1968 ... quantity released was not estimated. ...

For more History and Incidents (Complete) data for 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN (12 total), please visit the HSDB record page.

Fires involving this material can be controlled with a dry chemical, carbon dioxide or Halon extinguisher. (NTP, 1992)

In case of fire in the surroundings, use appropriate extinguishing media.

Fresh air, rest. Refer for medical attention.

Remove contaminated clothes. Rinse and then wash skin with water and soap. Refer for medical attention .

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.

Give a slurry of activated charcoal in water to drink. Induce vomiting (ONLY IN CONSCIOUS PERSONS!). Refer for medical attention .

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)

(General first aid procedures)；Eye: Irrigate immediately - If this chemical contacts the eyes, immediately wash (irrigate) the eyes with large amounts of water, occasionally lifting the lower and upper lids. Get medical attention immediately.；Skin: Soap flush immediately - If this chemical contacts the skin, immediately flush the contaminated skin with soap and water. If this chemical penetrates the clothing, immediately remove the clothing and flush the skin with water. If irritation persists after washing, get medical attention.；Breathing: Respiratory support；Swallow: Medical attention immediately - If this chemical has been swallowed, get medical attention immediately.

TIH (Toxic Inhalation Hazard) - Term used to describe gases and volatile liquids that are toxic when inhaled. Some are TIH materials themselves, e.g., chlorine, and some release TIH gases when spilled in water, e.g., chlorosilanes. [ERG 2016].

0.00000001 [mg/m3], inhalable fraction[German Research Foundation (DFG)]

Advice for firefighters: Wear self contained breathing apparatus for fire fighting if necessary.

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.

... Polychlorinated dibenzo-p-dioxins should be protected from light and kept at 4 °C during transportation and storage.

PRECAUTIONS FOR "CARCINOGENS": Storage site should be as close as practicable to lab in which carcinogens are to be used, so that only small quantities required for ... expt need to be carried. Carcinogens should be kept in only one section of cupboard, an explosion-proof refrigerator or freezer (depending on chemicophysical properties ...) that bears appropriate label. An inventory ... should be kept, showing quantity of carcinogen & date it was acquired ... Facilities for dispensing ... should be contiguous to storage area. /Chemical Carcinogens/

... Studies show that ruthenium tetroxide can be used for detoxification of glassware and artifacts, and for the periodic purging of industrial reactors to counteract the accumulation of polychloro-p-dioxin residues. ...

PRECAUTIONS FOR "CARCINOGENS": A high-efficiency particulate arrestor (HEPA) or charcoal filters can be used to minimize amt of carcinogen in exhausted air ventilated safety cabinets, lab hoods, glove boxes or animal rooms ... Filter housing that is designed so that used filters can be transferred into plastic bag without contaminating maintenance staff is avail commercially. Filters should be placed in plastic bags immediately after removal ... The plastic bag should be sealed immediately ... The sealed bag should be labelled properly ... Waste liquids ... should be placed or collected in proper containers for disposal. The lid should be secured & the bottles properly labelled. Once filled, bottles should be placed in plastic bag, so that outer surface ... is not contaminated ... The plastic bag should also be sealed & labelled. ... Broken glassware ... should be decontaminated by solvent extraction, by chemical destruction, or in specially designed incinerators. /Chemical Carcinogens/

SMALL SPILLS AND LEAKAGE: If you spill this chemical, FIRST REMOVE ALL SOURCES OF IGNITION, then dampen the solid spill material with toluene, then using absorbent paper 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: You should protect this container from damage. Store at room temperature and protect from light. Allow only your most experienced personnel access to this aliquot. (NTP, 1992)

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity 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 and plant life; and conformance with environmental and public health regulations.

SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.

Degradation by chemical means are necessary for polychlorophenol formulations because heat stable chlorodioxins are formed during incineration. Ruthenium tetroxide is a powerful oxidizing agent which reacts with a wide range of organic substances, including those aromatic compounds which are oxidized slowly, or not at all, by permanganate. It may be safely used in solution in water or in organic solvents with no nucleophilic character, such as chloroform, nitromethane or carbon tetrachloride. ... Preliminary work with TCDD showed that the rate of oxidation was increased at higher temperature and that the half-life was less than 15 min in carbon tetrachloride at 70 °C (TCDD concentration = 72 ug/mL carbon tetrachloride; ruthenium tetroxide = 2X10+3 ug/mL, about 10 equiv). There is no evidence of the nature of fragments formed during oxidation of the polychlorodibenzodioxins. However, the related chlorophenols undergo extensive decomposition to yield chloride ions and no significant levels of organic products.

Polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans could be degraded by ozonation in an alkaline aqueous medium, but no reaction occurred in acid solutions. Degradation rates of at least 99% were observed after the reaction conditions (pH, temperature) had been optimized. The investigated substances with three to eight chlorine atoms had different velocities of reaction depending on their number and configuration following reactions of second order. The selective detection and quantitative determination of polychlorinated dibenzo-p-dioxin and polychlorinated dibenzofuran traces was performed by capillary gas chromatography in combination with a mass selective detector.

For more Disposal Methods (Complete) data for 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN (10 total), please visit the HSDB record page.

