DIOXINS
HAZARDTEXT ®
Information to help in the initial response for evaluating chemical incidents
 -IDENTIFICATION
SYNONYMS
Dioxin Dioxin (agent orange) Agent orange Chlorinated dibenzo-p-dioxins Chlorinated dibenzofurans Chlorinated dioxins D48 Dibenzo(b,e)(1,4)dioxin, 2,3,7,8- tetrachloro- Dibenzo-p-dioxin, 2,3,7,8-tetrachloro- Dioksyny Dioxine Dioxin-like compounds PCDD 48 TCDBD TCDD 2,3,7,8-TCDD 2,3,7,8-TETRACDD Tetrachlorodibenzodioxin Tetrachlorodibenzo-p-dioxin 2,3,7,8-tetrachlorodibenzodioxin 2,3,7,8-tetrachlorodibenzo(b,e)(1,4) dioxan 2,3,7,8-tetrachlorodibenzo(b,e)(1,4) dioxin 2,3,7,8-tetrachlorodibenzo-p-dioxin 2,3,7,8-tetrachlorodibenzo-1,4-dioxin 2,3,7,8-tetrachloro-p-dioxin Tetradioxin Tetradioxin, D48 CAS 1746-01-6
- CONSTITUENTS OF THE GROUP
Dioxin Dioxin (agent orange) Agent orange Chlorinated dibenzo-p-dioxins Chlorinated dibenzofurans Chlorinated dioxins D48 Dibenzo(b,e)(1,4)dioxin, 2,3,7,8- tetrachloro- Dibenzo-p-dioxin, 2,3,7,8-tetrachloro- Dioksyny Dioxine Dioxin-like compounds PCDD 48 TCDBD TCDD 2,3,7,8-TCDD 2,3,7,8-TETRACDD Tetrachlorodibenzodioxin Tetrachlorodibenzo-p-dioxin 2,3,7,8-tetrachlorodibenzodioxin 2,3,7,8-tetrachlorodibenzo(b,e)(1,4) dioxan 2,3,7,8-tetrachlorodibenzo(b,e)(1,4) dioxin 2,3,7,8-tetrachlorodibenzo-p-dioxin 2,3,7,8-tetrachlorodibenzo-1,4-dioxin 2,3,7,8-tetrachloro-p-dioxin Tetradioxin Tetradioxin, D48 CAS 1746-01-6
IDENTIFIERS
Editor's Note: This material is not listed in the Emergency Response Guidebook. Based on the material's physical and chemical properties, toxicity, or chemical group, a guide has been assigned. For additional technical information, contact one of the emergency response telephone numbers listed under Public Safety Measures.
SYNONYM REFERENCE
- (HSDB , 2002; Lewis, 2000; RTECS , 2002; STNEasy , 2002)
USES/FORMS/SOURCES
The majority of data available is about the isomer 2,3,7,8-tetrachlorodibenzo-p-dioxin. The abbreviation TCDD is often used to refer to this isomer. When the term TCDD is employed in this document, the information refers to the 2,3,7,8-tetrachlorodibenzo-p-dioxin isomer or a sum of the TCDD isomers. Dioxins have no intended commercial use and are not produced intentionally; exposure is through their presence as a by-product or contaminant of certain defoliant herbicides (Baxter et al, 2000; Freeman, 1998; Sittig, 1991). However, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is produced in small quantities for use as a research chemical (Bingham et al, 2001). INTENTIONAL POISONING: A 50-year-old man developed severe toxicity after ingesting a meal containing TCDD (Sorg et al, 2009). TCDD has been tested for use in flame-proofing polyester materials and against insects and wood-destroying fungi (NTP, 2000). There is no evidence that these purposes were ever exploited commercially (ATSDR, 1998).
Dioxins are substituted dioxanes that are extremely toxic by-products of the manufacture of many chemicals (Lewis, 1998). The class of dibenzo-para-dioxins includes 75 isomers (Bingham et al, 2001). In 1983, the EPA canceled registration and prohibited the transfer, distribution, sale, or importation of these compounds. However, stockpiles exist and may be used in limited amounts. 2,4-Dichlorophenol does NOT contain dioxins, although TCDD may be a contaminant of some preparations (Baselt, 1997; NIOSH, 1984).
Dioxins are widespread in the environment (Bingham et al, 2001). They do not occur naturally; thus, they are present as a result of man-made (industrial) synthesis (Baxter et al, 2000; ILO, 1998; ATSDR, 1998). Environmental levels peaked around 1970 and have been decreasing since then, mainly because of changes in industrial processes and environmental regulation banning their use (Bingham et al, 2001; EPA, 1994a). Industrial emissions in the year 2002 are expected to be reduced by more than 90% from their levels in the 1980s ((EPA, 2000a)). Dioxins are released into the environment through incineration and combustion, chemical manufacturing processes, processes involving chlorine bleaching or municipal sludge, and recirculation of environmental reservoirs (EPA, 1994a; EPA, 1994b; Johnson, 1995). At present, a significant route of exposure is through the atmospheric fallout of particles and gases contaminated with TCDD (Bingham et al, 2001). Dioxins may be formed during the manufacture of hexachlorophene from 2,4,5-trichlorophenol, pentachlorophenol fungicides and wood preservatives, and from burning pentachlorophenol- or 2,4,5-trichlorophenoxyacetic acid-treated wood. Municipal and medical wastes containing phenol and hydrogen chloride, when burned, can generate dioxins (Eklund et al, 1986). 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is the most toxic of the 75 dioxins (Lewis, 2000). It is formed as a by-product during many industrial, thermal, photochemical and biochemical processes, in the production of certain chlorinated benzene compounds and polychlorinated phenols (Baxter et al, 2000; Bingham et al, 2001). It is also a toxic by-product and a contaminant of defoliant herbicides such as the once widely used 2,4,5-trichlorophenoxyacetic acid, contained in Agent Orange (Baxter et al, 2000). Formulations of the defoliant 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) and 2,4-dichlorophenoxyacetic acid (2,4-D), commonly known as Agent Orange, used in the Vietnam war contained from 0.1 to 30 ppm TCDD (Baselt, 2000). Exposure to TCDD has decreased since the U.S. EPA banned the use of herbicides containing 2,4,5-T in the late 1970s (NTP, 1998).
TCDD is also produced during the incineration of hospital and municipal wastes, toxic wastes, with gasoline and other fossil-fuel combustion, in smelters and in paper and pulp bleaching, and it is in wood preservatives (Baxter et al, 2000; Bingham et al, 2001; (EPA, 2000b)). It is considered by some to be the most toxic synthetic compound known (Baxter et al, 2000). Dioxins are also present in cigarette smoke. The total concentration of polychlorinated dibenzo-p-dioxins was approximately 5 mcg/m(3), corresponding to a TEQ of 1.81 ng/m(3). Smoking 20 cigarettes per day would account for an intake of approximately 4.3 pg/kg/day (Muto & Takizawa, 1989). Dioxins have been identified in ceramic clay, or "ball clay", typically used in ceramics and commercial operations (ie, tile, sanitary ware, and miscellaneous ceramics). It is unclear whether the contamination of the clay is the primary route of dioxin exposure or if volatilization of the dioxins occurs during the firing of the clay (Franzblau et al, 2008).
SYNONYM EXPLANATION
- When discussing dioxins, literature often does not distinguish between dibenzo-p-dioxins as a class of compounds and an individual isomer. When information specific to an isomer was given in the literature, that information is included within this document; however, when the terms dioxin or dioxins are used in this document, the assumption should be made that there was no clarification made in the literature reference or that the data refer to a mixture of isomers.
- The majority of data available is about the isomer 2,3,7,8-tetrachlorodibenzo-p-dioxin. The abbreviation TCDD is often used to refer to this isomer. When the term TCDD is employed in this document, the information refers to the 2,3,7,8-tetrachlorodibenzo-p-dioxin isomer or a sum of the TCDD isomers.
-CLINICAL EFFECTS
GENERAL CLINICAL EFFECTS
- USES: Dioxins have no intended commercial use; exposure is through their presence as a byproduct or contaminant of certain herbicides. However, 2, 3, 7, 8-tetrachlorodibenzo-p-dioxan (TCDD) is produced in small quantities for use as a research chemical. Dioxins are released into the environment through incineration and combustion, chemical manufacturing processes, processes involving chlorine bleaching or municipal sludge, and recirculation of environmental reservoirs. At present, a significant route of exposure is through the atmospheric fallout of particles and gases contaminated with TCDD.
- TOXICOLOGY: Dioxins bind to the aryl hydrocarbon receptor protein in cytoplasm, forming a heterodimer with nuclear proteins and inducing transcription of multiple genes. They are mutagenic and act as human carcinogens.
- EPIDEMIOLOGY: Low-level environmental exposure to dioxins is common. Dioxins have been responsible for several environmental disasters, but exposures rarely produce significant acute toxicity. Deliberate poisoning with dioxins is rare but may cause caustic injury and systemic symptoms.
MILD TO MODERATE TOXICITY: Acute early signs and symptoms include chemical burns of the skin, irritation of the mucous membranes and eyes, abdominal pain, nausea, vomiting, headache, dizziness, blurred vision, irritability, dyspnea, and severe muscle pains. TCDD affects various hormone systems, particularly sex steroids, corticosteroids, and thyroid hormones. It disrupts normal feedback mechanisms of the pituitary gland. Cardiovascular disorders such as atherosclerosis and myocardial infarction have been suggested but not conclusively shown to be related to TCDD exposure. SEVERE TOXICITY: After a latent period of several weeks, chloracne, an acne-like eruption of the skin, porphyria, cutaneous tarda, hirsutism, and hyperpigmentation may occur. Symptoms (itching, swelling, redness) may occur weeks or months before the eruptions appear and may last a few months or up to 15 years. Polyneuropathies and hepatotoxicity are frequently noted. Increased blood lipids are common and may persist. Pancreatitis, diabetes mellitus, and reduction in cognitive performance have also been noted. There are no known cases of human fatalities from acute exposure to dioxins. CARCINOGENIC EFFECT: TCDD is considered a human carcinogen by IARC. REPRODUCTIVE EFFECT: Dioxins may be human teratogens, specifically for ectodermal dysplasia, CNS, cardiac, and skeletal defects.
- POTENTIAL HEALTH HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 154 (ERG, 2004)
TOXIC; inhalation, ingestion or skin contact with material may cause severe injury or death. Contact with molten substance may cause severe burns to skin and eyes. Avoid any skin contact. Effects of contact or inhalation may be delayed. Fire may produce irritating, corrosive and/or toxic gases. Runoff from fire control or dilution water may be corrosive and/or toxic and cause pollution.
ACUTE CLINICAL EFFECTS
TOXICOLOGY: Dioxins bind to the aryl hydrocarbon receptor protein in cytoplasm, forming a heterodimer with nuclear proteins and inducing transcription of multiple genes. They are mutagenic and act as human carcinogens. EPIDEMIOLOGY: Low-level environmental exposure to dioxins is common. Dioxins have been responsible for several environmental disasters, but exposures rarely produce significant acute toxicity. Deliberate poisoning with dioxins is rare but may cause caustic injury and systemic symptoms. MILD TO MODERATE TOXICITY: Acute early signs and symptoms include chemical burns of the skin, irritation of the mucous membranes and eyes, abdominal pain, nausea, vomiting, headache, dizziness, blurred vision, irritability, dyspnea, and severe muscle pains. TCDD affects various hormone systems, particularly sex steroids, corticosteroids, and thyroid hormones. It disrupts normal feedback mechanisms of the pituitary gland. Cardiovascular disorders such as atherosclerosis and myocardial infarction have been suggested but not conclusively shown to be related to TCDD exposure. SEVERE TOXICITY: After a latent period of several weeks, chloracne, an acne-like eruption of the skin, porphyria, cutaneous tarda, hirsutism, and hyperpigmentation may occur. Symptoms (itching, swelling, redness) may occur weeks or months before the eruptions appear and may last a few months or up to 15 years. Polyneuropathies and hepatotoxicity are frequently noted. Increased blood lipids are common and may persist. Pancreatitis, diabetes mellitus, and reduction in cognitive performance have also been noted. There are no known cases of human fatalities from acute exposure to dioxins. CARCINOGENIC EFFECT: TCDD is considered a human carcinogen by IARC. REPRODUCTIVE EFFECT: Dioxins may be human teratogens, specifically for ectodermal dysplasia, CNS, cardiac, and skeletal defects.
MYOCARDIAL INFARCTION: Data from a 21 year follow-up of Vietnam veterans exposed to high levels of dioxins during Operation Ranch Hand spraying operations between 1962 and 1971 revealed that the most common cause of death from circulatory disease was MI (Ketchum & Michalek, 2005). CORONARY ARTERIOSCLEROSIS: A 15 year follow-up of the Vietnam veterans involved in Operation Ranch Hand, who were exposed to high levels of dioxins as contaminants in Agent Orange during spraying operations between 1962 and 1971, showed an increased number of deaths from diseases of the circulatory system among personnel exposed to the highest levels of dioxin, mainly from atherosclerotic heart disease (Michalek et al, 1998a).
DIABETES MELLITUS: The prevalence and severity of diabetes mellitus and the risk of abnormally high glucose increased, and time-to-onset of diabetes decreased in Vietnam veterans involved in Operation Ranch Hand ho were exposed to high levels of dioxins as contaminants in Agent Orange (Henriksen et al, 1997). DISORDER OF ENDOCRINE SYSTEM: Tetrachlorodibenzo-p-dioxin (TCDD) affects various hormone systems, particularly sex steroids, corticosteroids and thyroid hormones. It disrupts normal feedback mechanisms of the pituitary gland (Bingham et al, 2001; Kogevinas, 2001). ABNORMAL GLUCOSE TOLERANCE TEST: Pathological changes in glucose tolerance tests occurred in 40% of a group of 80 workers with chronic TCDD exposure (Pazderova-Vejlupkova et al, 1981).
EYES CONJUNCTIVITIS: Initial exposure may be accompanied by a burning irritation of the eye and blepharoconjunctivitis (Sittig, 1991; Zenz, 1994). ABNORMAL VISION: Exposure may result in blurred vision (Sittig, 1991).
NOSE
CIRRHOSIS OF LIVER: An increased number of deaths from digestive diseases, mainly chronic liver disease and cirrhosis, was reported in a 15-year follow-up of the Vietnam veterans involved in Operation Ranch Hand who were exposed to high levels of dioxins as contaminants in Agent Orange (Michalek et al, 1998a) LIVER DAMAGE: In severe exposures, about one-third of patients develop liver damage. Hepatotoxicity is the most consistent finding in acute occupational exposures and is manifested by increased liver enzyme activities, mild fibrosis, fatty changes, hemofuscin deposition, parenchymal cell degeneration, and hepatomegaly. (Dunagin, 1984). ABNORMAL LIVER ENZYMES: Increased serum transaminase levels occur with tetrachlorodibenzo-p-dioxin (TCDD) toxicity (ILO, 1998).
DISORDER OF METABOLIC FUNCTION: Disorders of fat and carbohydrate metabolism are a consequence of exposure to tetrachlorodibenzo-p-dioxin (TCDD) (ILO, 1998). SERUM CHOLESTEROL RAISED: Changes in lipid metabolism, including hypercholesterolemia, have been reported after occupational exposure to TCDD (Baxter et al, 2000; Hayes & Laws, 1991).
MUSCLE PAIN: Myalgia is a common manifestation in acute occupational exposure (Schecter & Ryan, 1992). Neuromuscular effects include severe joint and muscle pain exacerbated by exertion; this mainly affects the calves and thighs and thorax; fatigue and lower-limb weakness also occur (ILO, 1998; Sittig, 1991).
NEUROPATHY: Peripheral neuropathy, with sensory impairment, as well as central neuropathy, with lassitude, weakness, impotence, and loss of libido result from exposure to dioxin (Baxter et al, 2000; ILO, 1998). Neuritis and polyneuropathy have occurred after dermal exposure to 2,4-dichlorophenol, with incomplete recovery (Baselt, 1997). Polyneuropathy with sensory impairment and lower extremity weakness is a consistent finding in industrial exposure cases. In mild exposure, asymptomatic alteration in EMG and nerve conduction velocity studies may occur. In severe exposures, about one-third of patients have developed neuropathies (Dunagin, 1984). ALTERED MENTAL STATUS: ACUTE EXPOSURE: A reduction of cognitive performance in verbal conceptualization, amnestic organization of verbal and visual stimuli, psychomotor slowing, and subjective complaints such as irritability have been seen on neurologic examination (Peper et al, 1993).
FEELING NERVOUS: Emotional disorders, nervousness, and irritability have been found following inhalational exposure to tetrachlorodibenzo-p-dioxin (TCDD) (Sittig, 1991).
CHRONIC CLINICAL EFFECTS
- Dioxin is lipophilic and lipid-soluble, so it is found mainly in adipose tissue, skin, liver, pancreas and breast milk (Baselt, 2000; Baxter et al, 2000; Bingham et al, 2001). It is preferentially stored in adipose tissue and may be released systematically when an individual loses weight (Flowers et al, 1981).
- Dioxin is not known to be metabolized in man (Baselt, 2000). It may be metabolized as a detoxification process, possibly by cytochrome P450-associated mixed-function oxidases (Hayes & Laws, 1991).
- The serum elimination half-life was calculated to be about 7.1 years (Baselt, 2000). Other estimates of the half-life in humans include approximately 7 years, 5 to 8 years or 5.98 to 11.3 years (Baxter et al, 2000; Bingham et al, 2001; MMWR, 1988; Pirkle et al, 1989). The half-life based on experimental data from one human volunteer was 5.8 years (Poiger & Schlatter, 1986).