SRP: The scientific literature for the use of contact lenses by industrial workers is inconsistent. The benefits 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.

SRP: Contaminated protective clothing should be segregated in a manner such that there is no direct personal contact by personnel who handle, dispose, or clean the clothing. The completeness of the cleaning procedures should be considered before the decontaminated protective clothing is returned for reuse by the workers. Contaminated clothing should not be taken home at the end of shift, but should remain at employee's place of work for cleaning.

PRECAUTIONS FOR "CARCINOGENS": Smoking, drinking, eating, storage of food or of food & beverage containers or utensils, & the application of cosmetics should be prohibited in any laboratory. All personnel should remove gloves, if worn, after completion of procedures in which carcinogens have been used. They should ... wash ... hands, preferably using dispensers of liq detergent, & rinse ... thoroughly. Consideration should be given to appropriate methods for cleaning the skin, depending on nature of the contaminant. No standard procedure can be recommended, but the use of organic solvents should be avoided. Safety pipettes should be used for all pipetting. /Chemical Carcinogens/

PRECAUTIONS FOR "CARCINOGENS": In animal laboratory, personnel should remove their outdoor clothes & wear protective suits (preferably disposable, one-piece & close-fitting at ankles & wrists), gloves, hair covering & overshoes. ... clothing should be changed daily but ... discarded immediately if obvious contamination occurs ... /also,/ workers should shower immediately. In chemical laboratory, gloves & gowns should always be worn ... however, gloves should not be assumed to provide full protection. Carefully fitted masks or respirators may be necessary when working with particulates or gases, & disposable plastic aprons might provide addnl protection. If gowns are of distinctive color, this is a reminder that they should not be worn outside of lab. /Chemical Carcinogens/

For more Preventive Measures (Complete) data for 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN (15 total), please visit the HSDB record page.

In several studies that measured TCDD concentrations in blood and adipose tissue, the concentration was 10-20 pg/g (parts per trillion) lipid during the 1970s, and 2-10 parts per trillion lipid during the 1980s which suggests that concentrations are decreasing in human tissues(1). TCDD was found in human adipose tissue collected in 1984 and 1996 from the general population in Atlanta, GA at a range and mean concentration of 1.6-38.0 and 10.4 parts per trillion lipid, respectively(2). Analysis of 46 composite samples prepared from 900 adipose tissue specimens detected a mean TCDD concentration of 5.0 pg/g with a range of not detected (1.0 pg/g) to 10 pg/g as conducted by the USEPA National Human Adipose Tissue Survey for fiscal year 1982(3). Concentrations in adipose tissue were 3.5-750 parts per trillion wet weight basis, for 16 Missouri chemical plant workers(4). Adipose samples from workers (n=9) that made products contaminated with TCDD had levels of 42-750 parts per trillion; adipose samples from workers from other parts of the plant (n=7) had levels of 3.5-25.8 parts per trillion(4). TCDD was detected in 25 of 46 Canadian human adipose tissue samples collected in 1976 at a mean concentration of 6.4 pg/g(5).

The levels of TCDD in whole blood samples were as follows (concentration as parts per trillion lipid): Ho Chi Minh City, Vietnam, 3.4 (n=50); Don Nai, Vietnam (n=33), 12.0; Hanoi, Vietnam (n=32), <2.4; Germany, 3.6 (n=102); Baikalsk, Russia, 3.7 (n=8); St. Petersburg, Russia, 4.5; Guam, USA, 4.07(1). TCDD measured in serum specimens from residents who were potentially highly exposed to the 1976 explosion, Seveso, Italy, had levels as high as 56,000 parts per trillion(2). These TCDD levels are the highest ever reported, and yet almost all clinical laboratory tests on these individuals were normal; any abnormal test result was only transitory in nature(2). Concentrations of TCDD in plasma lipids of individuals residing in Quebec on the North Shore of the St. Lawrence River (fishing people; n=25) and in urban centers (n=30) were 13.8 and 2.2 ng/kg, respectively(3). Mean levels of TCDD in blood plasma from subjects living in Tarragona, Spain (non-occupationally exposed) were 1.9 pg I-TEQ (International toxicity equivalents)/g lipid (n=20; range, 0.9-5.3 pg I-TEQ/g lipid)(4). Blood levels of TCDD in residents of Mataro, Spain (North of Barcelona) were 1.6 and 1.5 parts per trillion/g fat weight in male and female residents, respectively, for samples collected in March-June 1995(5). Whole blood samples collected from German individuals in 1994 contain TCDD at a mean concentration of 2.9 pg/g lipid (n=134; range, 1.0-7.8 pg/g lipid)(6). Blood samples from 3 groups of men living in Norway (Fjord area) contained TCDD at average concentrations as follows (group, pg/g fat): reference, 3.6 (n=10; range, 0.2-7.0); moderate crab intake, 7.7 (n=15; range, 3-13.6); high crab intake, 11.0 (n=9; range, 6.3-22.4)(7). Between the period of 1989-1990, TCDD mean levels in plasma samples from Finish workers were reported as follows (industry group; pg/g lipid): control 4.1 (n=14; 1.3-10); bleaching plant, 5.7 (n=14; range, 0.6-22); paper mill, 3.1 (n=20; range, 0.2-9.3)(8). The concentrat

TCDD concentration (ng/kg lipid) in serum from a number of studies on highly exposed humans. Years equates to estimated years since last potential exposure and blood draw(1).[Table#4835]

The concentration of TCDD in tissue and fluid samples from 5 mothers women living in Upstate NY were as follows (sample, pg/g lipid): adipose tissue, 1.3; pre-delivery blood, 1.7; placenta, 2.7; cord blood, 1.3; postpartum blood, 1.5; breast milk, 1.4(1). Blood sampled in 1993 from men and women (non-occupationally exposed) living in the vicinity of a municipal waste incinerator in Schwandorf, Germany contained TCDD at <0.3-3.6 (mean, 1.3) and 0.4-3.3 (mean, 1.4) pg/g lipid, respectively(2). Human milk from women in this study had TCDD levels ranging from 0.6-2.0 pg/g milk fat (avg, 1.1 pg/g milk fat)(2). The concentration of TCDD in child-bearing women age group from an electronics recycling region (Taizhou) and reference region (Hangzhou) of Zhejiang Province, China was reported as 3.59 and 3.11 pg/g fat in human milk; 4.88 and 4.74 pg/g fat in the placenta and 2.31 and 4.48 pg/g dry weight in hair, respectively(3).

For more Body Burden (Complete) data for 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN (7 total), please visit the HSDB record page.

In mice, increased incidences in frequency of cleft palates .../were/ noted in combination experiments involving TCDD and other teratogens such as 2,4,5-T, dexamethasone, cyclophosphamide and 6-aminonicotinamide, admin at 'sub-threshold' and 'threshold' doses during days 6-15 of pregnancy. When 30 mg/kg bw 2,4,5-T, which produced no significant increase in incidence of cleft palate compared with that of controls, or half this dose, was combined with 2 ug/kg bw TCDD, potentiating effects were observed. However, 1/10 of TCDD dose (0.2 ug/kg bw) induced no detectable effect with either dose of 2,4,5-T.

Paw edema formation after subplantar injection of carrageenan was enhanced in rats treated with TCDD. It also enhances dextran-induced paw edema, which follows a time course different from that of carrageenan induced edema & is produced by a different mechanism.

The induction of cleft palate in C57BL/6N mice ... was used to look for potential interactions between two polychlorinated biphenyl congeners and TCDD. Both 2,3,4,5,3',4'-hexachlorobiphenyl and 2,4,5,2',4',5'-hexachlorobiphenyl are of relatively low toxic potency, but their biological properties differ. Pregnant mice were treated with TCDD and either hexachlorobiphenyl on gestation days 10 through 13, and the fetuses examined for the presence of cleft palate and renal abnormalities on gestation day 18. At a dose of TCDD which caused a low level of cleft palate, moderate hydronephrosis was observed. No renal or palatal anomalies were detected after 2,4,5,2',4',5'-hexachlorobiphenyl treatment, and the combination of this isomer with TCDD had no effect on the incidence of TCDD induced cleft palate. 2,3,4,5,3',4'-Hexachlorobiphenyl caused mild renal toxicity, but no cleft palate. However, treatment of pregnant mice with a combination of TCDD and 2,3,4,5,3',4'-hexachlorobiphenyl resulted in a 10 fold increase in the incidence of cleft palate.

Administration of 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) to 21 day old female Long Evans rats resulted in a dose dependent decrease in uterine and hepatic estrogen receptor levels. At a dose level of 80 ug/kg 2,3,7,8-TCDD, uterine and hepatic estrogen receptor levels were 54 and 41% of values observed in untreated animals. 2,3,7,8-TCDD also antagonized the estrogenicity of estradiol in the 21 day old rat. For example, administration of estradiol (15 ug/kg) resulted in a 194 and 155% increase in cytosolic and uterine estrogen receptor levels and a 42% increase in uterine wet weight 148 hr after treatment. Pretreatment of the rats with 2,3,7,8-TCDD (80 ug/kg) prior to administration of estradiol (15 ug/kg) completely blocked the estrogenic effects of estradiol. In fact, after cotreatment, the uterine and hepatic estrogen receptor levels were 51 and 54% lower than observed in the controls and the uterine wet weight was 20% lower than in the control animals.

For more Interactions (Complete) data for 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN (8 total), please visit the HSDB record page.

Developmental；Endocrine；Reproductive

Eyes, skin, liver, kidneys, reproductive system

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 pathologies, thyroid disorders, endometriosis, and diabetes. 2,3,7,8-Tetrachlorodibenzo-p-dioxin is also a known as a human carcinogen. (L177, L178)

LD50; Species: Colinus virginianus /(Northern Bobwhite)/ oral 0.0150 mg/kg (95% confidence limit: 0.00919-0.0245 mg/kg)

LD50; Species: Streptopelia risoria /(Ringneck dove)/ oral > 0.810 mg/kg

LD50; Species: Phasianus colchicus (Ring-Necked Pheasant) sexually mature organism, age 40-45 wk, weight 0.9-1.3 kg; ip 4.5 ug/kg

LD50; Species: Neovison vison (Mink) oral via capsule 4.2 ug/kg

For more Ecotoxicity Values (Complete) data for 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN (21 total), please visit the HSDB record page.