- Little is known of the human health effects as a result of long-term exposure to low concentrations (Stehr-Green et al, 1988). TEFs are based on relative acute toxicity and may underestimate repeated low-dose exposures (Hebert et al, 1990).
- Significant associations with exposure to dioxin were found in 1987 for diabetes, cholesterol, percent body fat, high-density lipoproteins (HDL), and cholesterol-HDL ratio in veterans of Operation Ranch Hand, who were exposed to high levels of dioxins as contaminants in Agent Orange during spraying operations in Vietnam between 1962 and 1971 (21).
Increases in serum triglycerides and high-density lipoprotein concentrations also correlated with serum TCDD concentration in a group of workers employed for at least 15 years (Calvert et al, 1996). A 15 year follow-up of the Vietnam veterans involved in Operation Ranch Hand showed an increased number of deaths from diseases of the circulatory system among personnel exposed to the highest levels of dioxin, mainly from atherosclerotic heart disease (Michalek et al, 1998a). Dose-dependent increases in risk of mortality from ischemic heart disease were seen in a retrospective cohort of 1189 male chemical workers exposed to TCDD and other higher chlorinated dioxins and furans. The highest relative risk was 2.48 in the highest decile. Quantitative exposures were obtained from analysis of blood and adipose tissue (Fleschjanys et al, 1995).
- A 15 year follow-up of the Vietnam veterans involved in Operation Ranch Hand also showed an increased number of deaths from digestive diseases, mainly chronic liver disease and cirrhosis (Michalek et al, 1998a).
- In Vietnam veterans involved in Operation Ranch Hand, the prevalence and severity of diabetes mellitus and the risk of abnormally high glucose increased, and time-to-onset of diabetes decreased, with dioxin exposure (Henriksen et al, 1997).
- Hemorrhagic cystitis was reported in a 6-year-old girl who was chronically exposed to TCDD-containing soil in a horse arena sprayed with contaminated oil. Symptoms resolved within 3 to 4 days (Beale et al, 1977).
- TCDD was shown to suppress T-helper cell function in workers exposed for 20 years (Goldfrank, 1998).
- In a NIOSH survey, there was no increased risk for porphyria cutanea tarda or subclinical uroporphyrinuria and/or coproporphyrinuria among 281 workers exposed to dioxin for more than 15 years (Calvert et al, 1994).
- One effect of exposure to TCDD is cachexia. It may suppress the formation of hunger signals, possibly through seratonergic mechanism. Diminished food intake and progressive weight loss are consequences of this (Bingham et al, 2001).
TCDD produces a wasting syndrome that is the ultimate cause of death in several species of animals (Zenz, 1994). Rats given 3 or 10 mcg/kg/day TCDD for 91 days developed wasting syndrome (Ivens et al, 1993). Death from acute exposure to TCDD is delayed by 2 to 6 weeks in experimental animals (Zenz, 1994).
-FIRST AID
FIRST AID AND PREHOSPITAL TREATMENT
DERMAL: Remove contaminated clothing and wash exposed area extremely thoroughly with soap and water. Personnel involved in washing patients should wear gloves and avoid contact with contaminated clothing. OCULAR: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persists after 15 minutes of irrigation, and ophthalmologic examination should be performed. ORAL: Activated charcoal: Most exposures are chronic and routine gastrointestinal decontamination is not indicated. In the unlikely event of acute ingestion, administer activated charcoal if conditions are appropriate.
-MEDICAL TREATMENT
LIFE SUPPORT
- Support respiratory and cardiovascular function.
SUMMARY
- FIRST AID - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 154 (ERG, 2004)
Move victim to fresh air. Call 911 or emergency medical service. Give artificial respiration if victim is not breathing. Do not use mouth-to-mouth method if victim ingested or inhaled the substance; give artificial respiration with the aid of a pocket mask equipped with a one-way valve or other proper respiratory medical device. Administer oxygen if breathing is difficult. Remove and isolate contaminated clothing and shoes. In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes. For minor skin contact, avoid spreading material on unaffected skin. Keep victim warm and quiet. Effects of exposure (inhalation, ingestion or skin contact) to substance may be delayed. Ensure that medical personnel are aware of the material(s) involved and take precautions to protect themselves.
FIRST AID Immediately wash the eyes with large amounts of water, occasionally lifting the lower and upper lids. Get medical attention immediately. Primary eye protection (spectacles or goggles), as defined by the Occupational Safety and Health Administration (OSHA), should be used when working with this chemical. Face shields should only be worn over primary eye protection. DERMAL EXPOSURE - 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. INHALATION EXPOSURE - Move the exposed person to fresh air at once. If breathing has stopped, perform artificial respiration. Keep the affected person warm and at rest. Get medical attention as soon as possible. ORAL EXPOSURE - If this chemical has been swallowed, get medical attention immediately. TARGET ORGANS - Eyes, skin, liver, kidneys and reproductive system [in animals: tumors at many sites](National Institute for Occupational Safety and Health, 2007; Chemsoft(R) , 2000),
INHALATION EXPOSURE INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
DERMAL EXPOSURE DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999). Personnel involved in washing patients should wear gloves and avoid contact with contaminated clothing. Chloracne may respond to topical retinoic acid, and oral tetracyclines to treat secondary pustular follicles. Resistant cases may require acne surgery or dermabrasion. Isotretinoin may be tried.
EYE EXPOSURE DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
ORAL EXPOSURE
-RANGE OF TOXICITY
MINIMUM LETHAL EXPOSURE
One review article by Reggiani (1978) reports a minimum lethal dose of 1 mcg/kg (Reggiani, 1978; Schardein, 2000). It is estimated that human lethal doses are greater than 100 mcg/kg (Neal, 1983).
MAXIMUM TOLERATED EXPOSURE
- The maximum tolerated human exposure to this agent has not been delineated.
- A cumulative dose of 100 mcg/kg is estimated as the minimum toxic dose, based on extrapolation of data from TCDF-contaminated cooking oil in Japan (Stevens, 1981).
DERMAL Assuming daily exposure, it appears that 10 to 30 ppm in oil and 100 to 3,000 ppm in soil-water mixtures are necessary to produce objective effects. Soil concentrations likely to produce chloracne with daily contact probably exceed 100 ppm (Dunagin, 1984). The lowest published toxic dose for a human (dermal route) is 107 mcg/kg (Lewis, 2000; RTECS , 2002).
INHALATION AIRBORNE SEVESO, ITALY INCIDENT - A plant producing trichlorophenol in Seveso, Italy, inadvertently overheated, creating a cloud of dioxin (TCDD) containing 650 to 1700 grams (35,000 ppt). Children and adults directly exposed to airborne dust complained of nausea, skin redness, and swelling. Others developed chloracne, which rapidly and spontaneously healed, subclinical peripheral neurological impairment, and liver enzyme abnormalities. The highest average soil levels were 584 ppb (Reggiani, 1978).
ORAL - SOIL LEVELS - Soil levels of 1 ppb are estimated to increase the risk of developing cancer by 1 in 1 million (MMWR, 1984). Soil concentrations likely to produce chloracne with daily contact probably exceed 100 ppm (Dunagin, 1984). A 6-year-old girl playing in a Missouri horse arena sprayed with dioxin (TCDD)-contaminated motor oil developed self-limited epistaxis, severe hemorrhagic cystitis, and gastrointestinal complaints. Samples taken from the soil contained 31.8 to 33 ppm of dioxin (TCDD) (Beale et al, 1977).
Hen pheasants injected with graded single doses of dioxin (TCDD) (6.25, 25 or 100 mcg/kg) had delayed-onset body weight loss and mortality, classic signs of the wasting syndrome (Nosek et al, 1992). The lowest single dose of dioxin (TCDD) to produce this effect was 25 mcg/kg. When hen pheasants were treated weekly with lower doses of dioxin (TCDD) (0.01 to 1.0 mcg/kg/wk) for 10 weeks, signs of the wasting syndrome and mortality were also produced. The lowest cumulative dioxin (TCDD) dose required to produce the wasting syndrome, using a weekly dosing regimen, was 10 mcg/kg. At this dosing regimen, egg production by hens treated with a cumulative dioxin (TCDD) dose of 10 mcg/kg was reduced, as was egg hatchability.
RATS: The maximum tolerated dose of TCDD in rats in a 91-day subchronic gavage study was 0.1 pg/kg/day (Ivens et al, 1993). RATS: The maximum tolerated dose of TCDD in rats was 0.01 mcg/kg/day when given 5 days/week for 13 weeks (Kociba et al, 1976). TCDD and two dioxin-like compounds, 2,3,4,7,8-pentachlorodibenzofuran (PCDF), and 1,2,3,4,7,8-hexachlorodibenzofuran (HCDF), were evaluated for relative dermal toxicity in 20-week subchronic skin painting studies in hairless mice (Hebert et al, 1990). Based on dermatotoxic effects and changes in body and organ weights, the last two compounds were relatively more toxic than their acute Toxicity Equivalency Factor (TEF) values would indicate. TEF values may underestimate the risk from repeated low-dose exposures, at least for these compounds.
Where TCDD has been assigned a Toxicity Equivalency Factor (TEF) of 1.0 (on a scale of 0 to 1.0, with 1.0 being the most toxic), the other chlorinated dibenzodioxins and chlorinated dibenzofurans have TEFs ranging from 0 to 0.5 (Freeman, 1998). TCDD is the most toxic of all the known dioxins. Of the 210 possible positional congeners, only 7 chlorinated dibenzodioxins and 10 chlorinated dibenzofurans are believed to have TCDD-like activity. These all have chlorine in the 2,3,7 and 8 positions (EPA, 1994a; EPA, 1994b; Freeman, 1998). The EPA's Exposure Estimation for Dioxin-Like Compounds mainly deals with chlorinated dibenzodioxins and, by extension, chlorinated dibenzofurans and other dioxin-like compounds. Analogous brominated dioxins and furans, and certain polychlorinated biphenyls, are known to have dioxin-like toxicity but have not yet been assigned TEFs (EPA, 1994a). Only 11 of the 209 possible polychlorinated biphenyl congeners are thought to have dioxin-like activity. These have at least four chlorine substituents (EPA, 1994a).
- Carcinogenicity Ratings for CAS1746-01-6 :
ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed EPA (U.S. Environmental Protection Agency, 2011): Not Listed IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): 1 ; Listed as: 2,3,7,8-Tetrachlorodibenzo-para-dioxin 1 : The agent (mixture) is carcinogenic to humans. The exposure circumstance entails exposures that are carcinogenic to humans. This category is used when there is sufficient evidence of carcinogenicity in humans. Exceptionally, an agent (mixture) may be placed in this category when evidence of carcinogenicity in humans is less than sufficient but there is sufficient evidence of carcinogenicity in experimental animals and strong evidence in exposed humans that the agent (mixture) acts through a relevant mechanism of carcinogenicity.
NIOSH (National Institute for Occupational Safety and Health, 2007): Ca ; Listed as: 2,3,7,8-Tetrachloro-dibenzo-p-dioxin MAK (DFG, 2002): Category 4 ; Listed as: 2,3,7,8-Tetrachlorodibenzo-p-dioxin Category 4 : Substances with carcinogenic potential for which genotoxicity plays no or at most a minor part. No significant contribution to human cancer risk is expected provided the MAK value is observed. The classification is supported especially by evidence that increases in cellular proliferation or changes in cellular differentiation are important in the mode of action. To characterize the cancer risk, the manifold mechanisms contributing to carcinogenesis and their characteristic dose-time-response relationships are taken into consideration.
NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): K ; Listed as: 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), Dioxin
TOXICITY AND RISK ASSESSMENT VALUES
- EPA Risk Assessment Values for CAS1746-01-6 (U.S. Environmental Protection Agency, 2011):
References: Bingham et al, 2001 HSDB, 2002 Lewis, 2000 NTP, 2001;) Pohjanvirta et al, 1993 RTECS, 2002 Verschueren, 2001 LD50- (ORAL)DOG: LD50- (ORAL)GUINEA_PIG: 500 ng/kg 0.6 mcg/kg (HSDB, 2002)
LD50- (INTRAPERITONEAL)HAMSTER: LD50- (ORAL)HAMSTER: 1157 mcg/kg -- gastrointestinal changes, weight loss, changes in serum composition 1157-5051 mcg/kg (HSDB, 2002)
LD50- (INTRAPERITONEAL)MOUSE: LD50- (ORAL)MOUSE: LD50- (ORAL)PRIMATE: LD50- (INTRAPERITONEAL)RABBIT: LD50- (ORAL)RABBIT: 115 mcg/kg 10 mcg/kg (HSDB, 2002)
LD50- (SKIN)RABBIT: LD50- (INTRAPERITONEAL)RAT: LD50- (ORAL)RAT: 20 mcg/kg Male, 22.0 mcg/kg (HSDB, 2002) Sprague-Dawley, 43 mcg/kg (Bingham et al, 2001) Female, 45.0 mcg/kg (HSDB, 2002) >7200 mcg/kg -- H/W strain (Pohjanvirta et al, 1993) Female, 9.8 mcg/kg -- L-E strain (Pohjanvirta et al, 1993) Male, 17.7 mcg/kg -- L-E strain (Pohjanvirta et al, 1993)
LDLo- (INTRAPERITONEAL)CHICKEN: LDLo- (ORAL)CHICKEN: LDLo- (SKIN)MOUSE: TD- (ORAL)MOUSE: 1 mcg/kg for 2Y-Intermittent -- equivocal tumorigenic agent by RTECS criteria, tumors of the liver and thyroid 36 mcg/kg for 52W-Intermittent -- neoplastic, tumors of the lung, thorax, liver
TD- (SKIN)MOUSE: TD- (ORAL)RAT: 1 mcg/kg for 2Y-Intermittent -- equivocal tumorigenic agent by RTECS criteria, tumors of the liver and thyroid 27 mcg/kg for 65W-Continuous-- equivocal tumorigenic agent by RTECS criteria, tumors of the liver and thyroid 73 mcg/kg for 2Y-Continuous -- carcinogenic by RTECS criteria, tumors of the liver 190 mcg/kg for 95W-Continuous -- equivocal tumorigenic agent by RTECS criteria, tumors of the liver and kidney 137 mcg/kg for 65W-Continuous -- equivocal tumorigenic agent by RTECS criteria, tumors of the liver and kidney 328 mcg/kg for 78W-Continuous -- equivocal tumorigenic agent by RTECS criteria, tumors of the lung, thorax
TDLo- (ORAL)GUINEA_PIG: 5 mcg/kg for 5W- Intermittent -- changes in the bladder, kidney, ureter and endocrine system, death 1600 ng/kg for 8W- Intermittent -- changes in thymus weight, weight loss 441 ng/kg for 90D- Continuous -- changes in liver and thymus weights, weight loss
TDLo- (ORAL)HAMSTER: Female, 2 mcg/kg at 11D of pregnancy -- reduced weight gain in offspring Female, 18 mcg/kg at 9D of pregnancy -- fetal death 600 mcg/kg for 3D- Intermittent -- changes in the liver, oxidoreductases and transferases
TDLo- (SKIN)HUMAN: TDLo- (INTRAPERITONEAL)MOUSE: Female, 20 mcg/kg at 11D of pregnancy -- craniofacial developmental abnormalities Female, 25 mcg/kg at 7-11D of pregnancy -- fetotoxicity, craniofacial developmental abnormalities 120 mcg/kg for 12W-Intermittent -- changes in liver and thymus weight, changes in cell count (unspecified) 180 mcg/kg for 6W-Intermittent -- changes in liver weight and serum composition, transaminases
TDLo- (ORAL)MOUSE: 9260 ng/kg for 4W-Intermittent -- changes in liver and thymus weight, changes in erythrocyte count Female, 1 mcg/kg at 10D of pregnancy -- developmental abnormalities of the urogenital system Female, 9 mcg/kg at 12D of pregnancy -- craniofacial (including mouth and tongue) developmental abnormalities Female, 12 mcg/kg at 10-13D of pregnancy -- post-implantation mortality, fetal death Female, 20 mcg/kg at 14D of pregnancy and 3D after birth -- reduced weight gain in offspring 52 mcg/kg for 2Y-Intermittent -- carcinogenic by RTECS criteria, tumors of the liver, thyroid Female, 235 mcg/kg at 28D prior to mating and 21D after birth -- immune and reticuloendothelial system developmental abnormalities Female, 13,500 mg/kg at 6-14D of pregnancy -- developmental abnormalities of the endocrine system 20 mcg/kg for 4W-Intermittent -- changes in thymus weight and endocrine system, decrease in cellular immune response 336 mcg/kg for 8W-Continuous -- changes in leukocyte count, decrease in humoral immune response 520 mcg/kg for 13W-Intermittent -- changes in the liver, death 150 mcg/kg for 6W-Intermittent -- fatty liver degeneration, changes in thymus weight and serum composition 588 mcg/kg for 14D-Intermittent -- changes in the weights of the liver, spleen and thymus
TDLo- (SKIN)MOUSE: 97 mcg/kg for 13W-Intermittent -- hepatitis, changes in spleen, death 62 mcg/kg for 2Y-Intermittent -- carcinogenic by RTECS criteria, tumors of the skin and appendages
TDLo- (SUBCUTANEOUS)MOUSE: Female, 30 mcg/kg at 10D of pregnancy -- craniofacial (including mouth and tongue) developmental abnormalities Female, 100 mcg/kg at 2D of pregnancy -- post-implantation mortality Female, 100 mcg/kg at 10D of pregnancy -- craniofacial (including mouth and tongue) developmental abnormalities Female, 250 mcg/kg at 7-16D of pregnancy -- fetal death, reduced litter size Female, 250 mcg/kg at 7-16D of pregnancy -- craniofacial (including mouth and tongue), musculoskeletal, and urogenital developmental abnormalities
TDLo- (ORAL)PRIMATE: Female, 2 mcg/mg at 12D of pregnancy -- abortion Male, 107 mg/kg at 4Y prior to mating -- behavioral effects in offspring Female, 163 ng/kg at 3.5Y prior to mating -- behavioral effects on offspring Female, 92 ng/kg at 46W prior to mating and 17W after birth -- behavioral effects on offspring Female, 123 ng/kg at 30W prior to mating and 17W after birth -- behavioral effects in offspring 10 mcg/kg for 12D-Continuous -- ulceration or bleeding from the stomach, nutritional and metabolic changes, death
TDLo- (ORAL)RABBIT: Female, 1 mcg/kg at 6-15D of pregnancy -- developmental abnormalities of the musculoskeletal system Female, 10 mcg/kg at 6-15D of pregnancy -- pre-implantation mortality, abortion Female, 2500 ng/kg at 6-15D of pregnancy -- post-implantation mortality, developmental abnormalities of the urogenital system 80 mcg/kg for 8W-Intermittent -- decrease in cellular and humoral immune responses, death
TDLo- (INTRAPERITONEAL)RAT: TDLo- (ORAL)RAT: Female, 1 mcg/kg at 15D of pregnancy -- developmental abnormalities of endocrine system in offspring Female, 1 mcg/kg at 15D of pregnancy -- physical effects in offspring Female, 1 mcg/kg at 15D of pregnancy -- developmental abnormalities of urogenital system, fetal death Female, 12 mcg/kg at 10D of pregnancy -- cytological changes to embryo, developmental abnormalities of urogenital system Female, 20 mcg/kg at 1D prior to pregnancy -- affected uterus, cervix, vagina 52 mcg/kg for 2Y-Intermittent -- carcinogenic by RTECS criteria, tumors of the liver, thyroid Female, 1250 ng/kg at 6-15D of pregnancy -- fetal death, developmental abnormalities Female, 1270 ng/kg -- decreased fertility, developmental abnormalities of blood and lymphatic system Female, 1500 ng/kg at 1-3D of pregnancy -- fetotoxicity, developmental abnormalities of urogenital system 16 mcg/kg for 16W-Intermittent -- changes of the liver and urine composition, porphyrin including bile pigments 30 mcg/kg for 30D-Intermittent -- changes in serum composition and platelet count, multiple enzyme effects 120 mcg/kg for 3D-Intermittent -- changes of the liver and iron metabolism, hepatic microsomal mixed oxidase 140 mcg/kg for 14D-Intermittent -- changes in clotting factors, erythrocyte count and platelet count 450 ng/kg for 45W-Intermittent -- changes in urine composition 6500 ng/kg for 13W-Intermittent -- changes in liver and thymus weights, pigmented or nucleated red blood cells 7300 mg/kg for 2Y-Continuous -- hepatitis, changes in liver weight and urine composition 164 mcg/kg for 78W-Continuous -- carcinogenic by RTECS criteria, tumors of the liver, lung and thorax
TDLo- (SUBCUTANEOUS)RAT: Female, 5 mg/kg at 6-15D of pregnancy -- urogenital system abnormalities Female, 2200 ng/kg at 19D of pregnancy and 21D after birth -- reduced weight gain in offspring
CALCULATIONS
-STANDARDS AND LABELS
WORKPLACE STANDARDS
- ACGIH TLV Values for CAS1746-01-6 (American Conference of Governmental Industrial Hygienists, 2010):
- AIHA WEEL Values for CAS1746-01-6 (AIHA, 2006):
- NIOSH REL and IDLH Values for CAS1746-01-6 (National Institute for Occupational Safety and Health, 2007):
- OSHA PEL Values for CAS1746-01-6 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
- OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS1746-01-6 (U.S. Occupational Safety and Health Administration, 2010):
ENVIRONMENTAL STANDARDS
- EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS1746-01-6 (U.S. Environmental Protection Agency, 2010):
Listed as: TCDD Final Reportable Quantity, in pounds (kilograms): Additional Information: Listed as: 2,3,7,8-Tetrachlorodibenzo-p-dioxin Final Reportable Quantity, in pounds (kilograms): Additional Information:
- EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS1746-01-6 (U.S. Environmental Protection Agency, 2010):
- EPA RCRA Hazardous Waste Number for CAS1746-01-6 (U.S. Environmental Protection Agency, 2010b):
- EPA SARA Title III, Extremely Hazardous Substance List for CAS1746-01-6 (U.S. Environmental Protection Agency, 2010):
- EPA SARA Title III, Community Right-to-Know for CAS1746-01-6 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):
Listed as: 2,3,7,8 Tetrachlorodibenzo-p-dioxin Effective Date for Reporting Under 40 CFR 372.30: Lower Thresholds for Chemicals of Special Concern under 40 CFR 372.28: 0.1 grams Listed as: Dioxin and dioxin-like compounds (Manufacturing; and the processing or otherwise use of dioxin and dioxin-like compounds if the dioxin and dioxin-like compounds are present as contaminants in a chemical and if they were created during the manufacturing of that chemical)(This category includes only those chemicals listed below) Effective Date for Reporting Under 40 CFR 372.30: 1/00 Lower Thresholds for Chemicals of Special Concern under 40 CFR 372.28: Listed as: 2,3,7,8-Tetrachlorodibenzo-p-dioxin Effective Date for Reporting Under 40 CFR 372.30: 1/00 Lower Thresholds for Chemicals of Special Concern under 40 CFR 372.28:
- DOT List of Marine Pollutants for CAS1746-01-6 (49 CFR 172.101 - App. B, 2005):
- EPA TSCA Inventory for CAS1746-01-6 (EPA, 2005):
SHIPPING REGULATIONS
- DOT -- Table of Hazardous Materials and Special Provisions (49 CFR 172.101, 2005):
- ICAO International Shipping Name (ICAO, 2002):
LABELS
- NFPA Hazard Ratings for CAS1746-01-6 (NFPA, 2002):
-HANDLING AND STORAGE
SUMMARY
TCDD is a confirmed carcinogen and a deadly experimental poison by ingestion and dermal contact. It is toxic by inhalation and is an eye irritant. Exposure should be avoided (Lewis, 2000; NIOSH , 2002).
HANDLING
- Personal protective equipment, including respiratory protection, should be worn at all times when working with or around TCDD (NIOSH , 2002).
- Use dioxin (TCDD) in a ventilated hood in an adequately ventilated area. Take every precaution to limit airborne concentrations of this compound. Use a plastic backed absorbent and segregated tools and glassware (Sittig, 1991).
- After each manipulation and before personnel leave the work area, hands and forearms should be thoroughly washed. The same precautions that are required for radioactive work should be used when working with this compound (Sittig, 1991).
- Only the most experienced personnel should be allowed to handle this compound (NTP, 2001).
STORAGE
- ROOM/CABINET RECOMMENDATIONS
Dioxin (TCDD) should be stored in a ventilated area (Sittig, 1991). During transportation and storage, it should be kept at 4 degrees C and should be protected from light (HSDB , 2002). Eyewash fountains should be provided in areas where there is any possibility of exposure to TCDD (NIOSH , 2002). TCDD should be stored as close as practicable to lab in which it is to be used (HSDB , 2002).
Under ordinary storage conditions, TCDD is stable (HSDB , 2002). This compound is relatively stable toward acids, alkalies, and heat. Solutions of dioxin (TCDD) in isooctane or n-octanol may be changed chemically when exposed to ultra-violet light; it undergoes catalytic perchlorination (HSDB , 2002; IARC, 1977) NTP, 2001). Photodecomposition is neglible in aqueous solutions (NTP, 2001). Dioxin (TCDD) is decomposed by ultra-violet light (NIOSH , 2002) NTP, 2001).
-PERSONAL PROTECTION
SUMMARY
- RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 154 (ERG, 2004)
Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection. Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.
- Wear appropriate protective clothing and eye protection, including disposable gloves, a disposable apron or lab coat, and safety glasses, to prevent skin and eye contact when working with dioxin (TCDD) (NIOSH , 2002; Sittig, 1991).
- Any work area where there is a possibility of exposure to dioxin (TCDD) should include facilities for quickly drenching the body for emergency use. Immediately wash contaminated skin and remove and replace any clothing which becomes contaminated. Training should be provided for the proper removal of contaminated gloves and clothing to avoid contact with exterior surfaces. Leave contaminated clothing at the workplace for cleaning. Personnel should wash at the end of each work shift (HSDB , 2002; NIOSH , 2002; Sittig, 1991).
- Only experienced personnel should be allowed to work with TCDD. Non-essential personnel should be restricted from areas in which dioxins are used (NTP, 2001).
- Workers engaged in decontamination processes after the release or spill of TCDD are advised to wear complete disposable equipment to protect the skin and prevent exposure to dust and vapor from contaminated materials (HSDB , 2002).
EYE/FACE PROTECTION
- Appropriate eye protection should be worn when working with dioxin (TCDD) to prevent the chemical coming into contact with the eyes. Contact lenses should not be worn (NIOSH , 2002).
- Eyewash fountains should be placed where there is any possibility of workers being exposed to this compound, whether or not eye protection is worn (NIOSH , 2002).
RESPIRATORY PROTECTION
- Refer to "Recommendations for respirator selection" in the NIOSH Pocket Guide to Chemical Hazards on TOMES Plus(R) for respirator information.
- Where TCDD is used in the laboratory, wear a NIOSH-approved half face respirator equipped with a combination filter cartridge (e.g., organic vapor/acid gas/HEPA) (NTP, 2001).
PROTECTIVE CLOTHING
- CHEMICAL PROTECTIVE CLOTHING. Search results for CAS 1746-01-6.
ENGINEERING CONTROLS
- Vertical laminar-flow biological safety cabinets may be used for laboratory procedures so long as the exhaust air flow is sufficient to provide inward air flow at the face opening of the cabinet. Horizontal laminar-flow safety cabinets in which filtered air is blown out toward the operator should never be used (HSDB , 2002).
-PHYSICAL HAZARDS
FIRE HAZARD
Editor's Note: This material is not listed in the Emergency Response Guidebook. Based on the material's physical and chemical properties, toxicity, or chemical group, a guide has been assigned. For additional technical information, contact one of the emergency response telephone numbers listed under Public Safety Measures. POTENTIAL FIRE OR EXPLOSION HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 154 (ERG, 2004) Non-combustible, substance itself does not burn but may decompose upon heating to produce corrosive and/or toxic fumes. Some are oxidizers and may ignite combustibles (wood, paper, oil, clothing, etc.). Contact with metals may evolve flammable hydrogen gas. Containers may explode when heated.
TCDD is generally thought to be nonflammable (NTP, 2001).
- FLAMMABILITY CLASSIFICATION
- NFPA Flammability Rating for CAS1746-01-6 (NFPA, 2002):
- FIRE CONTROL/EXTINGUISHING AGENTS
- SMALL FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 154 (ERG, 2004)
- LARGE FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 154 (ERG, 2004)
Dry chemical, CO2, alcohol-resistant foam or water spray. Move containers from fire area if you can do it without risk. Dike fire control water for later disposal; do not scatter the material.
- TANK OR CAR/TRAILER LOAD FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 154 (ERG, 2004)
Fight fire from maximum distance or use unmanned hose holders or monitor nozzles. Do not get water inside containers. Cool containers with flooding quantities of water until well after fire is out. Withdraw immediately in case of rising sound from venting safety devices or discoloration of tank. ALWAYS stay away from tanks engulfed in fire.
- NFPA Extinguishing Methods for CAS1746-01-6 (NFPA, 2002):
- Fires involving dioxins can be controlled using dry chemical, carbon dioxide or Halon extinguishers (NTP, 2001).
EXPLOSION HAZARD
- TCDD is considered relatively stable toward heat, acids, and alkalies (HSDB , 2002).
DUST/VAPOR HAZARD
- Inhalation of TCDD vapors can cause headache, dizziness, nausea, vomiting, pain in the joints, fatigue, emotional disorders, blurred vision, muscle pain, irritability and intolerance to cold temperatures. Itching, swelling and redness followed by the appearance of chloroacne is a common development following exposure. Abnormalities of the liver, pancreas, circulatory and respiratory systems and death may also result (Sittig, 1991).
- Toxic chloride fumes are emitted when dioxin (TCDD) is heated to decomposition (Lewis, 2000).
- Inceneration of chemical wastes (e.g., chlorophenols, chlorinated benzenes, biphenyl ethers) can result in particulate matter (e.g., flue gases, fly ash, soot particles) that contains TCDD (Lewis, 2000).
REACTIVITY HAZARD
- TCDD is considered relatively stable toward heat, acids, and alkalies (HSDB , 2002).
- Combustion of TCP-contaminated 2,4,5-T can result in conversion to small amounts of TCDD (Tvers & Anderson, 1986).
- Toxic chloride fumes are emitted when dioxin (TCDD) is heated to decomposition (Lewis, 2000).
EVACUATION PROCEDURES
- Initial Isolation and Protective Action Distances (ERG, 2004)
Data presented from the Emergency Response Guidebook Table of Initial Isolation and Protective Action Distances are for use when a spill has occurred and there is no fire. If there is a fire, or if a fire is involved, evacuation information presented under FIRE - PUBLIC SAFETY EVACUATION DISTANCES should be used. Generally, a small spill is one that involves a single, small package such as a drum containing up to approximately 200 liters, a small cylinder, or a small leak from a large package. A large spill is one that involves a spill from a large package, or multiple spills from many small packages. Suggested distances to protect from vapors of toxic-by-inhalation and/or water-reactive materials during the first 30 minutes following the spill. - SPILL - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 154 (ERG, 2004)
Increase, in the downwind direction, as necessary, the isolation distance of at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids in all directions.
- FIRE - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 154 (ERG, 2004)
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.
- PUBLIC SAFETY MEASURES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 154 (ERG, 2004)
CALL Emergency Response Telephone Number on Shipping Paper first. If Shipping Paper not available or no answer, refer to appropriate telephone number: MEXICO: SETIQ: 01-800-00-214-00 in the Mexican Republic; For calls originating in Mexico City and the Metropolitan Area: 5559-1588; For calls originating elsewhere, call: 011-52-555-559-1588.
CENACOM: 01-800-00-413-00 in the Mexican Republic; For calls originating in Mexico City and the Metropolitan Area: 5550-1496, 5550-1552, 5550-1485, or 5550-4885; For calls originating elsewhere, call: 011-52-555-550-1496, or 011-52-555-550-1552; 011-52-555-550-1485, or 011-52-555-550-4885.
ARGENTINA: CIQUIME: 0-800-222-2933 in the Republic of Argentina; For calls originating elsewhere, call: +54-11-4613-1100.
BRAZIL: PRÓ-QUÍMICA: 0-800-118270 (Toll-free in Brazil); For calls originating elsewhere, call: +55-11-232-1144 (Collect calls are accepted).
COLUMBIA: CISPROQUIM: 01-800-091-6012 in Colombia; For calls originating in Bogotá, Colombia, call: 288-6012; For calls originating elsewhere, call: 011-57-1-288-6012.
CANADA: UNITED STATES:
For additional details see the section entitled "WHO TO CALL FOR ASSISTANCE" under the ERG Instructions. 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. Keep unauthorized personnel away. Stay upwind. Keep out of low areas. Ventilate enclosed areas.
- TCDD is extremely toxic through all routes of exposure. Workers should wear appropriate personal protective clothing and equipment at all times to reduce the risk of exposure (HSDB , 2002; NIOSH , 2002) NTP, 2001).
- In escape situations, use any air-purifying, full-facepiece respirator or gas mask with a chin-style, front- or back- mounted organic vapor canister with a HEPA filter. Any escape-type self-contained breathing apparatus may be used as well (NIOSH , 2002) NTP, 2001).
- Move exposed persons to fresh air at once. Keep the affected person warm and at rest (NIOSH , 2002).
- Seek immediate medical attention for any persons that were exposed to TCDD even if no symptoms are present (NIOSH , 2002) NTP, 2001; (Sittig, 1991).
- Any clothing that becomes contaminated should be immediately removed and isolated then replaced (NIOSH , 2002).
- AIHA ERPG Values for CAS1746-01-6 (AIHA, 2006):
- DOE TEEL Values for CAS1746-01-6 (U.S. Department of Energy, Office of Emergency Management, 2010):
Listed as Dioxine; (TCDD; 2,3,7,8-tetrachlorodibenzo-p-dioxin) TEEL-0 (units = mg/m3): 0.00000001 TEEL-1 (units = mg/m3): 0.0015 TEEL-2 (units = mg/m3): 0.0075 TEEL-3 (units = mg/m3): 0.0075 Definitions: TEEL-0: The threshold concentration below which most people will experience no adverse health effects. TEEL-1: The airborne concentration (expressed as ppm [parts per million] or mg/m(3) [milligrams per cubic meter]) of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic, nonsensory effects. However, these effects are not disabling and are transient and reversible upon cessation of exposure. TEEL-2: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long-lasting, adverse health effects or an impaired ability to escape. TEEL-3: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience life-threatening adverse health effects or death.
- AEGL Values for CAS1746-01-6 (National Research Council, 2010; National Research Council, 2009; National Research Council, 2008; National Research Council, 2007; NRC, 2001; NRC, 2002; NRC, 2003; NRC, 2004; NRC, 2004; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; United States Environmental Protection Agency Office of Pollution Prevention and Toxics, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; 62 FR 58840, 1997; 65 FR 14186, 2000; 65 FR 39264, 2000; 65 FR 77866, 2000; 66 FR 21940, 2001; 67 FR 7164, 2002; 68 FR 42710, 2003; 69 FR 54144, 2004):
- NIOSH IDLH Values for CAS1746-01-6 (National Institute for Occupational Safety and Health, 2007):
CONTAINMENT/WASTE TREATMENT OPTIONS
SPILL OR LEAK PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 154 (ERG, 2004) ELIMINATE all ignition sources (no smoking, flares, sparks or flames in immediate area). Do not touch damaged containers or spilled material unless wearing appropriate protective clothing. Stop leak if you can do it without risk. Prevent entry into waterways, sewers, basements or confined areas. Absorb or cover with dry earth, sand or other non-combustible material and transfer to containers. DO NOT GET WATER INSIDE CONTAINERS.
RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 154 (ERG, 2004) Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection. Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.
TCDD is an extremely toxic compound and efforts should be taken to avoid exposure. Standard precautions for handling carcinogens should be followed when dealing with a spill or exposure to TCDD (HSDB , 2002). Only persons wearing protective clothing, including disposable gloves, a disposable apron or lab coat, safety glasses, and a supplied-air respirator or a self-contained breathing apparatus with a full facepiece should be allowed in the contaminated area (Sittig, 1991). Editors' Note: There are numerous environmental regulations that apply to the disposal of wastes contaminated with dioxins (TCDD). Before undertaking disposal of materials that are known or suspected to contain dioxins, refer to the Code of Federal Regulations for guidance and consult federal regulatory agencies for the most current standards and regulations.
If TCDD is spilled, dampen the spilled material with toluene and use absorbant paper to transfer the material to a vapor-tight container. Wipe up any remaining material with an absorbant paper dampened with toluene. Seal used absorbant paper in a vapor-tight plastic bag for later disposal. Contaminated surfaces should be washed with toluene followed by a solution of soap and water (NTP, 2001). After absorbing the spilled material and placing it in a suitable container, rinse the area of the spill with 1,1,1-trichloroethane and then wash the area with detergent and water (Sittig, 1991). Any contaminated clothing should be removed and placed in a vapor-tight plastic bag for later disposal (NTP, 2001).
Potential treatment methods for destroying or detoxifying dioxins include the following technologies (Freeman, 1998): Solvent Extraction; Solidification/Stabilization; Chemical Dechlorination. Treatment with ruthenium tetraoxide can cause oxidative degeneration of dioxins and can be employed for decontamination of glassware or artifacts and to counteract the accumulation of dioxins in industrial reactors (ATSDR, 1998; HSDB , 2002). Dioxins have been successfully destroyed in liquid wastes through treatment with alkali polyethylene glycolate reagents. This involves the reaction of potassium hydroxide with polyethylene glycol to form an alkoxide that reacts with a chlorine atom on the dioxin and produces an ether and potassium chloride. Bio-assays indicate that the resultant products are far less toxic than TCDD (ATSDR, 1998). A modified alkali-metal method has been used for dechlorination of dioxins. The destruction reagent was prepared by dissolving either potassium hydroxide or sodium hydroxide in 1,3-dimethyl-2-imidazolidinone. Destruction efficiency under various conditions ranged from 99.95 to 99.80 percent (ATSDR, 1998). Greater than 99 percent removal of TCDD from incinerator flue gases was effected through contact with a catalyst containing titanium oxide/silica and platinum at 450 degrees C (Verschueren, 2001). Removal of TCDD from waste gases can be acheived through scrubbing with a calcium hydroxide solution and sorbant materials (e.g., activated carbon, metallurgic coke, activated alumnia, silica gel, kieselguhr) (Verschueren, 2001). TCDD is regulated by the U.S. Environmental Protection Agency as a hazardous constituent of waste and, as such, is subject to special handling and report/recordkeeping requirements (NTP, 1998). Waste management activities associated with material disposition are unique to individual situations. Proper waste characterization and decisions regarding waste management should be coordinated with the appropriate local, state, or federal authorities to ensure compliance with all applicable rules and regulations.
Dioxin (TCDD) is thought to be generally resistant to biodegradation (HSDB , 2002). In a laboratory environment, a white rot fungus, Phanerochaete chrysosporium, has shown the ability to slowly degrade TCDD (ATSDR, 1998; Verschueren, 2001).
High-temperature incineration is the most extensively tested and generally most accepted method of disposal of dioxins (ATSDR, 1998). TCDD is classified by the U.S. Environmental Protection Agency as a Principal Organic Hazardous Constiuent (POHC) and as such, incineration conditions used for its destruction are required to acheive 99.9999 percent destruction and removal efficiency (DRE). Please see 40 CFR Section 63.1203 for specific requirements (EPA, 2002f). Potential treatment methods for destroying or detoxifying dioxins include the following technologies (ATSDR, 1998; Freeman, 1998): Stationary Rotary Kiln Incineration; Transportable Rotary Kiln Incineration; Liquid Waste Incineration; Fluidized Bed Incineration (circulating or bubbling fluidized bed combustor); High-Temperature Electric Reactor; Infrared Incineration; Supercritical Water Oxidation; Plasma Arc Systems; In Situ Vitrification; Thermal Desorption; Photolysis; Soil Washing; Carbon Adsorption. Incineration has been approved by the U.S. Environmental Protection Agency for the remediation of Superfund wastes that contain dioxins (Freeman, 1998). The regulation at 40 CFR Section 266.104(3), states the following (EPA, 2002g): "Dioxin-listed waste. A boiler or industrial furnace burning hazardous waste containing (or derived from) EPA Hazardous Wastes Nos. F020, F021, F022, F023, F026, or F027 must achieve a destruction and removal efficiency (DRE) of 99.9999% for each POHC designated (under paragraph (a)(2) of this section) in its permit. This performance must be demonstrated on POHCs that are more difficult to burn than tetra-, penta-, and hexachlorodibenzo-p-dioxins and dibenzofurans. DRE is determined for each POHC from the equation in paragraph (a)(1) of this section. In addition, the owner or operator of the boiler or industrial furnace must notify the Director of intent to burn EPA Hazardous Waste Nos. F020, F021, F022, F023, F026, or F027." Please refer to the Code of Federal Regulations for complete and current incineration requirements.
In situ photodegradation of TCDD in soil has been investigated; it was found that up to 86 percent of TCDD can be degraded through this process. The addition of a solvent mixture of 2:1 tetradecane and 1-butonal was used to facilitate the photolysis (ATSDR, 1998). Gamma radiation in the presence of surfactants has been used to destroy TCDD in soil samples. A destruction of greater than 92 percent was acheived in soils contaminated with 100 ppb TCDD, 25 percent water and 2 percent nonionic surfactant using cobalt-60 as a source of radiation (ATSDR, 1998). Degradation of dioxins by ozonation in alkaline aqueous medium has been observed. No degradation occurred in acidic media (HSDB , 2002; Verschueren, 2001).
-ENVIRONMENTAL HAZARD MANAGEMENT
POLLUTION HAZARD
- Dioxins are ubiquitous in the environment. Significant sources of current environmental levels of TCDD include past releases to sediment, soil, and sewage from the application and production of chlorophenoxyacetic acid herbicides (Bingham et al, 2001). A study of TCDD contamination undertaken in 1994 estimates that as much as 500,000 tons of soil and sediment in the United States were contaminated with TCDD (NTP, 2000).
- Dioxins are not known to occur naturally; rather, they are by-products of certain industrial, chemical manufacturing or combustion processes involving precursor compounds and heat (HSDB, 2004; Freeman, 1998).
- Dioxin (TCDD) is released to the environment in exhaust from automobiles that use leaded gasoline, in emissions from wood burning in the presence of chlorine, in accidental fires involving transformers that contain polychlorinated biphenyls and chlorinated benzenes, in stack emissions from the incineration of municipal and medical refuse and certain chemical wastes, and from the improper disposal of certain chlorinated chemical wastes (Bingham et al, 2001; HSDB, 2004)(NTP, 2000).
- Dioxin (TCDD) may be released to the environment in flue gases, fly ash, and soot particles as a result of incinerating chemical wastes, including chlorophenols, chlorinated benzenes, and biphenyl ethers (Lewis, 2000).
- Pulp bleaching processes for paper production and dye and pigment manufacture are additional sources of TCDD pollution (Bingham et al, 2001; Budavari, 2000). However, the federal effluent guidelines promulgated in 1998 are expected to reduce this industry's dioxin discharge by at least 96 percent ((EPA, 2000b)).
- Sludge from seven pulp and paper mills was analyzed for dioxin (TCDD). The level of dioxin (TCDD) ranged from not detectable (1 pg/g) to over 400 pg/g (Kuehl et al, 1987).
- Approximately two to ten pounds of TCDD were released into the environment due to an industrial accident during the manufacture of 2,4,5-trichlorophenol in Seveso, Italy on July 10, 1976. Some samples contained concentrations as high as 51.3 ppm dioxin (TCDD) (Budavari, 2000).
- Many industrial processes have been changed to reduce the release of TCDD into the environment (Bingham et al, 2001). This, in combination with stricter environmental regulations regarding its handling and disposal should result in decreased levels in the future; industrial emissions in the year 2002 are expected to be reduced by more than 90 percent from their levels in the 1980's ((EPA, 2000a); (EPA, 2000b)).
ENVIRONMENTAL FATE AND KINETICS
Despite its extremely low vapor pressure (7.4x10(-10) mmHg (at 25 degrees C)), dioxin (TCDD) has been shown to be volatile; it occurs in air in both gas- and particulate-phases (HSDB , 2002). Particulate-phase dioxin (TCDD) may be transported long distances through the atmosphere. It may be removed from the atmosphere by wet and dry deposition (HSDB, 2004). Wet and dry deposition are the major routes of removal of dioxins from the environment. This includes precipitation, gravitational settling of particles, sorption of vapor-phase dioxins onto plant surfaces. Wet depositions are thought to dominate dry processes in removing small particulates from the air (ATSDR, 1998).
Vapor-phase TCDD may be degraded by reaction with hydroxyl radicals or through direct photolysis (HSDB, 2004). The half-life for the reaction of vapor-phase dioxin (TCDD) with photochemically produced hydroxyl radicals is estimated to be 8.3 days. The potential photolysis rate of particulate-phase dioxin (TCDD) has not been estimated due to insufficient data (Dragun, 1988; HSDB , 2002). Direct photolysis of gas-phase dioxin (TCDD) may occur at a faster rate than the reaction with hydroxyl radicals (HSDB, 2004). The estimated photooxidation half-life of dioxin (TCDD) in air is 22.3 hours to 9.3 days. The atmospheric photolysis half-life is estimated to be 1.1 to 3.4 days; however, based on its high soil adsorption coefficient and the observed persistence of dioxin (TCDD) in the environment, photolysis in the environment is not expected to be significant (Howard et al, 1991).
SURFACE WATER The ultimate environmental sink for all global releases of dioxin pollutants is believed to be aquatic sediments. Dioxins entering the water column will undergo sedimentation with some uptake by aquatic organisms (ATSDR, 1998; HSDB , 2002). Photodegradation is not significant in aqueous solution (Verschueren, 2001). Run-off/erosion from dioxin-contaminated land is thought to be the major route of entry into most bodies of water (ATSDR, 1998). Dioxin (TCDD) is expected to adsorb to sediments and suspended material due to its very low water solubility (HSDB, 2004). Dioxin (TCDD) is generally resistant to biodegradation, but may be removed from water by photolysis and volatilization (HSDB, 2004). Dioxin has an estimated aqueous photolysis half-life of 1.1-3.4 days; however, based on the high soil adsorption coefficient of dioxin (TCDD) and its observed persistence in the environment, photolysis in the environment is not expected to be significant (Howard et al, 1991a). The estimated photolysis half-life in surface water ranges from 21 hours in summer to 118 hours in winter. These rates decrease significantly as the depth of the water increases; therefore, many bottom sediments may not undergo significant photodegradation. Hydrolysis from environmental waters and free-radical oxidation are not expected to be significant (Dragun, 1988; HSDB, 2004). The estimated volatilization half-life from the water column of an environmental pond is 46 days. When adsorption to sediment is accounted for, however, the volatilization model predicts an overall volatilization half-life of over 50 years (HSDB , 2002).
The most significant transport mechanism for the removal of dioxins from the water column is thought to be sedimentation and burial in sediment (ATSDR, 1998). A persistence half-life of greater than 1.5 years has been estimated for dioxin (TCDD) in lakes (HSDB , 2002). The half-life for surface water may range from 1.15-1.62 years (Howard et al, 1991). TCDD (2,3,7,8-isomer) had a 600D half-life in a model aquatic environment (Verschueren, 2001).
GROUND WATER
TERRESTRIAL Dioxin (TCDD) does not leach in soil. Any movement in soil is generally caused by surface erosion of soil particles or flooding. This compound is generally resistant to biodegradation; however, photodegradation may occur in surface soils (Dragun, 1988; HSDB , 2002; IARC, 1977). The disappearance of TCDD from soil is believed to be due to physical removal rather than degradation (ATSDR, 1998). The major removal mechanism from soil surfaces during warm, summer months is thought to be volatilization. Volatilization is extremely slow during cold, winter months, as well as from soil depths several centimeters below the boundary layer. However, during warm summer months, volatilization may be significant (HSDB, 2004). Recent studies suggest that the tetra-chlorinated dioxin congeners undergo very little movement up- or downward in subsurface soil due to volatilization unless surfactants or carriers such as waste oil are present to serve as a solvent. It was found that TCDD moved readily through the soil when combined with components of waste oil; its mobility was also enhanced by the addition of surfactants (e.g., sodium lauryl sulfate) (ATSDR, 1998).
Dioxins are a persistent pollutant in soils, with half-lives estimated to range from 1 to 15 years in surface soils and 12 to 100 years in subsurface soils (ATSDR, 1998). TCDD may undergo volatilization from surface soils during warm summer months (HSDB, 2004). The half-life of dioxin (TCDD) on soil surfaces ranges from less than 1 year to 3 years. The half-life in soil interiors may be up to 12 years (ATSDR, 1998). The estimated half-life in soil is 1.15-1.62 years (Howard et al, 1991). Soil tested in Seveso, Italy a few years following the release of TCDD due to an industrial accident showed a mean half-life for TCDD of 9.1 years (HSDB , 2002). A review of recent studies on the persistence of dioxins indicate that TCDD has an estimated half-life of 25 to 100 years in subsurface soils and 9 to 15 years in surface soils. There was some indication that the binding of dioxin compounds to soil is irreversible after a length of time due to the encapsulation of the compounds in organic and mineral matter in the soil (ATSDR, 1998). Half-lives for dioxins in sludge-amended soil were on the order of 20 years (ATSDR, 1998).
ABIOTIC DEGRADATION
- Dioxins are persistent in soil (half-life 1-15Y in surface soil and 12-100Y in subsurface soil). They may irreversibly bind to soil over time due to encapsulation in organic and mineral substances. Removal from soil is chiefly due to physical mechanisms rather than chemical or biological degradation. The material does not leach, and migration in soil is usually through surficial erosion or flooding. Runoff and erosion of contaminated soil contributes to levels in aquatic systems. The tetra-chlorinated dioxin congeners (TCDDs) can migrate more easily when surfactants or carriers, such as sodium lauryl sulfate or waste oil, are co-contaminants. Volatilization from surface soil is possible, especially during warm summer months. Dioxins are generally resistant to biodegradation; however, photodegradation may occur in surface soils (HSDB, 2004; ATSDR, 1998; Dragun, 1988; IARC, 1977).
- Aquatic sediments act as a sink for dioxins. Major contributors to aquatic systems are runoff and erosion of contaminated soil. Dioxins are not very soluble in water and likely adsorb to sediments and suspended material in the water column. Biouptake by aquatic organisms occurs, although dioxins are generally resistant to biodegradation. They may be removed from water by photolysis or volatilization. However, bottom sediments may not undergo significant photodegradation as photolysis rates decrease with depth. Photodegradation, hydrolysis, and free-radical oxidation are not likely significant in water (HSDB, 2004; Verschueren, 2001; ATSDR, 1998; Dragun, 1988).
- Dioxins exist as a vapor or in particulate form in air. Migration over great distances occurs in the atmosphere, and removal is mainly by wet and dry deposition, such as precipitation, gravitational settling, and sorption of the vapor-phase onto plant surfaces. The vapor-phase (TCDD) can degrade by direct photolysis or reaction with hydroxyl radicals. Photolysis is not expected to be significant based on the high soil adsorption coefficient and observed persistence (HSDB , 2002; ATSDR, 1998; Howard et al, 1991).
BIODEGRADATION
- Phanerochaete chrysosporium (white rot fungus) degrades dioxins (Verschueren, 2001).
- Dioxin (TCDD) was not subject to microbial degradation in lake water and aquatic sediments in laboratory studies. Microbial degradation of dioxin (TCDD) occurs rarely in nature (HSDB, 2004; IARC, 1977).
- In a screening analysis, only 5 of 100 microbial strains had some ability to degrade dioxin (TCDD) (HSDB , 2002).
- The estimated anaerobic half-life ranges from 4.58-6.45 years in an unacclimated aqueous environment (Howard et al, 1991).
- The estimated aerobic half-life ranges from 1.15-1.62 years in an unacclimated aqueous environment (Howard et al, 1991).
BIOACCUMULATION
TCDD accumulates in human tissue, particularly liver and adipose tissues, and has a half-life in the body of 5.8 to 12 years (ATSDR, 1998)(NTP, 2000).