TERRESTRIAL FATE: Based on a classification scheme(1), a mean Koc value of 2.45X10+7(2), indicates that TCDD is expected to be immobile in soil(SRC). Volatilization of TCDD from moist soil surfaces is expected to be an important fate process(SRC) given an estimated Henry's Law constant of 3.2X10-6 atm-cu m/mole(SRC), based upon its vapor pressure, 1.5X10-9 mm Hg(3), and water solubility, 2.0X10-4 mg/L(4). However, adsorption to soil is expected to attenuate volatilization(SRC). TCDD is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(3). TCDD was photo-degraded 99.9% during and immediately after soil application in test site studies(5). Once below the surface, TCDD remained in the top 15 cm 14 years after application(5). After 350 days, 56% of the initially applied TCDD was recovered from the sandy soil, while 63% was recovered from the silty clay loam for all concentrations; incubation was at 28 °C in foil-sealed beakers(6). Estimates of the half-life of TCDD in subsurface soil may range from 25 to 100 years(7). These results indicate that biodegradation is not an important environmental fate process in soil(SRC).

AQUATIC FATE: Based on a classification scheme(1), a mean Koc value of 2.45X10+7(2), indicates that TCDD 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 3.2X10-6 atm-cu m/mole(SRC), derived from its vapor pressure, 1.5X10-9 mm Hg(4), and water solubility, 2.0X10-4 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 160 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 5.1X10+4 years if adsorption is considered(6). TCDD does not hydrolyze in environmental waters and is not expected to react with photochemically produced singlet oxygen or peroxy radicals in water(7). According to a classification scheme(8), BCF values of 1585 to 5.1X10+6 for fish(9-11) suggest bioconcentration in aquatic organisms is very high(SRC). The photolysis half-life for TCDD in natural waters from marshes, ponds and lakes in New York was 3.5-5.9 hours(12). In laboratory studies using aquatic sediments and lake water, TCDD was found to be recalcitrant to microbial attack(13). Screening analyses using 100 microbial strains (which had previously shown the ability to degrade persistent pesticides) determined that only 5 strains showed some ability to degrade TCDD(14). These results indicate that biodegradation is not an important environmental fate process in water(SRC). Based on studies of Agent Orange containing TCDD as a contaminant, photodegradation is expected to be the most relevant fate(15).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), TCDD, which has a vapor pressure of 1.5X10-9 mm Hg at 25 °C(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase TCDD may be removed from the air by wet and dry deposition(SRC). After 40 hours of illumination in simulated sunlight, TCDD sorbed onto small-diameter fly ash particulates suspended in air exhibited no loss to as much as 8% photo-degradation(3).

TCDD concentration in infant formulas from America, Australia, Denmark, Germany, Netherlands, New Zealand and Taiwan were 0.079, 0.057, 0.089, 0.080, 0.061, 0.054 and 0.073 pg/g lipid, respectively(1).

TCDD was not detected in food samples of rough rice, soybeans, crawfish, or bovine fat collected 1979-1980 in Missouri, Arkansas, and Louisiana(1). Food from Southern Mississippi sampled in 1994 contained TCDD as follows (all pg/g fat): oyster, 7.2-12; blue crab, body, 4.2-6.4; blue crab, claw, 3.2-4.9; crawfish, head, 1.3-1.4; crawfish, tail, 2-2.1; catfish, farm-raised, 2.5-6.3; mullet, fillet, 0.41-10; Spanish mackerel, 7.1; chicken, meat, 0.15-0.19; chicken, liver, 0.18-0.45; ground beef, 0.037-0.048; sausage, 0.088-0.22; milk, whole, 0.06-0.071; cheese, cheddar, 0.051-0.067; butter, 0.051-0.088; eggs, 0.050-0.069(2). Foods collected from supermarkets in Binghamton, NY, Chicago, IL, Louiseville, KY, Atlanta, GA, San Diego, CA contained TCDD at the following concentrations (food item, pg/g wet wt): fresh fish, 0.15; ocean fish, 0.03; butter, 0.10(3). Meat samples from nine US cities were collected and tested in 2001; TCDD was not detected (detection limit 0.1 pg/g lipid in 11 bacon, 22 chicken, 11 pork or 10 beef samples, but was detected at 0.1-0.6 pg/g lipid in 11 hamburger samples(4).

Samples of food were collected in Germany as part of the official inspection from 1993 to 1996(1). Samples of milk, butter, eggs, meat, and fish were found to contain TCDD at mean concentrations of 0.09 (n=538; range, 0-1.19), 0.08 (n=222; range, 0-0.26), 0.34 (n=218; range, 0-3.42), 0.14 (n=107; range, 0.04-0.85), and 5.45 (n=138; range, 0-245.73) pg/g fat, respectively(1). In 9 of 11 commercial butter samples from Spanish supermarkets, TCDD was found at concentrations ranging from not detected (detection limit not specified) to 1.11 pg/g fat(2). The concentration of TCDD in butter samples from Australia was reported as <0.01-0.12 pg/g fat (n=9)(3). TCDD was detected in 3% of 60 beef samples and 3% of 60 raw milk samples at respective concentrations of 0.024-0.46 and 0.024-0.54 pg/g fat; beef samples were collected from 52 farms Feb to Oct 2004 and milk was collected from 21 gathering stations involving 129 farms in Apr 2005; nine regions in South Korea were represented(1).