The biota-sediment accumulation factor (BSAF) for Lake Ontario Lake Trout was calculated at 0.059. The bioaccumulation equivalency factor (BEF) was calculated to be 1.0 (ATSDR, 1998). Since 1988, the State of Maine has monitored dioxin levels in the tissues of predatory and bottom feeding species of fish taken from the state's major water bodies, including five rivers which receive the effluent of bleached kraft paper mills. Monitoring results were analyzed using simple models to yield field bioaccumulation factors (BAF) for dioxin (TCDD) in Maine rivers (Frakes et al, 1993). Mean BAFs (across rivers) ranged from 11,500-24,600 for smallmouth bass fillets, from 17,900-28,300 for brown trout fillets, from 3000-7500 for white perch fillets, and from 78,500-106,000 for white sucker whole bodies (Frakes et al, 1993).
TCDD can be strongly bioaccumulated by fish and invertebrates (ATSDR, 1998).
TERRESTRIAL A comparative analysis of two types of soils showed that the bioavailability of dioxin (TCDD) from soils may be related to the specific compositions of the soils (Umbreit et al, 1986). Young oats and soybeans grown on a sandy loam that was contaminated with 60 ppb TCDD accumulated 40 ppb TCDD (Verschueren, 2001).
Log biotransfer factor for beef (mammals): -1.26(Verschueren, 2001) Log biotransfer factor for milk (mammals): -1.99(Verschueren, 2001)
OTHER Dioxin (TCDD) may bioaccumulate in animals (IARC, 1977; Lewis, 2000). Dioxin (TCDD) may bioconcentrate in aquatic organisms (ATSDR, 1998; HSDB, 2004).
Mean BCF values: FATHEAD MINNOW: 29,200 for 28D -- dry weight (HSDB, 2004) FATHEAD MINNOW: 5840 for 28D -- wet weight (HSDB, 2004) MOSQUITO FISH: 4,875 for 7D (Verschueren, 2001) BRINE SHRIMP: 1,570 (at 0.01 ppb in water) -- TCDD introduced into system through residue on sand (Verschueren, 2001) MOSQUITO LARVAE: 5,000 to 9,222 (at 0.45 to 2.4 mcg/L in water) -- TCDD introduced into system through residue on sand (Verschueren, 2001) ALGAE: 2,000 to 18,600 (Verschueren, 2001) DUCKWEED: 1,200 to 5,000 (Verschueren, 2001) SNAIL: 1,400 to 47,100 (Verschueren, 2001)
Log BCF values: RAINBOW TROUT: approximately 3.2 to 3.9 -- laboratory flow-through studies during 4-5 exposures (HSDB , 2002) FATHEAD MINNOW: approximately 3.2 to 3.9 -- laboratory flow-through studies during 4-5 exposures (HSDB , 2002) SNAILS, FISH (GAMBUSIA), DAPHNIA: 4.3 to 4.4 (HSDB, 2004) DUCKWEED, ALGAE, CATFISH: 3.6 to 3.95 (HSDB, 2004) Various Species: 3.73 to 5.90 ((EPA, 2000c)) GUPPY: 5.24 (measured): 5.48 (calculated) ((EPA, 2000c)) VEGETATION, unspecified: -1.87 (Verschueren, 2001)
ENVIRONMENTAL TOXICITY
Dioxin (TCDD) doses of 25 and 125 mcg/kg (intraperitoneally) caused 85% lethality 2 to 4 weeks after treatment in rainbow trout, juvenile Shasta or Wytheville strain fish, obtained from 4 hatcheries (Spitsbergen et al, 1988a). Dioxin (TCDD) doses of 25 and 125 mcg/kg (intraperitoneally) caused 95% mortality by 28 days after treatment in juvenile, hatchery-reared yellow perch, Perca flavescens (Spitsbergen et al, 1988b).
LD50 - (ORAL) Colinus virginianus: 0.0150 mg/kg -- 95% confidence limit 0.00919-0.0245 (HSDB, 2004) LD50 - (ORAL) Streptopelia risorias: >0.810 mg/kg (HSDB, 2004)
-PHYSICAL/CHEMICAL PROPERTIES
MOLECULAR WEIGHT
DESCRIPTION/PHYSICAL STATE
- Dioxin exists as colorless to white needles or crystals (NIOSH, 2005; Budavari, 2000; Lewis, 2000) . It has no odor or warning characteristics (Bingham et al, 2001).
VAPOR PRESSURE
- 1.7x10(-6) mmHg (at 25 degrees C) (Freeman, 1989)
- 7.4x10(-10) mmHg (at 25 degrees C) (ATSDR, 1998; HSDB , 2002)
- 2.0 x 10(-5) mmHg (at 77 degrees F) (NIOSH, 2005; Harbison, 1998)
- 1.5x10(-9) to 3.4x20(-5) mmHg (ATSDR, 1998; (EPA, 2000c))
- 2.0x10(-7) Pa (at 25 degrees C) (Bingham et al, 2001)
DENSITY
- TEMPERATURE AND/OR PRESSURE NOT LISTED
FREEZING/MELTING POINT
Needles: 295 degrees C (Budavari, 2000) Crystals from anisole: 320-325 degrees C (Budavari, 2000) 305 degrees C (Bingham et al, 2001; Lewis, 2000) 302-305 degrees C (Sittig, 1991) 305-306 degrees C (ATSDR, 1998; (EPA, 2000c); Verschueren, 2001) 581 degrees F (NIOSH, 2005)
BOILING POINT
FLASH POINT
EXPLOSIVE LIMITS
SOLUBILITY
OCTANOL/WATER PARTITION COEFFICIENT
- log Kow = 6.8 (HSDB, 2005; Bingham et al, 2001; (EPA, 2000c))
- log Kow = 7.39 to 7.58 (ATSDR, 1998)
- log Kow (estimated) = 7.02 ((EPA, 2000c))
HENRY'S CONSTANT
- 1.62x10(-5) atm-m(3)/mol (at 25 degrees C) (estimated) (HSDB , 2002)
- 16.1x10(-6) to 101.7x10(-6) atm-m(3)/mol (at 25 degrees C) (ATSDR, 1998)
- 3.29x10(-5) atm-m(3)/mol ((EPA, 2000c))
- 3.34 Pa-m(3)/mol (Bingham et al, 2001)
OTHER/PHYSICAL
- ORGANIC CARBON PARTITION COEFFICIENT
- DECOMPOSITION TEMPERATURE
>700 degrees C (Freeman, 1998; Hayes & Laws, 1991) Decomposition begins at 500 degrees C and is nearly complete after 21 seconds at 800 degrees C (HSDB, 2005; Sittig, 1991).
-REFERENCES
GENERAL BIBLIOGRAPHY- 't Mannetje A, McLean D, Cheng S, et al: Mortality in New Zealand workers exposed to phenoxy herbicides and dioxins. Occup Environ Med 2005; 62:34-40.
- 40 CFR 372.28: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Lower thresholds for chemicals of special concern. National Archives and Records Administration (NARA) and the Government Printing Office (GPO). Washington, DC. Final rules current as of Apr 3, 2006.
- 40 CFR 372.65: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Chemicals and Chemical Categories to which this part applies. National Archives and Records Association (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Apr 3, 2006.
- 49 CFR 172.101 - App. B: Department of Transportation - Table of Hazardous Materials, Appendix B: List of Marine Pollutants. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 29, 2005.
- 49 CFR 172.101: Department of Transportation - Table of Hazardous Materials. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 11, 2005.
- 62 FR 58840: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 1997.
- 65 FR 14186: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
- 65 FR 39264: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
- 65 FR 77866: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
- 66 FR 21940: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2001.
- 67 FR 7164: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2002.
- 68 FR 42710: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2003.
- 69 FR 54144: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2004.
- AIHA: 2006 Emergency Response Planning Guidelines and Workplace Environmental Exposure Level Guides Handbook, American Industrial Hygiene Association, Fairfax, VA, 2006.
- ATSDR: Toxicological Profile for Chlorinated Dibenzo-p-dioxins (CDDs), TP 104, Agency for Toxic Substances and Disease Registry, US Dept of Health and Human Services, Atlanta, GA, 1998.
- Abernethy DJ, Greenlee WF, & Huband JC: 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) promotes the transformation of C3H/10T1/2 cells. Carcinogenesis 1985; 6:651-653.
- Alavanja MC, Merkle S, & Teske J: Mortality among forest and soil conservationists. Arch Environ Health 1989; 44:94-101.
- Albanese RA: United States Air Force Personnel and Exposure to Herbicide Orange. USAFSAM-TR-88-3, (NTIS ADA 191985). National Technical Information Services (NTIS), 1988.
- Alsharif NZ, Lawson T, & Shohs SJ: Oxidative stress induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin is mediated by the aryl hydrocarbon (Ah) receptor complex. Toxicology 1994; 92:39-51.
- American Conference of Governmental Industrial Hygienists : ACGIH 2010 Threshold Limit Values (TLVs(R)) for Chemical Substances and Physical Agents and Biological Exposure Indices (BEIs(R)), American Conference of Governmental Industrial Hygienists, Cincinnati, OH, 2010.
- Anon: Association of Selected Cancers with Service in the US Military in Vietnam, Govt Reports Announcements & Index (GRA&I), Issue 10. National Technical Information Services (NTIS), 1991.
- Anon: Bioassay of a Mixture of 1,2,3,6,7,8-Hexachlorodibenzo-p-Dioxin and 1,2,3,7,8,9-Hexachlorodibenzo-p-Dioxin (Gavage) for Possible Carcinogenicity, Govt Reports Announcements & Index (GRA&I), Issue 05. National Technical Information Services (NTIS), 1981.
- Anon: Carcinogenesis Bioassay of 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (CAS No 1746-01-6) in Osborne-Mendel Rats and B6C3F1 Mice (Gavage Study); Govt Reports Announcements & Index (GRA&I); Issue 11. National Technical Information Services (NTIS), 1982a.
- Anon: Carcinogenesis Bioassay of 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (CAS No 1746-01-6) in Swiss-Webster Mice (Dermal Study), Govt Reports Announcements & Index (GRA&I); Issue 11. National Technical Information Services (NTIS), 1982ba.
- Anon: Chemical review: Dioxin. Dang Proper Ind Mater Rep 1988; 8:2-48.
- Anon: No excess in cancer deaths found in largest group ever studied for long-term effects of dioxin exposure. Am Ind Hyg Assoc J 1980; 41:73.
- Ansbaugh N, Shannon J, Mori M, et al: Agent Orange as a risk factor for high-grade prostate cancer. Cancer 2013; 119(13):2399-2404.
- Assennato G, Cervino D, & Emmett EA: Follow-up of subjects who developed chloracne following TCDD exposure at Seveso. Am J Ind Med 1989; 16:119-125.
- Axelson O & Sundell L: Herbicide exposure, mortality and tumor incidence. An epidemiological investigation on Swedish railroad workers. Scand J Work Environ Health 1974; 11:21-28.
- Axelson O, Persson B, & Wingren G: Dioxin and diabetes mellitus (letter). Epidemiology 1998; 9(3):358-359.
- Baccarelli A, Giacomini SM, Corbetta C, et al: Neonatal thyroid function in Seveso 25 years after maternal exposure to dioxin. PLoS med 2008; 5(7):e161.
- Badesha JS, Maliji G, & Flaks B: Immunotoxic effects of exposure of rats to xenobiotics via maternal lactation. 1. 2,3,7,8-tetrachlorodibenzo-p-dioxin. Internat J Exp Pathol 1995; 76:425-439.
- Barbieri S, Pirovano C, & Scarlato G: Long-term effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin on the peripheral nervous system. Clinical and neurophysiological controlled study on subjects with chloracne from the Seveso area. Neuroepidemiology 1988; 7:29-37.
- Baselt RC: Biological Monitoring Methods for Industrial Chemicals, 3rd ed, PSG Publishing Company, Littleton, MA, 1997.
- Baselt RC: Disposition of Toxic Drugs and Chemicals in Man, 5th ed, Chemical Toxiology Institute, Foster City, CA, 2000.
- Baxter PJ, Adams PH, & Aw TC: Hunter's Diseases of Occupations, 9th ed, Oxford University Press Inc, New York, NY, 2000.
- Beale MG, Shearer WT, & Karl MM: Long term effects of dioxin exposure. Lancet 1977; 1:748.
- Becher H, Fleschjanys D, & Kauppinen T: Cancer mortality in German male workers exposed to phenoxy herbicides and dioxins. Cancer Causes Contr 1996; 7:312-321.
- Beck H, Dross A, & Ende M: Ergebnisse von Ruckstandsuntersuchungen auf polychlorierte Dibenzofurane und Dibenzodioxine in Frauenmilch aus der Bundesrepublik Deutschland (Results of the analysis for residue of polychlorinated dibenzodioxins and dibenzofurans in human milk from the Federal Republic of Germany) (German). Bundesgesundheitsblatt 1991; 34:564-568.
- Beebe LE, Fornwald LW, & Diwan BA: Promotion of N-nitrosodiethylamine-initiated hepatocellular tumors and hepatoblastomas by 2,3,7,8-tetrachlorodibenzo-p-dioxin or Aroclor 1254 in C57BL/6, DBA/2, and B6D2F1 mice. Cancer Res 1995; 55:4875-4880.
- Bertazzi A, Pesatori AC, & Consonni D: Cancer incidence in a population accidentally exposed to 2,3,7,8-tetrachlorodibenzo-para-dioxin. Epidemiology 1993; 4:398-406.
- Bertazzi PA, Zocchetti C, & Guercilena S: Dioxin exposure and cancer risk: a 15-year mortality study after the "Seveso accident". Epidemiology 1997; 8:646-652.
- Bertazzi PA, Zocchetti C, & Pesatori AC: Ten-year mortality study of the population involved in the Seveso incident in 1976. Am J Epidemiol 1989; 129:1187-1200.
- Bingham E, Cohrssen B, & Powell CH: Patty's Toxicology, 5th ed, 1, 5 & 8, John Wiley & Sons, New York, NY, 2001.
- Birnbaum LS & Slezak BP: Research highlights: dietary exposure to PCBs and dioxins in children. Environ Health Perspect 1999; 107:1.
- Birnbaum LS, McDonald MM, & Blair PC: Differential toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in C57BL/6J mice congenic at the Ah locus. Fundam Appl Toxicol 1990; 15:186-200.
- Birnbaum LS, Morrissey RE, & Harris MW: Teratogenic effects of 2,3,7,8-tetrabromodibenzo-p-dioxin and three polybrominated dibenzofurans in C57BL/6N mice. Toxicol Appl Pharmacol 1991; 107:141-152.
- Bjerke DL, Mably TA, & Moore RW: Effects of perinatal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on reproductive function in male rats. Toxicologist 1990; 10:313.
- Blair A, Grauman DJ, & Lubin JH: Lung cancer and other causes of death among licensed pesticide applicators. J Natl Cancer Inst 1983; 71:31-37.
- Bleiberg J, Wallen M, & Brodkin R: Industrially acquired porphyria. Arch Dermatol 1964; 89:793-797.
- Boffetta P, Stellman SD, & Garfinkel L: A case-control study of multiple myeloma nested in the American Cancer Society prospective study. Intl J Cancer 1989; 43:554-559.
- Bois FY & Eskenazi B: Possible risk of endometriosis for Seveso, Italy, Residents: an assessment of exposure to dioxin. Environ Health Prespect 1994; 102:476-477.
- Bond GG, McLaren EA, & Brenner FE: Incidence of chloracne among chemical workers potentially exposed to chlorinated dioxins. J Occup Med 1989b; 31:771-774.
- Bond GG, McLaren EA, & Lipps TE: Update of mortality among chemical workers with potential exposure to the higher chlorinated dioxins. J Occup Med 1989a; 31:121-123.
- Brewster DW, Banks YB, & Clark AM: Comparative dermal absorption of 2,3,7,8-tetrachlorodibenzo-p-dioxin and three polychlorinated dibenzofurans. Toxicol Appl Pharmacol 1989; 97:156-166.
- Brewster DW, Bombick DW, & Matsumura F: Rabbit serum hypertriglyceridemia after administration of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). J Toxicol Environ Health 1988; 25:495-507.
- Brooks AL, Jordan SW, & Bose KK: The cytogenetic and hepatotoxic effects of dioxin on mouse liver cells. Cell Biol Toxicol 1988; 4:31-40.
- Budavari S: The Merck Index, 12th ed. on CD-ROM. Version 12:3a. Chapman & Hall/CRCnetBASE. Whitehouse Station, NJ. 2000.
- Burgess JL, Kirk M, Borron SW, et al: Emergency department hazardous materials protocol for contaminated patients. Ann Emerg Med 1999; 34(2):205-212.
- Burmeister LF, Everett GD, & Van Lier SF: Selected cancer mortality and farm practices in Iowa. Am J Epidemiol 1983; 118:72-77.
- Calvert GM, Hornung RW, & Sweeney MH: Hepatic and gastrointestinal effects in an occupational cohort exposed to 2,3,7,8-tetrachlorodibenzo-para-dioxin. JAMA 1992; 267:2209-2214.
- Calvert GM, Sweeney MH, & Fingerhut MA: Evaluation of porphyria cutanea tarda in US workers exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin. Am J Ind Med 1994; 25:559-571.
- Calvert GM, Wille KK, & Sweeney MH: Evaluation of serum lipid concentrations among US workers exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin. Arch Environ Health 1996; 51:100-107.
- Cantor KP & Blair A: Farming and mortality from multiple myeloma: a case-control study with the use of death certificates. J Natl Cancer Inst 1984; 72:251-255.
- Caputo R, Monti M, & Ermacora E: Cutaneous manifestations of tetrachlorodibenzo-p-dioxin in children and adolescents. J Am Acad Dermatol 1988; 19:812-819.
- Caravati EM, Knight HH, & Linscott MS: Esophageal laceration and charcoal mediastinum complicating gastric lavage. J Emerg Med 2001; 20:273-276.
- Chahoud I, Hartmann J, & Rune GM: Reproductive toxicity and toxicokinetics of 2,3,7,8-tetrachlorodibenzo-p-dioxin. 3. Effects of single doses on the testis of male rats. Arch Toxicol 1992; 66:567-572.