The concentration of TCDD in meats and poultry reported in a US survey conducted May 2002 to May 2003(1).[Table#4841]

Local and commercial food products were collected from 20 locations in 4 regions of Turkey. TCDD concentration results were not given for fruits, fruiting vegetables, rooty vegetables or flour(1).[Table#4842]

Occupational hepatotoxin - Secondary hepatotoxins: the potential for toxic effect in the occupational setting is based on cases of poisoning by human ingestion or animal experimentation.；Reproductive Toxin - A chemical that is toxic to the reproductive system, including defects in the progeny and injury to male or female reproductive function. Reproductive toxicity includes developmental effects. See Guidelines for Reproductive Toxicity Risk Assessment.；Dermatotoxin - Chloracne.；IARC Carcinogen - Class 1: International Agency for Research on Cancer classifies chemicals as established human carcinogens.；NTP Carcinogen - Known to be a human carcinogen.

The substance can be absorbed into the body by inhalation of dust, through the skin and by ingestion.

inhalation, skin absorption, ingestion, skin and/or eye contact

Oral (L177) ; inhalation (L177) ; dermal (L177)

The concentration of TCDD in one mother's breast milk decreased over a period of 3 years of lactation as follows (date; concentration in parts per trillion lipid basis): Feb 1992, 3.3; Mar 1993, 2.7; Jun 1994, 0.7; Dec 1994, 0.5; Sep 1995, 0.4 (1). In 1997, the mean concentration of TCDD in human milk from Keewatin (a rural area in Northwest Territories, Canada) was 0.76 ng/kg lipid(5). In 1992, a Canadian National Survey of human milk found TCDD at 2.1 ng/kg lipid(2). A pooled sample of mother's milk (n=40) from Rio de Janeiro, Brazil contained TCDD at a mean of 0.6 pg/g milk fat(3). Between the years late-1993 and 1994, the concentration of TCDD in human milk samples from Japan ranged from 0.042 to 0.15 pg/g whole wt (n=27; mean, 0.08 pg/g whole wt)(4). TCDD levels in human milk samples collected 1970, 1973 and 1985 from women in South Vietnam were 484, 121 and 12 pg/g lipid, respectively(5). The average body burden of TCDD in the nursing mothers from 1970 and 1973 was estimated to be 3.6 and 0.98 ug, respectively(5). TCDD was detected in primapara breast milk fat at 13 parts per trillion average, 255 samples, from preserved samples collected over a seven-year period, 1978-1984, in Osaka prefecture, Japan(6). It was not detected in multipara samples(6).

Between the years 1992-1994, the range and mean concentration of TCDD in mother's milk from an urban area (Helsinki) of Finland was 1.11-5.81 and 2.66 pg/g fat, respectively(1). At a rural area (Kuopio) of Finland, the range and mean concentration was 0.4-3.03 and 1.71 pg/g fat, respectively(1). Pooled samples of human milk collected from 1972-1992 from Swedish mother's living in the Stockholm region contained 2,3,7,8-tetrachlorodibenzo-p-dioxin at levels ranging from 1-5 pg/g fat(2). The range and mean level of TCDD in pooled samples of breast milk from mothers living in the Tarragona area (southern Catalonia, Spain) were 0.59-1.53 and 1.07 pg/g fat, respectively(3). Human milk samples collected in 1990 from mothers living in Madrid (Spain) and Paris (France) contained 2,3,7,8-tetrachlorodibenzo-p-dioxin at 1.2 and 2.4 pg/g fat, respectively(4). Human milk sampled between the period of 1986-1991 from North-Rhine-Westphalia, Germany contained TCDD at a mean concentration of 3.2 pg/g fat (range, 0.7-12.0 pg/g fat)(5). The mean and maximum concentration of TCDD reported in the blood of 48 people from Munich or nearby region of Germany was 0.30 and 3.92 g/g lipid, respectively; samples were collected Apr to Oct 2005(6). Women (n=169) living in an industrial area of Germany had blood and breast milk levels of 2,3,7,8-tetrachlorodibenzo-p-dioxin of 0.085-4.9 and 0.075-5.3 pg/g lipid, respectively; samples were collected Sep 2000 to Jan 2001(7). Breast milk samples collected 1998 to 2001 in Venice and Rome, Italy contained 2,3,7,8-tetrachlorodibenzo-p-dioxin at 1.79, 1.54, 1.25 and 1.11 pg/g lipid from women in Venice with low fish consumption (n=10), medium fish consumption (n=13), high fish consumption (n=6) and pooled sample (n=10) from women in Rome, respectively(8). Breast milk samples collected Apr 2008 to Nov 2009, from women one to three months after giving birth from Piacenza, Milan and Giugliano, Italy contained TCDD at 0.04-0.51 pg/g fat in 10 of 22 samples, 0.