- Chahoud I, Krowke R, & Bochert G: Reproductive toxicity and toxicokinetics of 2,3,7,8-tetrachlorodibenzo-p-dioxin. 2. Problem of paternally-mediated abnormalities in the progeny of rat. Arch Toxicol 1991; 65:27-31.
- Chahoud I, Krowke R, & Schimmel A: Reproductive toxicity and pharmacokinetics of 2,3,7,8-tetrachlorodibenzo-p-dioxin. 1. Effects of high doses on the fertility of male rats. Arch Toxicol 1989; 63:432-439.
- Chapman EE & Schiller CM: Dose-related effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in C57BL/6J and DBA/2J mice. Toxicol Appl Pharmacol 1985; 78:147-157.
- Chemsoft(R) : Electronic EPA, NIOSH, & OSHA Methods(TM). Windowchem(TM) Software. Fairfield, CA. 2000.
- Chen YCJ, Guo YL, & Hsu CC: Cognitive development of Yu-Chen ("Oil Disease") children prenatally exposed to heat-degraded PCBs. JAMA 1992; 268:3213-3218.
- Chyka PA, Seger D, Krenzelok EP, et al: Position paper: Single-dose activated charcoal. Clin Toxicol (Phila) 2005; 43(2):61-87.
- Clayton GD & Clayton FE: Patty's Industrial Hygiene and Toxicology, Volume 2D, Toxicology, 4th ed, John Wiley & Sons, New York, NY, 1994, pp 2513-2536.
- Collins JJ, Strauss ME, & Levinskas GJ: The mortality experience of workers exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin in a trichlorophenol process,accident. Epidemiology 1993; 4:7-13.
- Cook RR: Dioxin, chloracne, and soft tissue sarcoma. Lancet 1981; 1:618-619.
- Courtney CD & Moore JA: Teratology studies with 2,4,5-trichlorophenoxyacetic acid and 2,3,7,8-tetrachlorodibenzo-p-dioxin. Toxicol Appl Pharmacol 1971; 20:396-403.
- Couture LA, Abbott BD, & Birnbaum LS: A critical review of the developmental toxicity and teratogenicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin: recent advances toward understanding the mechanism. Teratology 1990; 42:619-627.
- DFG: List of MAK and BAT Values 2002, Report No. 38, Deutsche Forschungsgemeinschaft, Commission for the Investigation of Health Hazards of Chemical Compounds in the Work Area, Wiley-VCH, Weinheim, Federal Republic of Germany, 2002.
- Dalderup LM & Zellenrath D: Dioxin exposure: 20 year follow-up. Lancet 1983; 2:1134-1135.
- Davis BJ, Mccurdy EA, & Miller BD: Ovarian tumors in rats induced by chronic 2,3,7,8-tetrachlorodibenzo-p-dioxin treatment. Cancer Res 2000; 60:5414-5419.
- Della Porta G, Dragani TA, & Sozzi G: Carcinogenic effects of infantile and long-term 2,3,7,8-tetrachlorodibenzo-p-dioxin treatment in the mouse. Tumori 1987; 73:99-107.
- DiDomenico A & Zapponi GA: 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in the environment: human health risk estimation and its application to the severe case as an example. Regulatory Toxicol Pharmacol 1986; 6:248-260.
- Dimich-Ward H, Hertzman C, & Teschke K: Reproductive effects of paternal exposure to chlorophenate wood perservatives in the sawmill industry. Scand J Work Environ Health 1996; 22:267-273.
- Dragun J: The Soil Chemistry of Hazardous Materials, Hazardous Materials Control Research Institute, Silver Spring, MD, 1988.
- Dunagin WG: Cutaneous signs of systemic toxicity due to dioxins and related chemicals. J Am Acad Dermatol 1984; 10:688-700.
- EPA: 40 CFR 266.104(3). Standards to control organic emissions, Government Printing Office, Washington, DC, 2002g.
- EPA: 40 CFR 63.1203. Final Rules for standards for hazardous waste incinerators, Government Printing Office, Washington, DC, 2002f.
- EPA: Estimating Exposure to Dioxin-Like Compounds. Volume I: Executive Summary, US Government Printing Office, Washington, DC, 1994a.
- EPA: Health Assessment Document for 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and Related Compounds, Volume III, US Government Printing Office, Washington, DC, 1994b.
- EPA: Health Reassessment for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related compounds (EPA/600/p-00/001Ae).. U.S. Environmental Protection Agency. Washington, DC, USA. 2000c. Available from URL: www.epa.gov/nceawww1/pdfs/dioxin/index.html.
- EPA: Questions and Answers about Dioxins.. U.S. Environmental Protection Agency, Office of Research and Development. Washington, DC, USA. 2000a. Available from URL: www.epa.gov/nceawww1/pdfs/dioxin/dioxin questions and answers.pdf.
- EPA: Search results for Toxic Substances Control Act (TSCA) Inventory Chemicals. US Environmental Protection Agency, Substance Registry System, U.S. EPA's Office of Pollution Prevention and Toxics. Washington, DC. 2005. Available from URL: http://www.epa.gov/srs/.
- EPA: Summary of Major EPA Control Efforts. U.S. Environmental Protection Agency, Office of Research and Development. Washington, DC, USA. 2000b. Available from URL: www.epa.gov/nceawww1/pdfs/dioxin/factsheets/dioxin_regs.pdf.
- EPA: Summary of the Dioxin Reassessment Science, Update. U.S. Enivronmental Proctection Agency, Office of Research and Development. Washington, DC, USA. 2001a. Available from URL: www.epa.gov/nceawww1/pdfs/dioxin/factsheets/dioxin_short2.pdf.
- ERG: Emergency Response Guidebook. A Guidebook for First Responders During the Initial Phase of a Dangerous Goods/Hazardous Materials Incident, U.S. Department of Transportation, Research and Special Programs Administration, Washington, DC, 2004.
- Egeland GM, Sweeney MH, & Fingerhut MA: Total serum testosterone and gonadotropins in workers exposed to dioxin. Am J Epidemiol 1994; 139:272-281.
- Eklund G, Pedersen JR, & Stromberg B: Phenol and HCl at 550 degree C yield a large variety of chlorinated toxic compounds. Nature 1986; 320:155-156.
- Elliot CG, Colby TV, & Kelly TM: Charcoal lung. Bronchiolitis obliterans after aspiration of activated charcoal. Chest 1989; 96:672-674.
- Erickson JD, Mulinare J, & McClain PW: Vietnam veteran's risks for fathering babies with birth defects. JAMA 1984; 252:903-912.
- Eriksson M, Hardell L, & Adami HO: Exposure to dioxins as a risk factor for soft tissue sarcoma: a population-based case-control study. J Natl Cancer Inst 1990; 82:486-490.
- Eschenroeder A, Jaeger RJ, & Ospital JJ: Health risk analysis of human exposures to soil amended with sewage sludge contaminated with polychlorinated dibenzodioxins and dibenzofurans. Vet Human Toxicol 1986; 28:435-442.
- Evans RG, Webb KB, & Knutsen AP: A medical follow-up of the health effects of long-term exposure to 2,3,7,8-tetrachorodibenzo-p-dioxin. Arch Environ Health 1988; 43:273-278.
- FDA: Poison treatment drug product for over-the-counter human use; tentative final monograph. FDA: Fed Register 1985; 50:2244-2262.
- Field B & Kerr C: Reproductive behaviour and consistent patterns of abnormality in offspring of Vietnam veterans. J Med Genet 1988; 25:819-826.
- Fierens S, Mairesse H, Jean-Francois H, et al: Dioxin/polychlorinated biphenyl body burden, diabetes and endometriosis: findings in a population-based study in Belgium. Biomarkers 2003; 8(6):529-534.
- Fingerhut MA, Halperin WE, & Marlow DA: Cancer mortality in workers exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin. N Engl J Med 1991; 324:212-218.
- Fleschjanys D, Becher H, & Gurn P: Elimination of polychlorinated dibenzo-p-dioxins and dibenzofurans in occupationally exposed persons. J Toxicol Environ Health 1996; 47:363-378.
- Fleschjanys D, Berger J, & Gurn P: Exposure to polychlorinated dioxins and furans (PCDD/F) and mortality in a cohort of workers from a herbicide-producing plant in Hamburg, Federal Republic of Germany. Am J Epidemiol 1995; 142:1165-1175.
- Flodstroem S & Ahlborg UG: Relative liver tumor promoting activity of some polychlorinated dibenzo-p-dioxin-, dibenzofuran- and biphenyl-congeners in female rats. Chemosphere 1992; 25:169-172.
- Floret N , Mauny F , Challier B , et al: Dioxin emissions from a solid waste incinerator and risk of non-Hodgkin lymphoma. Epidemiology 2003; 14(4):392-398.
- Flowers FP, Fenske NA, & Whisman PA: Agent orange: What's it all about?. J Florida Med Assoc 1981; 68:991-992.
- Forawi HA, Tchounwou PB, & McMurray RW: Xenoestrogen modulation of the immune system: effects of dichlorodiphenyltrichloroethane (DDT) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) . Rev Environ Health 2004; 19(1):1-13.
- Frakes RA, Zeeman CQ, & Mower B: Bioaccumulation of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) by fish downstream of pulp and paper mills in Maine. Ecotoxicol Environ Safety 1993; 25:244-52.
- Franzblau A , Hedgeman E , Chen Q , et al: Case report: human exposure to dioxins from clay. Environ Health Perspect 2008; 116(2):238-242.
- Freeman HM: Standard Handbook of Hazardous Waste Treatment and Disposal, 2nd ed, McGraw-Hill Book Company, New York, NY, 1998.
- Freeman HM: Standard Handbook of Hazardous Waste Treatment and Disposal, McGraw-Hill Book Company, New York, NY, 1989.
- Geusau A , Jurecka W , Nahavandi H , et al: Punctate keratoderma-like lesions on the palms and soles in a patient with chloracne: a new clinical manifestation of dioxin intoxication?. Br J Dermatol 2000; 143(5):1067-1071.
- Geusau A , Tschachler E , Meixner M , et al: Cutaneous elimination of 2,3,7,8-tetrachlorodibenzo-p-dioxin. Br J Dermatol 2001; 145(6):938-943.
- Giavini E, Prati M, & Vismara C: Embryotoxic effects of 2,3,7,8 tetrachlorodibenzo-p-dioxin administered to female rats before mating. Environ Res 1983; 31:105-110.
- Giesy JP, Jones PD, & Kannan K: Effects of chronic dietary exposure to environmentally relevant concentrations to 2,3,7,8-tetrachlorodibenzo-p-dioxin on survival, growth, reproduction and biochemical repsonses of female rainbow troug (Oncorhynchus mykiss). Aquat Toxicol 2002; 59:35-53.
- Goldfrank LR: Goldfrank's Toxicological Emergencies, 6th ed, McGraw-Hill, New York, NY, 1998.
- Golej J, Boigner H, Burda G, et al: Severe respiratory failure following charcoal application in a toddler. Resuscitation 2001; 49:315-318.
- Graff GR, Stark J, & Berkenbosch JW: Chronic lung disease after activated charcoal aspiration. Pediatrics 2002; 109:959-961.
- Greenlee WE, Hushka LJ, & Hushka DR: Molecular basis of dioxin actions: evidence supporting chemoprotection. Toxicol Pathol 2001; 29:6-7.
- Greenwald P, Kovasznay B, & Collins DN: Sarcomas of soft tissues after Vietnam service. J Natl Cancer Inst 1984; 73:1107-1109.
- Grehl H, Grahmann F, & Claus D: Histologic evidence for a toxic polyneuropathy due to exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in rats. ACTA Neurol Scand 1993; 88:354-357.
- Guo SW: The link between exposure to dioxin and endometriosis: A critical reappraisal of primate data. Gyn Obst Investigation 2004; 57:157-173.
- Guo YL, Hsu PC, & Hsu CC: Semen quality after prenatal exposure to polychlorinated biphenyls and dibenzofurans. Lancet 2000; 356:1240-1241.
- Guo YL, Lin CJ, & Yao WJ: Musculoskeletal changes in children prenatally exposed to polychlorinated biphenyls and related compounds (Yu-Cheng children). J Toxicol Environ Health 1994; 41:83-93.
- HSDB : Hazardous Substances Data Bank. National Library of Medicine. Bethesda, MD (Internet Version). Edition expires 2002; provided by Truven Health Analytics Inc., Greenwood Village, CO.
- HSDB : Hazardous Substances Data Bank. National Library of Medicine. Bethesda, MD (Internet Version). Edition expires 2004; provided by Truven Health Analytics Inc., Greenwood Village, CO.
- HSDB : Hazardous Substances Data Bank. National Library of Medicine. Bethesda, MD (Internet Version). Edition expires 2005; provided by Truven Health Analytics Inc., Greenwood Village, CO.
- Halperin W, Kalow W, & Sweeney MH: Induction of P-450 in workers exposed to dioxin. Occup Environ Med 1995; 52:86-91.
- Hannah RR, Lund J, & Poellinger L: Characterization of the DNA-binding properties of the receptor for 2,3,7,8-tetrachlorodibenzo-p-dioxin. Eur J Biochem 1986; 156:237-242.
- Harbison RM: Hamilton and Hardy's Industrial Toxicology, 5th ed, Mosby, St. Louis, MO, 1998.
- Hardell L & Bengtsson NO: Epidemiological study of socioeconomic factors and clinical findings in Hodgkin's disease, and reanalysis of previous data regarding chemical exposure. Br J Cancer 1983; 48:217-225.
- Hardell L & Eriksson M: The association between soft tissue sarcomas and exposure to phenoxyacetic acids: a new case-referent study. Cancer 1988; 62:652-656.
- Hardell L & Sandrom A: Case-control study: soft tissue sarcoma and exposure to phenoxyacetic acids or chlorophenols. Br J Cancer 1979; 39:711-717.
- Hardell L, Eriksson M, & Lenner P: Malignant lymphoma and exposure to chemicals, especially organic solvents, chlorophenols and phenoxy acids: a case-control study. Br J Cancer 1981; 43:169-176.
- Hardell L: Malignant lymphoma of histiocytic type and exposure to phenoxyacetic acids or chlorophenols. Lancet 1979; 1:55-56.
- Hardell L: Relation of soft-tissue sarcoma, malignant lymphoma and colon cancer to phenoxy acids, chlorophenols and other agents. Scand J Work Environ Health 1981; 7:119-130.
- Harper N, Connor K, & Safe S: Immunotoxic potencies of polychlorinated biphenyl (PCB), dibenzofuran (PCDF) and dibenzo-p-dioxin (PCDD) congeners in C57BL/6 and DBA/2 mice. Toxicology 1993; 80:217-227.
- Harris CR & Filandrinos D: Accidental administration of activated charcoal into the lung: aspiration by proxy. Ann Emerg Med 1993; 22:1470-1473.
- Hassan MQ, Stohs SJ, & Murray WJ: Dietary selenium, glutathione peroxidase activity, and toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin. J Toxicol Environ Health 1985; 15:405-415.
- Hassoun EA & Stohs SJ: Comparative teratological studies on TCDD, endrin and lindane in C57BL/6J and DBA/2J mice. Comp Biochem Physiol 1996; 113:393-398.
- Hatch MC & Stein ZA: Agent orange and risks to reproduction: the limits of epidemiology. Teratogen Carcinogen Mutagen 1986; 6:185-202.
- Hayes HM, Tarone RE, & Casey HW: Excess of seminomas observed in Vietnam service US military working dogs. J Natl Cancer Inst 1990; 82:1042-1046.
- Hayes WJ Jr & Laws ER Jr: Handbook of Pesticide Toxicology, Volume 1, Academic Press, Inc, San Diego, CA, 1991, pp 330-3371217-1243.
- Hayes WJ Jr: Pesticides Studied in Man, Williams & Wilkins, Baltimore, MD, 1982.
- Hebert CD, Harris MW, & Elwell MR: Relative toxicity and tumor-promoting ability of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 2,3,4,7,8-pentachlorodibenzofuran (PCDF), and 1,2,3,4,7,8-hexachlorodibenzofuran (HCDF) in hairless mice. Toxicol Appl Pharmacol 1990; 102:362-377.
- Henriksen GL, Ketchum NS, & Michalek JE: Serum dioxin, diabetes mellitus in veterans of Operation Ranch Hand. Epidemiology 1997; 8:252-258.
- Hoar SK, Blair A, & Holmes FF: Agricultural herbicide use and risk of lymphoma and soft-tissue sarcoma. JAMA 1986; 256:1141-1147.
- Hoffman RE, Stehr-Green PA, & Webb KB: Health effects of long-term exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin. JAMA 1986; 255:2031-2038.
- Holsapple MP, McNerney PJ, & Barnes DW: Suppression of humoral antibody production by exposure to 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin. J Pharmacol Exp Ther 1984; 231:518-526.
- Honchar PA & Halperin WE: 2,4,5-T, trichlorophenol, and soft tissue sarcoma. Lancet 1981; 1:268-269.
- Howard PH, Boethling RS, & Jarvis WF: Handbook of Environmental Degradation Rates, Lewis Publishers, Chelsea, MI, 1991.
- Howard PH, Boethling RS, & Jarvis WF: Handbook of Environmental Degradation Rates, Lewis Publishers, Chelsea, MI, 1991a.
- Hruska RE & Olson JR: Species differences in estrogen receptors and in the response to 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure. Toxicol Lett 1989; 48:289-299.
- Hsu CC, Hu HF, & Lai RJ: Behavioral development of Yucheng children as compared to their matched controls. Dioxin '93 1993; 14:239-242.
- Huff JE, Salmon AG, & Hooper NK: Long-term carcinogenesis studies on 2,3,7,8-tetrachlorodibenzo-p-dioxin and hexachlorodibenzo-p-dioxins. Cell Biol Toxicol 1991; 7:67-94.
- Huisman M, Koopmanesseboom C, & Fidler V: Perinatal exposure to polychlorinated biphenyls and dioxins and its effect on neonatal neurological development. Early Human Dev 1995; 41:111-127.
- Hurst CH, Abbott B, & Schmid JE: 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) disrupts early morphogenetic events that form the lower reproductive tract in female rat fetuses. Toxicol Sci 2002; 65:87-98.
- Huuskonen H, Unkila M, & Pohjanvirta R: Developmental toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in the most TCDD-resistant and -susceptible rat strains. Toxicol Appl Pharmacol 1994; 124:174-180.
- IARC : Monographs on the Evaluation of the Carcinogenicity of Chemicals to Humans. Polychlorinated Dibenzo-para-dioxins [1746-01-6]. Available at International Agency for Research on Cancer. 69. International Agency for Research on Cancer, World Health Organization. Geneva, Switzerland. 1997. Available from URL: http://www.iarc.fr). As accessed Accessed 10 May 01.
- IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: 1,3-Butadiene, Ethylene Oxide and Vinyl Halides (Vinyl Fluoride, Vinyl Chloride and Vinyl Bromide), 97, International Agency for Research on Cancer, Lyon, France, 2008.
- IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Formaldehyde, 2-Butoxyethanol and 1-tert-Butoxypropan-2-ol, 88, International Agency for Research on Cancer, Lyon, France, 2006.
- IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Household Use of Solid Fuels and High-temperature Frying, 95, International Agency for Research on Cancer, Lyon, France, 2010a.
- IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Smokeless Tobacco and Some Tobacco-specific N-Nitrosamines, 89, International Agency for Research on Cancer, Lyon, France, 2007.
- IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Some Non-heterocyclic Polycyclic Aromatic Hydrocarbons and Some Related Exposures, 92, International Agency for Research on Cancer, Lyon, France, 2010.
- IARC: International Agency for Research on Cancer: IARC Monographs on the Evaluation of Carcinogenic Risk of Chemicals to Humans, 15, International Agency for Research on Cancer, World Health Organization, Geneva, Switzerland, 1977.
- IARC: List of all agents, mixtures and exposures evaluated to date - IARC Monographs: Overall Evaluations of Carcinogenicity to Humans, Volumes 1-88, 1972-PRESENT. World Health Organization, International Agency for Research on Cancer. Lyon, FranceAvailable from URL: http://monographs.iarc.fr/monoeval/crthall.html. As accessed Oct 07, 2004.
- ICAO: Technical Instructions for the Safe Transport of Dangerous Goods by Air, 2003-2004. International Civil Aviation Organization, Montreal, Quebec, Canada, 2002.
- ILO: Encyclopaedia of Occupational Health and Safety, 4th ed. Vol 1-4. JM Stellman (Ed) , International Labour Organization, Geneva, Switzerland, 1998.
- IOM: Veterans and Agent Orange (Executive Summary), Institute of Medicine, Division of Health Promotion and Disease Prevention, Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides, National Academy Press, Washington, DC, 1993.
- International Agency for Research on Cancer (IARC): IARC monographs on the evaluation of carcinogenic risks to humans: list of classifications, volumes 1-116. International Agency for Research on Cancer (IARC). Lyon, France. 2016. Available from URL: http://monographs.iarc.fr/ENG/Classification/latest_classif.php. As accessed 2016-08-24.
- International Agency for Research on Cancer: IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. World Health Organization. Geneva, Switzerland. 2015. Available from URL: http://monographs.iarc.fr/ENG/Classification/. As accessed 2015-08-06.
- Ivens IA, Loser E, & Rinke M: Subchronic toxicity of 2,3,7,8-tetrabromodibenzo-p-dioxin in rats. Toxicology 1993; 83:181-201.
- Ivnitski I, Elmaoued R, & Walker MK: 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) inhibition of coronary development is preceded by a decrease in myocyte proliferation and an increase in cardiac apoptosis. Teratology 2001; 64:201-212.
- Jansson B & Voog L: Dioxin from Swedish municipal incinerators and the occurrence of cleft lip and palate malformations. Int J Environ Stud 1989; 34:99-104.
- Johnson ES, Parsons W, & Weinberg CR: Current serum levels of 2,3,7,8-tetrachlorodibenzo-p-dioxin in phenoxy acid herbicide applicators and characterization of historical levels. J Natl Cancer Inst 1992; 84:1648-1653.
- Johnson J: Dioxin risk: are we sure yet?. Environ Sci Technol 1995; 29:24A-25A.
- Johnson L, Walker CE, & Safe SH: 2,3,7,8-tetrachlorodibenzo-p-dioxin reduces the number, size and organelle content of Leydig cells in adult rat testes. Toxicology 1994; 89:49-65.
- Jones RE & Chelsky M: Further discussion concerning porphyria cutanea tarda and TCDD exposure. Arch Environ Health 1986; 41:100-103.
- Kahn PC, Gochfeld M, & Nygren M: Dioxins and dibenzofurans in blood and adipose tissue of Agent Orange - exposed Vietnam veterans and matched controls. JAMA 1988; 259:1661-1667.
- Karmaus W & Wolf N: Reduced birthweight and length in the offspring of females exposed to PCDFs, PCP, and lindane. Environ Health Perspect 1995; 103:1120-1125.
- Kayajanian G: Dioxin is a promoter blocker, a promoter, and a net anticarcinogen. Regul Toxicol Pharmacol 1997; 26:134-137.
- Keenan RE, Paustenbach DJ, & Wenning RJ: Pathology reevaluation of the Kociba et al (1978) bioassay of 2,3,7,8-TCDD: implications for risk assessment. J Toxicol Environ Health 1991; 34:279-296.
- Kerkvliet NI, Wagner SL, & Schmotzer WB: Dioxin intoxication from chronic exposure to horses to pentachlorophenol-contaminated wood shavings. JAVMA 1992; 201:296-302.
- Ketchum NS & Michalek JE: Postservice mortality of Air Force veterans occupationally exposed to herbicides during the Vietnam War: 20-year follow-up results. Mil Med 2005; 170(5):406-413.
- Ketchum NS, Michalek JE, & Burton JE: Serum dioxin and cancer in veterans of Operation Ranch Hand. Am J Epidemiol 1999; 149:630-639.
- Kimbrough RD, Carter CD, & Liddle JA: Epidemiology and pathology of a tetrachlorodibenzodioxin poisoning episode. Arch Environ Health 1977; 32:77.
- Klawans HL: Dystonia and tremor following exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin. Movement Disorders 1987; 2:255-261.
- Kociba RJ, Keeler PA, & Park CN: 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD): results of a 13-week oral toxicity study in rats. Toxicol Appl Pharmacol 1976; 35:553-574.
- Kociba RJ, Keyes DG, & Beyer JE: Results of a two-year chronic toxicity and oncogenicity study of 2,3,7,8-tetrachlorodibenzo-p-dioxin in rats. Toxicol Appl Pharmacol 1978; 46:279-303.
- Kogan MD & Clapp RW: Soft tissue sarcoma mortality among Vietnam veterans in Massachusetts, 1972 to 1983. Int J Epidemiol 1988; 17:39-43.
- Kogevinas M : Human health effects of dioxins: cancer, reproductive and endocrine system effects. Hum Reprod Update 2001; 7(3):331-339.
- Kogevinas M, Kauppinen T, & Winkelmann R: Soft tissue sarcoma and non-Hodgkins lymphoma in workers exposed to phenoxy herbicides, chlorophenols, and dioxins - two nested case-control studies. Epidemiol 1995; 6:396-402.
- Koopman-Esseboom C, Weisglaskuperus N, & Deridder MAJ: Effects of polychlorinated biphenyl dioxin exposure and feeding type on infants mental and psychomotor development. Pediatrics 1996; 97:700-706.
- Koppe JG, Olie K, & van Wijen J: Placental transport of dioxins from mother to fetus. Dev Pharmacol Ther 1992; 18:9-13.
- Koppe JG: Dioxins and furans in the mother and possible effects on the fetus and newborn breast-fed baby. ACTA Paediatr Scand 1989; 360(Suppl):146-153.
- Kuehl DW, Butterworth BC, & DeVita WM: Environmental contamination by polychlorinated dibenzo-p-dioxins and dibenzofurans associated with pulp and paper mill discharge. Biomed Environ Mass Spectrum 1987; 14:443-7.
- Lai TJ, Chen YC, & Chou WJ: Cognitive development in Yucheng children. Dioxin '93 1993; 14:247-250.
- Lamb JC 4th, Marks TA, & Gladen BC: Male fertility, sister chromatid exchange, and germ cell toxicity following exposure to mixtures of chlorinated phenoxy acids containing 2,3,7,8-tetrachlorodibenzo-p-dioxin. J Toxicol Environ Health 1981a; 8:825-834.
- Lamb JC 4th, Moore JA, & Marks TA: Development and viability of offspring of male mice treated with chlorinated phenoxy acids and 2,3,7,8-tetrachlorodibenzo-p-dioxin. J Toxicol Environ Health 1981b; 8:835-844.
- Landi MT, Consonni D, & Patterson DG Jr: 2,3,7,8-Tetrachlorodibenzo-p-dioxin plasma levels in Seveso 20 years after the accident. Environ Health Perspect 1998; 106(5):273-7.
- Lang DS, Becker S, & Clark GC: Lack of direct immunosuppressive effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on human peripheral blood lymphocyte subsets in vitro. Arch Toxicol 1994; 68:296-302.
- Levy CJ: Agent orange exposure and posttraumatic stress disorder. J Nervous Mental Dis 1988; 176:242-245.
- Lewis RA: Lewis' Dictionary of Toxicology, Lewis Publishers, Boca Raton, FL, 1998.
- Lewis RJ: Sax's Dangerous Properties of Industrial Materials, 10th ed, John Wiley & Sons, New York, NY, 2000.
- Lim M, Jacobson-Kram D, & Bowman RE: Effect of chronic exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin on sister chromatid exchange levels in peripheral lymphocytes of the Rhesus monkey. Cell Biol Toxicol 1987; 3:279-284.
- Lorber M & Phillips L : Infant exposure to dioxin-like compounds in breast milk. Environ Health Perspect 2002; 110(6):A325-A332.
- Luster MI, Boorman GA, & Dean JH: Examination of bone marrow, immunologic parameters and host susceptibility following pre- and postnatal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Internat J Immunopharmacol 1980; 2:301-310.
- MMWR: Serum 2,3,7,8-tetrachlorodibenzo-p-dioxin levels in Air Force Health Study participants report. MMWR (May 27), 1988.
- Mably TA, Bjerke DL, & Moore RW: In utero and lactational exposure of male rats to 2,3,7,8-tetrachlorodibenzo-p-dioxin. 3. Effects on spermatogenesis and reproductive capability. Toxicol Appl Pharmacol 1992c; 114:118-126.
- Mably TA, Moore RW, & Goy RW: In utero and lactational exposure of male rats to 2,3,7,8-tetrachlorodibenzo-p-dioxin. 2. Effects on sexual behavior and the regulation of luteinizing hormone secretion in adulthood. Toxicol Appl Pharmacol 1992b; 114:108-117.
- Mably TA, Moore RW, & Peterson RE: Effects of perinatal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on pre- and postnatal plasma testosterone (T) concentrations in male rats. Toxicologist 1991; 11:262.
- Mably TA, Moore RW, & Peterson RE: In utero and lactational exposure of male rats to 2,3,7,8-tetrachlorodibenzo-p-dioxin. 1. Effects on androgenic status. Toxicol Appl Pharmacol 1992a; 114:97-107.
- Manz A, Berger J, & Dwyer JH: Cancer mortality among workers in chemical plant contaminated with dioxin. Lancet 1991; 338:959-964.
- Martin JV: Lipid abnormalities in workers exposed to dioxin. Br J Ind Med 1984; 41:254-256.
- Massa T, Esmaeili A, & Fortmeyer H: Cell transforming and oncogenic activity of 2,3,7,8--tetrachloro--and 2,3,7,8 tetrabromodibenzo-p-dioxin. Anticancer Res 1992; 12:2053-2060.
- Mastroiacovo P, Spagnolo A, & Marni E: Birth defects in the Seveso area after TCDD contamination. JAMA 1988; 259:1668-1672.
- Matsumura F: Stimulation of c-ras expression by 2,3,7,8-tetrachlorodibenzo-p-dioxin. Chemosphere 1992; 25:959-966.
- May G: Chloracne from the accidental production of tetrachlorobenzodioxin. Br J Ind Med 1973; 30:276-283.
- McKinney J & McConnell E: Structural specificity and the dioxin receptor, in Hutzinger O: Chlorinated Dioxins and Related Compounds, Pergamon Press, Oxford, UK, 1982.
- Meyne J, Allison DC, & Bose K: Hepatotoxic doses of dioxin do not damage mouse bone marrow chromosomes. Mutat Res 1985; 157:63-69.
- Michalek JE, Akhtar FZ, & Kiel JL: Serum dioxin, insulin, fasting glucose, and sex hormone-binding globulin in veterans of Operation Ranch Hand. J Clin Endocrinol Metab 1999; 84:1540-1543.
- Michalek JE, Ketchum NS, & Akhtar FZ: Postservice mortality of US Air Force veterans occupationally exposed to herbicides in Vietnam: 15-year follow-up. Am J Epidemiol 1998a; 148:786-792.
- Michalek JE, Ketchum NS, & Check IJ: Serum dioxin and immunologic response in veterans of Operation Ranch Hand. Am J Epidemiol 1999a; 149:1038-1046.
- Michalek JE, Pirkle JL, & Caudill SP: Pharmacokinetics of TCDD in veterans of operation ranch hand -- 10-year follow-up. J Toxicol Environ Health 1996; 47:209-220.
- Michalek JE, Rahe AJ, & Boyle CA: Paternal dioxin, preterm birth, intrauterine growth retardation, and infant death. Epidemiology 1998b; 9:161-167.
- Mocarelli P , Gerthoux PM , Patterson DG , et al: Dioxin exposure, from infancy through puberty, produces endocrine disruption and affects human semen quality. Environ Health Perspect 2008; 116(1):70-77.
- Mocarelli P, Needham LL, & Marocchi A: Serum concentrations of 2,3,7,8-tetrachlorodibenzo-p-dioxin and test results from selected residents of Seveso, Italy. J Toxicol Environ Health 1991; 32:357-366.
- Moore RW, Mably TA, & Peterson RE: Effects of perinatal 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure on the development of male rats and their androgenic status. Toxicologist 1990; 10:247.
- Morrison H, Savitz D, & Semenciw R: Farming and prostate cancer mortality. Am J Epidemiol 1993; 137:270-280.
- Moses M, Lilis R, & Thornton J: Health status of workers with past exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin in the manufacture of 2,4,5-trichlorophenoxyacetic acid: comparison of findings with and without chloracne. Am J Ind Med 1984; 5:161-182.
- Murray FJ, Smith FA, & Nitschke KD: Three-generation reproduction study of rats ingesting 2,3,7,8-tetrachlorodibenzo-p-dioxin. Toxicol Appl Pharmacol 1977; 41:200-201.
- Mustonen R, Elovaara E, & Zitting A: Effects of commercial chlorophenolate, 2,3,7,8-TCDD, and pure phenoxyacetic acids on hepatic peroxisome proliferation, xenobiotic metabolism and sister chromatid exchange in the rat. Arch Toxicol 1989; 63:203-208.
- Muto H & Takizawa Y: Dioxins in cigarette smoke. Arch Environ Health 1989; 44:171-174.
- NFPA: Fire Protection Guide to Hazardous Materials, 13th ed., National Fire Protection Association, Quincy, MA, 2002.
- NIOSH : Pocket Guide to Chemical Hazards. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires March/2002; provided by Truven Health Analytics Inc., Greenwood Village, CO.
- NIOSH: Current Intelligence Bulletin 40, 2,3,7,8-tetrachlorodibenzo-p-dioxin, No 84-104, National Institute for Occupational Safety and Health, Cincinnati, OH, 1984.
- NIOSH: Pocket Guide to Chemical Hazards. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires 2005; provided by Truven Health Analytics Inc., Greenwood Village, CO.
- NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 1, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2001.
- NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 2, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2002.
- NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 3, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2003.
- NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 4, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2004.
- Nagayama J , Nagayama M , Iida T , et al: Frequency of SCEs in Japanese infants exposed to dioxins and PCBs through the breast milk. Fukuoka Igaku Zasshi 2003; 94(5):158-165.
- Nakano S, Noguchi T, Takekoshi H, et al: Maternal-fetal distribution and transfer of dioxins in pregnant women in Japan, and attempts to reduce maternal transfer with Chlorella (Chlorella pyrenoidosa) supplements. Chemosphere 2005; 61:1244-1255.