Milk samples from 45 dairy plants across the US expected to represent 20% of the national supply were collected Jun 2000 and again in Jan 2001, a grand composite of these samples had a reported concentration of 0.03 pg/g lipid of TCDD(1). TCDD found in cow's milk from six locations in Switzerland ranged from below detection limits (0.01 ng/kg) to 0.049 ng/kg(2). Cow's milk collected Jan to Dec 2008 in Campania, Italy contained TCDD at 0.0025-2.71 pg/g milk fat; 79 samples were collected from 63 farms(3).

Two studies of nursing infants suggest that ingestion of breast milk with a higher dioxin-furan TEQ value may alter thyroid function. ... /Polychlorinated dibenzo-p-dioxins and dibenzofurans/

Hazard Traits - Bioaccumulation; Carcinogenicity; Dermatotoxicity; Developmental Toxicity; Endocrine Toxicity; Environmental Persistence; Hematotoxicity; Hepatotoxicity and Digestive System Toxicity; Reproductive Toxicity; Respiratory Toxicity；Authoritative List - CA MCLs; CA TACs; CWA 303(c); CWA 303(d); IARC Carcinogens - 1; NTP RoC - known; OEHHA RELs; OSPAR Priority Action Part A; Prop 65; WA PBTs；Report - regardless of intended function of ingredient in the product

Regulation (EC) No 178/2002 (amended)

The New Jersey Worker and Community Right to Know Act requires public and private employers to provide information about hazardous substances at their workplaces. (N.J.S.A. 34:5A-1 et. seq.)

Listed as a hazardous air pollutant (HAP) generally known or suspected to cause serious health problems. The Clean Air Act, as amended in 1990, directs EPA to set standards requiring major sources to sharply reduce routine emissions of toxic pollutants. EPA is required to establish and phase in specific performance based standards for all air emission sources that emit one or more of the listed pollutants. 2,3,7,8-Tetrachlorodibenzo-p-dioxin is included on this list.

Persons in charge of vessels or facilities are required to notify the National Response Center (NRC) immediately, when there is a release of this designated hazardous substance, in an amount equal to or greater than its reportable quantity of 1lb or 0.454 40kg. The toll free number of the NRC is (800) 424-8802. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV. D.3.b).

(FL) FLORIDA 0.000003 ug/L

(ME) MAINE 0.000007 ug/L

The LD50 value shows a positive log/log correlation with the lipid content of mammals. This is due to the high lipophilicity of the compound which, after entering the body, tends to partition into the lipid fraction, where it is prevented from reaching the target organs (liver, nervous system), and/or receptors. The main toxic effect in all animals is a loss of body weight (wasting syndrome) which is mainly contributed to loss of body fat; thus, animals having greater fat reserves are more resistant. Some similarities in the chemical structure of 2,3,7,8-TCDD and thyroid hormones suggest an influence on the thyroid physiology and thus on lipid metabolism, which would explain the wasting syndrome. ...The mediator of the toxicity of 2,3,7,8-TCDD is via Ah-receptor. Binding to this receptor is a precondition for most of the toxic action of 2,3,7,8-TCDD and related compounds. The ligand-receptor complex interacts in the cell nucleus with certain DNA sequences ('Ah locus' and other gene loci), to cause an increase in mRNA synthesis followed by a dose-related induction of various proteins, especially cytochrome P450-associated monooxygenases. The induction of enzymes is observed after both acute and chronic application of 2,3,7,8-TCDD. The receptor is principally localized in the liver, but is also found in other organs.

The Ah receptor (AhR), a soluble cytosolic protein, mediates most of the toxic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related environmental contaminants. The mechanism of ligand-mediated AhR activation has been, in part, elucidated. The sequence of events following the binding of the AhR/AhR nuclear translocator protein (ARNT) heterodimer to dioxin response elements has yet to be completely understood. The role of coactivator, RIP140, in the modulation of transcriptional activity of AhR/ARNT heterodimer was examined. RIP140 enhanced TCDD-mediated, dioxin response element-driven reporter gene activity in three cell lines. ...These results demonstrate that the AhR recruits coactivators that are capable of enhancing transcription and, thus, the AhR may compete with steroid receptors for a common coactivator pool.

To determine the molecular mechanisms underlying the "cross talk" between the activity of 2,3,7,8-tetra-chlorodibenzo-p-dioxin (TCDD), which binds to arylhydrocarbon receptor (AHR) and estradiol (E2)-liganded estrogen receptor (ER), ...the initial step of estrogen action, ligand binding to ER /was examined/. None of the AHR ligands tested, i.e. TCDD, benzo[a]pyrene, 3,3',4,4',5-pentachlorobiphenyl, beta-naphthoflavone, or alpha-naphthoflavone, bound to ER alpha. ...TCDD inhibited E2-activated reporter gene activity from a consensus /estrogen response element/ (ERE) and from EREs in the pS2, /progesterone receptor/ (PR), and Fos genes in transiently transfected MCF-7 human breast cancer cells. However, this inhibition was not reciprocal since E2 did not inhibit TCDD-stimulated luciferase activity from the CYP1A1 promoter in transiently transfected MCF-7 or human endometrial carcinoma HEC-1A cells.

Whole body: 7.1 years (2.9 to 26.9 years); [TDR, p. 1111] Estimated at around 7 years; [Reference #2, p. 379]

(14)C-labeled tetrachlorodibenzo-p-dioxin was administered by gavage to guinea pigs. Half-life for elimination was estimated to be between 22 and 43 days.

Rats were given a single oral dose of 1.0 ug of (14)C-2,3,7,8-tetrachlorodibenzo-p-dioxin (14)C-TCDD/kg/day, or repeated oral doses of 0.01, 0.1, or 1.0 ug of (14)C-TCDD/kg/day Monday through Friday for 7 weeks. Following a single oral dose of 1.0 ug of (14)C-TCDD/kg, (14)C activity could be detected only in feces, but not in urine. The half-life of (14)C activity in the body was 31 + or - 6 days ... .

Dioxins are present in milk of dairy cattle following feeding of technical grade pentachlorophenol. A dioxin concentration as high as 85 ug/kg is found in milk after feeding pentachlorophenol for 10 days at 20 mg/kg/day and then for an additional 60 days at 10 mg/kg/day. The elimination half-life of dioxin in milk is approximately 50 days.

After a single oral dose administration of (14C)-TCDD to rats, (14C) was detected in feces but not urine with a body t(1/2) = 31 +/- 6 days.

For more Biological Half-Life (Complete) data for 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN (10 total), please visit the HSDB record page.

This study presents evidence for the in vivo biotransformation of TCDD in the rat. Three male rats were implanted with indwelling bile loop cannulas. They were then given oral doses of 15 ug (14)C-TCDD/kg. After 2, 4, or 6 doses, the bile loop of one rat was opened and bile was collected for 24 hr. Biliary (14)C was excreted at a rate similar to the excretion of (14)C in the feces of rats fed (14)C-TCDD in a previous study. Selective solvent extraction revealed that the biliary (14)C activity was due to compound more polar than TCDD itself. Incubation of bile with beta-glucuronidase resulted in the extraction of more (14)C activity, implying the presence of glucuronide conjugates of (14)C-TCDD metabolites. Liquid chromatography of bile has revealed the presence of at least 5 distinct radioactive peaks, none of which was due to (14)C-TCDD. The data did not indicate extensive enterohepatic circulation of radioactivity derived from (14)C-TCDD. These results, in conjunction with the results of previous studies, indicate that TCDD is slowly metabolized in the liver to a variety of polar metabolites, which are then excreted in the bile.

Thin layer and gas chromatographic examination of the bile of dogs which were given tritium labelled TCDD revealed the presence of several polar biotransformation products. The structure of 5 phenolic metabolites was elucidated by combined gas chromatography-mass spectrometry. A metabolic breakdown scheme for TCDD in the dog is proposed /which includes 1,3,7,8-tetrachloro-2-methoxydibenzo-p-dioxin, 2,7,8-trichloro-3-methoxydibenzo-p-dioxin, trichloro-dimethoxydibenzo-p-dioxins, tetrachloro-dimethoxy diphenylether, and 1,2-dichloro-4,5-dimethyoxybenzene/.

The in vitro metabolism of 2,3,7,8-tetrachlorodibenzo-p-dioxin in isolated rat hepatocytes /was investigated/. ... The metabolites were ... identified as 1-hydroxy-2,3,7,8-TCDD and 8-hydroxy-2,3,7-trichlorodibenzo-p-dioxin.

The major metabolite /of 2,3,7,8-TCDD in dogs/ is 1,3,7,8-tetrachloro-2-hydroxydibenzo-p-dioxin.

For more Metabolism/Metabolites (Complete) data for 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN (6 total), please visit the HSDB record page.

CDDs are absorbed through oral, inhalation, and dermal routes of exposure. CDDs are carried in the plasma by serum lipids and lipoproteins, and mainly distributed in the liver and adipose tissue. CDDs are slowly metabolized to polar metabolites by the microsomal monooxygenase system. These metabolites can undergo conjugation with glucuronic acid and glutathione. They may increase the rate of their own metabolism by inducing both phase I and phase II enzymes. The major routes of excretion of CDDs are the bile and the faeces, though smaller amounts are excreted in the urine and via lactation. (L177)

Substances or energies, for example heat or light, which when introduced into the air, water, or land threaten life or health of individuals or ECOSYSTEMS.

An agent that causes the production of physical defects in the developing embryo.

Following single oral administration of 50 ug/kg bw (14)C-TCDD to rats, almost 30% was eliminated in feces during first 48 hr; excretion of (14)C activity via feces after this time was from 1-2%/day. After its absorption in the body, most of the activity derived from (14)C-TCDD is localized in liver and fat: the level in these tissues is 10 times that in other tissues. A total of 53.2% of the dose was eliminated via feces and 13.2% and 3.2% via urine and expired air respectively within 21 days.

In female guinea pigs administered a single oral dose of 2,3,7,8-TCDD only 1/2 of dose was absorbed. 22 days after dosing, fat, liver, adrenals and thymus contained 0.75, ...0.40, ...0.33, ...and 0.72% ...respectively.

... Distribution of (14)C-TCDD in the young following a single oral dose to the mother at the rate of 0.005 mg/kg was consistent with enzyme induction following a single oral dose. TCDD was found in fetuses sampled on gestation days 14, 18, or 21 but at far lower concentrations than in young examined 3, 7, 10, or 14 days after birth. Cross fostering tests indicated that TCDD was excreted in milk, and this accounted for the greater transfer to the neonate.

The liver concentration of TCDD was measured as a means of following the uptake of this chemical by the intestinal and dermal routes. Accumulation of the (radiolabelled) compound in the liver was found to provide a good and reproducible method of comparing TCDD uptake from different formulations. After oral administration of 14.7 ng TCDD using 50% ethanol as vehicle, 36.7% of the total dose was found in the liver after 24 hr. When the cmpd was administered in a mixture with soil particles, adsorption occurred and only about half of this amount was found in the liver. The liver level also decreased with increasing duration of contact between the soil and the dioxin. Adsorption onto activated carbon almost completely prevented uptake of the cmpd. Similar effects were observed after dermal application of TCDD in the various formulations. The highest liver content, 14.8% of the dose, was found after contact of the pure cmpd with the skin surface. The inhibiting effects of soil and activated carbon were even more pronounced. After incorporation of the dioxin into vaseline (a lipophilic ointment), 1.4% of the dose was found in the liver, wheras, after incorporation into polyethylene glycol 1500 (a hydrophilic ointment) containing 15% water, 14.1% was found in the liver.

For more Absorption, Distribution and Excretion (Complete) data for 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN (19 total), please visit the HSDB record page.

2,3,7,8-TCDD is not intentionally produced by industry. It can be inadvertently produced in very small amounts as an impurity during the incineration of municipal and industrial wastes and during the manufacture of certain chemicals.

No commercial uses; By-product of waste incineration, pulp and paper mill bleaching, and chemical production of 2,4,5-T, hexachlorophene, vinyl chloride, trichlorophenol, and pentachlorophenol; [Reference #2, p. 377] Levels in 2,4,5-T manufactured in the 1960s was as high as 100 mg/kg; High-exposure populations in the past included workers producing the herbicide 2,4,5-T and residents in Seveso, Italy contaminated by a factory explosion in 1976; [Reference #1]

NIOSH recommends lowest feasible level of exposure. TCDD product contamination is limited to 0.01 to 0.05 ppm. For drinking water, MCL is 0.05 ppt. FDA limit for dioxins in fish is 25 ppt. [ATSDR Case Studies]

For 2,3,7,8-tetrachlorodibenzo-p-dioxin (USEPA/OPP Pesticide Code: 600000) there are 0 labels match. /SRP: Not registered for current use in the U.S., but approved pesticide uses may change periodically and so federal, state and local authorities must be consulted for currently approved uses./

RESEARCH CHEMICAL

NOT USED COMMERCIALLY IN USA

(1978) NOT PRODUCED COMMERCIALLY IN USA

(1982) NOT PRODUCED COMMERCIALLY IN USA

(1985) Not produced commercially in the USA

Conventional methods for the laboratory preparation ... involve 2 types of processes: (1) condensation of polychlorophenol, or (2) direct halogenation of parent dibenzo-para-dioxin or monochloro derivative. ... Condensation between a catechol dianion and either an appropriate polychlorobenzene in boiling dimethyl sulfoxide or an appropriate ortho-chloropolychloronitrobenzene /may be done to increase yield/.

Tetrachlorodibenzo-p-dioxin is formed in the distillate /as a by-product during synthesis of 2,4,5-trichlorophenol/ by condensation of 2 molecules of sodium trichlorophenate under influence of highly exothermic decomposition of sodium-2-hydroxyethanol.

TCDD can be formed by the pyrolysis at 500 °C for 5 hr of sodium alpha-(2,4,5-trichlorophenoxy)propionate.

Produced as a by-product during the manufacture of chlorinated phenols ... and phenoxyherbicides, chlorine bleaching of paper pulp and combustion of chlorine-containing waste.

2,3,7,8-Tetrachlorodibenzo-p-dioxin is produced as an unwanted contaminant during the manufacture of chlorobenzenes, chlorophenols and their derivatives such as 2,4,5-trichlorophenoxyacetic acid and 2-(2,4,5-trichlorophenoxy)propionic acid.

Tetrachlorodibenzo-p-dioxin is formed during the production of 2,4,5-TCP (trichlorophenol); by the alkaline hydrolysis of 1,2,4,5-tetrachlorobenzene. ... It is an inadvertant contaminant in herbicide precursors and thus in the herbicides themselves. ... Thus, it is applied in herbicide formulations, but is not used per se.

Dow Chem Co supplied most of 2,4,5-T used in defoliation programs during vietnam war in form of cmpd known as agent orange, which contained the contaminant TCDD in amt in excess of 30 ppm.

2,3,7,8-Tetrachlorodibenzodioxin ... has not been detected in products other than 2,4,5-T and fenoprop.

May be produced in the preparation of 2,4,5-trichlorophenol from 1,2,4,5- tetrachlorobenzene and sodium hydroxide

USEPA/OPP Pesticide Code: 600000

For more General Manufacturing Information (Complete) data for 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN (7 total), please visit the HSDB record page.