- Naradzay J & Barish RA: Approach to ophthalmologic emergencies. Med Clin North Am 2006; 90(2):305-328.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2,3-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2,4-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2-Butylene Oxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648083cdbb&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2-Dibromoethane (Proposed). United States Environmental Protection Agency. Washington, DC. 2007g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064802796db&disposition=attachment&contentType=pdf. As accessed 2010-08-18.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,3,5-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 2-Ethylhexyl Chloroformate (Proposed). United States Environmental Protection Agency. Washington, DC. 2007b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648037904e&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Acrylonitrile (Proposed). United States Environmental Protection Agency. Washington, DC. 2007c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648028e6a3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Adamsite (Proposed). United States Environmental Protection Agency. Washington, DC. 2007h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Agent BZ (3-quinuclidinyl benzilate) (Proposed). United States Environmental Protection Agency. Washington, DC. 2007f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ad507&disposition=attachment&contentType=pdf. As accessed 2010-08-18.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Allyl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648039d9ee&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Aluminum Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Arsenic Trioxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2007m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480220305&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Automotive Gasoline Unleaded (Proposed). United States Environmental Protection Agency. Washington, DC. 2009a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cc17&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Biphenyl (Proposed). United States Environmental Protection Agency. Washington, DC. 2005j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064801ea1b7&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bis-Chloromethyl Ether (BCME) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006n. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648022db11&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Boron Tribromide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ae1d3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bromine Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2007d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648039732a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bromoacetone (Proposed). United States Environmental Protection Agency. Washington, DC. 2008e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809187bf&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Calcium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Carbonyl Fluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ae328&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Carbonyl Sulfide (Proposed). United States Environmental Protection Agency. Washington, DC. 2007e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648037ff26&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Chlorobenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2008c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803a52bb&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Cyanogen (Proposed). United States Environmental Protection Agency. Washington, DC. 2008f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809187fe&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Dimethyl Phosphite (Proposed). United States Environmental Protection Agency. Washington, DC. 2009. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbf3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Diphenylchloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648091884e&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyl Phosphorodichloridate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480920347&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2008g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809203e7&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Germane (Proposed). United States Environmental Protection Agency. Washington, DC. 2008j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963906&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Hexafluoropropylene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064801ea1f5&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ketene (Proposed). United States Environmental Protection Agency. Washington, DC. 2007. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ee7c&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Magnesium Aluminum Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Magnesium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Malathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2009k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809639df&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Mercury Vapor (Proposed). United States Environmental Protection Agency. Washington, DC. 2009b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a8a087&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl Isothiocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963a03&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl Parathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2008l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963a57&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl tertiary-butyl ether (Proposed). United States Environmental Protection Agency. Washington, DC. 2007a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064802a4985&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methylchlorosilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2005. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5f4&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyldichlorosilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2005a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c646&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN1 CAS Reg. No. 538-07-8) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN2 CAS Reg. No. 51-75-2) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN3 CAS Reg. No. 555-77-1) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Tetroxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008n. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648091855b&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Trifluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963e0c&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Parathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2008o. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963e32&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Perchloryl Fluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e268&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Perfluoroisobutylene (Proposed). United States Environmental Protection Agency. Washington, DC. 2009d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e26a&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008p. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096dd58&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyl Mercaptan (Proposed). United States Environmental Protection Agency. Washington, DC. 2006d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020cc0c&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phorate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008q. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096dcc8&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phosgene (Draft-Revised). United States Environmental Protection Agency. Washington, DC. 2009e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a8a08a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phosgene Oxime (Proposed). United States Environmental Protection Agency. Washington, DC. 2009f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e26d&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Potassium Cyanide (Proposed). United States Environmental Protection Agency. Washington, DC. 2009g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbb9&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Potassium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Propargyl Alcohol (Proposed). United States Environmental Protection Agency. Washington, DC. 2006e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec91&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Selenium Hexafluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2006f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec55&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Silane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d523&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sodium Cyanide (Proposed). United States Environmental Protection Agency. Washington, DC. 2009h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbb9&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sodium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Strontium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sulfuryl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2006h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec7a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tear Gas (Proposed). United States Environmental Protection Agency. Washington, DC. 2008s. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e551&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tellurium Hexafluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e2a1&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tert-Octyl Mercaptan (Proposed). United States Environmental Protection Agency. Washington, DC. 2008r. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e5c7&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tetramethoxysilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d632&disposition=attachment&contentType=pdf. As accessed 2010-08-17.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethoxysilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d632&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethyl Phosphite (Proposed). United States Environmental Protection Agency. Washington, DC. 2009j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7d608&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethylacetyl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008t. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e5cc&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Zinc Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
- National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for n-Butyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064808f9591&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
- National Heart,Lung,and Blood Institute: Expert panel report 3: guidelines for the diagnosis and management of asthma. National Heart,Lung,and Blood Institute. Bethesda, MD. 2007. Available from URL: http://www.nhlbi.nih.gov/guidelines/asthma/asthgdln.pdf.
- National Institute for Occupational Safety and Health: NIOSH Pocket Guide to Chemical Hazards, U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, Cincinnati, OH, 2007.
- National Research Council : Acute exposure guideline levels for selected airborne chemicals, 5, National Academies Press, Washington, DC, 2007.
- National Research Council: Acute exposure guideline levels for selected airborne chemicals, 6, National Academies Press, Washington, DC, 2008.
- National Research Council: Acute exposure guideline levels for selected airborne chemicals, 7, National Academies Press, Washington, DC, 2009.
- National Research Council: Acute exposure guideline levels for selected airborne chemicals, 8, National Academies Press, Washington, DC, 2010.
- None Listed: Position paper: cathartics. J Toxicol Clin Toxicol 2004; 42(3):243-253.
- Nosek JA, Craven SR, & Sullivan JR: Toxicity and reproductive effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin in ring-necked pheasant hens. J Toxicol Environ Health 1992; 35:187-98.
- Ohsako S, Miyabara Y, & Sakaue M: Developmental stage-specific effects of perinatal 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure on reproductive organs of male rat offspring. Toxicol Sci 2002; 66:283-292.
- Oliver RM: Toxic effects of 2,3,7,8-tetrachlorodibenzo-1, 4-dioxin in laboratory workers. Br J Ind Med 1975; 32:49-53.
- Olson JR & McGarrigle BP: Comparative developmental toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Chemosphere 1992; 25:71-74.
- Olson JR: Metabolism and disposition of 2,3,7,8-tetrachlorodibenzo-p-dioxin in guinea pigs. Toxicol Appl Pharmacol 1986; 85:263-273.
- Osborne R & Greenlee WF: 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) enhances terminal differentiation of cultured human epidermal cells. Toxicol Appl Pharmacol 1985; 77:434-443.
- Ott MG, Olson RA, & Cook RR: Cohort mortality study of chemical workers with potential exposure to the higher chlorinated dioxins. J Occup Med 1987; 29:422-429.
- Patterson AT , Kaffenberger BH , Keller RA , et al: Skin diseases associated with Agent Orange and other organochlorine exposures. J Am Acad Dermatol 2016; 74(1):143-170.
- Patterson DG Jr, Fingerhut MA, & Roberts DW: Levels of polychlorinated dibenzo-p-dioxins and dibenzofurans in workers exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin. Am J Ind Med 1989; 16:135-146.
- Patterson DG Jr, Needham LL, & Pirkle JL: Correlation between serum and adipose tissue levels of 2,3,7,8-tetrachlorodibenzo-p-dioxin in 50 persons from Missouri. Arch Environ Contam Toxicol 1988; 17:139-143.
- Pazderova-Vejlupkova J, Nemcova M, & Pickova J: The development and prognosis of chronic intoxication by tetrachlorodibenzo-p-dioxin in man. Arch Environ Health 1981; 35:5-11.
- Pearn JH: Herbicides and congenital malformations: a review for the paediatrician. Aust Paediatr J 1985; 21:237-242.
- Peate WF: Work-related eye injuries and illnesses. Am Fam Physician 2007; 75(7):1017-1022.
- Peper M, Klett M, & Frentzel-Beyme R: Neuropsychological effects of chronic exposure to environmental dioxins and furans. Environ Res 1993; 60:124-135.
- Persson B, Dahlander A-M, & Fredriksson M: Malignant lymphomas and occupational exposures. Br J Ind Med 1989; 46:517-520.
- Pesatori AC, Consonni D, & Tironi A: Cancer in a young population in a dioxin-contaminated area. Intl J Epidemiol 1993; 22:1010-1013.
- Peterson RE, Theobald HM, & Kimmel GL: Developmental and reproductive toxicity of dioxins and related compounds - cross-species comparisons. Crit Rev Toxicol 1993; 23:283-335.
- Pirkle JL, Wolfe WH, & Patterson DG: Estimates of the half-life of 2,3,7,8-tetrachlorodibenzo-p-dioxin in Vietnam Veterans of Operation Ranch Hand. J Toxicol Environ Health 1989; 27:165-171.
- Plewig G: Vitamin A acid treatment of chloracne. Hautarzt 1971; 22:341-345.
- Pluim HJ, Devijlder JJM, & Olie K: Effects of prenatal and postnatal exposure to chlorinated dioxins and furans on human neonatal thyroid hormone concentrations. Environ Health Perspect 1993; 101:504-508.
- Pluim HJ, Koppe JG, & Olie K: Effects of dioxins on thyroid function in newborn babies. Lancet 1992; 339:1303.
- Poiger H & Schlatter C: Influence of solvents and absorbents on dermal and intestinal absorption of TCDD. Drug Cosmet Toxicol 1980; 18:477-481.
- Poiger H & Schlatter C: Pharmacokinetics of 2,3,7,8-TCDD in man. Chemosphere 1986; 15:1489-1494.
- Poland A & Glover E: Genetic expression of aryl hydrocarbon hydroxylase by 2,3,7,8-tetrachlorodibenzo-p-dioxin: evidence for a receptor mutation in genetically non-responsive mice. Mol Pharmacol 1975; 11:389-398.
- Poland AP, Smith D, & Metter G: A health survey of workers in a 2,4,D and 2,4,5-T plant, with special attention to chloracne, porphyria cutanea tarda and psychologic parameters. Arch Environ Health 1971; 22:316-327.
- Pollack MM, Dunbar BS, & Holbrook PR: Aspiration of activated charcoal and gastric contents. Ann Emerg Med 1981; 10:528-529.
- Puga A, Nebert DW, & Carrier F: Dioxin induces expression of c-fos and c-jun proto-oncogenes and a large increase in transcription factor AP-1. DNA Cell Biol 1992; 4:269-281.
- RTECS : Registry of Toxic Effects of Chemical Substances. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires 2001; provided by Truven Health Analytics Inc., Greenwood Village, CO.
- RTECS : Registry of Toxic Effects of Chemical Substances. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires 2002; provided by Truven Health Analytics Inc., Greenwood Village, CO.
- Raisanen S, Hiltunen R, & Arstila AU: Determination of 2,3,7,8-tetrachlorodibenzo-p-dioxin in goat milk and tissues by glass capillary gas chromatography and medium resolution mass fragmentography. J Chromatogr 1981; 208:323-330.
- Randerath K, Putman KL, & Randerath E: Organ-specific effects of long term feeding of 2,3,7,8-tetrachlorodibenzo-p-dioxin and 1,2,3,7,8-pentachlorodibenzo-p-dioxin on I-compounds in hepatic and renal DNA of female Sprague-Dawley rats. Carcinogenesis 1988; 9:2285-2289.
- Rannug A, Alexandrie AK, & Persson I: Genetic polymorphism of cytochromes P450 1A1, 2D6 AND 2E1 - regulation and toxicological significance. J Occup Environ Med 1995; 37:25-36.
- Rao MS, Subbarao V, & Prasad JD: Carcinogenicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin in the Syrian golden hamster. Carcinogenesis 1988; 9:1677-1679.
- Rau NR, Nagaraj MV, Prakash PS, et al: Fatal pulmonary aspiration of oral activated charcoal. Br Med J 1988; 297:918-919.
- Reggiani G: Estimations of the TCDD toxin potential in light of the Seveso accident. Arch Toxicol (Suppl) 1979; 2:291-302.
- Reggiani G: Medical problems raised by the TCDD contamination in Seveso, Italy. Arch Toxicol 1978; 40:161-188.
- Rier SE, Martin DC, & Bowman RE: Endometriosis in rhesus monkeys (Macaca mulatta) following chronic exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin. Fundam Appl Toxicol 1993; 21:433-441.
- Riihimaki V, Asp S, & Hernberg S: Mortality of 2,4-dichlorophenoxyacetic acid and 2,4,5-trichlorophenoxyacetic acid herbicide applicators in Finland: first report of an ongoing prospective cohort study. Scand J Work Environ Health 1982; 8:37-42.
- Roegner RH, Grubbs WD & Lustik MB et al: GRA&I, Air Force Health Study. An Epidemiologic Investigation of Health Effects in Air Force Personnel Following Exposure to Herbicides. Volume 1. National Technical Information Service, 1991.
- Rozman K: A critical view of the mechanism(s) of toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin. Implications for human safety assessment. Derm Beruf Umwelt 1989; 37:81-92.
- Rylander L & Hagmar L: Mortality and cancer incidence among women with a high consumption of fatty fish contaminated with persistent organochlorine compounds. Scand J Work Environ Health 1995; 21:419-426.
- STNEasy : Scientific & Technical Information Network, Search results for 2,3,7,8-tetrachlorodibenzo-p-dioxin. Chemical Abstract Service. Columbus, OH. 2002. Available from URL: http://stneasy.cas.org. As accessed accessed 2002 March 5.
- Saracci R, Kogevinas M, & Bertazzi P: Cancer mortality in workers exposed to chlorophenoxy herbicides and chlorophenols. Lancet 1991; 38:1027-1032.
- Schantz SL & Bowman RE: Learning in monkeys exposed perinatally to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Neurotoxicol Teratol 1989; 11:13-19.
- Schardein JL: Chemically Induced Birth Defects, 3rd ed, Marcel Dekker, Inc, New York, NY, 2000.
- Schecter A & Ryan JJ: Persistent brominated and chlorinated dioxin blood levels in a chemist. Am Coll Occup Environ Med 1992; 34:702-707.
- Schecter A, Dai LC, & Le TBT: Agent Orange and the Vietnamese -- the persistence of elevated dioxin levels in human tissues. Am J Public Health 1995; 85:516-522.
- Schecter A, Papke O, & Ball M: Dioxin and dibenzofuran levels in food from the United States as compared to levels in food from other industrialized countries. 12th Intl Symp Dioxins Rel Cmpds, Tampere, Finland, Finish Institute of Occupational Health, Helsinki, Finland, 1992, pp 243-246.
- Schecter A, Ryan JJ, & Masuda Y: Chlorinated and brominated dioxins and dibenzofurans in human tissue following exposure. Environ Health Perspect 1994; 102(Suppl1):135-147.
- Schecter A: Dioxins and related compounds in humans and the environment, in: Gallo M, Scheuplein R, Van der Heijden K (Eds), Biological basis for risk assessment of dioxin and related compounds. Banbury report No 35, Cold Spring Harbor Laboratory Press, Plainview, NY, 1991.
- Schiestl RH, Aubrecht J, & Yap WY: Polychlorinated biphenyls and 2,3,7,8-tetrachlorodibenzo-p-dioxin induce intrachromosomal recombination in vitro and in vivo. Cancer Res 1997; 57:4378-4383.
- Schulz KH: Dermatologic aspects of dioxin intoxication. Z Hautkr 1977; 52:198-199.
- Sharma RP & Reddy RV: Toxic effects of chemicals on the immune system. in: Halley TJ & Berndt WO (Eds), Handbook of Toxicology, Hemisphere Publishing Corp, Washington, DC, 1987, pp 581.
- Sherr DH: 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and long term immunologic memory. Toxicol Sci 2004; 79:211-213.
- Silbergeld EK & Mattison DR: Experimental and clinical studies on the reproductive toxicology of 2,3,7,8-tetrachlorodibenzo-p-dioxin. Am J Ind Med 1987; 11:131-144.
- Sirimanne SR, Barr JR, & Patterson DG: Quantification of polycyclic aromatic hydrocarbons and polychlorinated dibenzo-p-dioxins in human serum by combined micelle mediated extraction. (cloud-point extraction) and HPLC. Anal Chem 1996; 68:1556-1560.
- Sittig M: Handbook of Toxic and Hazardous Chemicals and Carcinogens, 3rd ed, Noyes Publications, Park Ridge, NJ, 1991.
- Smialowicz RJ, Riddle MM, & Williams WC: Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on humoral immunity and lymphocyte subpopulations: differences between mice and rats. Toxicol Appl Pharmacol 1994; 124:248-256.
- Smith AH, Pearce NE, & Fisher DO: Soft tissue sarcoma and exposure to phenoxyherbicides and chlorophenols in New Zealand. J Natl Cancer Aust 1984; 73:1111-1117.
- Smith FA, Schwetz BA, & Nitschke KD: Teratogenicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin in CF-1 mice. Toxicol Appl Pharmacol 1976; 38:517-523.
- Sorg O, Zennegg M, Schmid P, et al: 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) poisoning in Victor Yushchenko: identification and measurement of TCDD metabolites. Lancet 2009; 374(9696):1179-1185.
- Spitsbergen JM, Kleeman JM, & Peterson RE: 2,3,7,8-Tetrachlorodibenzo-p-dioxin toxicity in yellow perch (Perca flavescens). J Toxicol Environ Health 1988b; 23:359-83.
- Spitsbergen JM, Kleeman JM, & Peterson RE: Morphologic lesions and acute toxicity in rainbow trout (Salmo gairdneri) treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin. J Toxicol Environ Health 1988a; 23:333-58.
- Stanker L, Watkins B, & Vanderlaan M: Development of an immunoassay for chlorinated dioxins based on a monoclonal antibody and an enzyme linked immunosorbent assay (ELISA). Chemosphere 1987; 16:1635-1639.
- Steenland K, Piacitelli L, & Deddens J: Cancer, heart disease, and diabetes in workers exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin. J Natl Cancer Inst 1999; 91:779-786.
- Stehr-Green PA, Andrews JS Jr, & Hoffman RE: An overview of the Missouri dioxin studies. Arch Environ Health 1988; 43:174-177.
- Stellman SD, Stellman JM, & Sommer JF Jr: Health and reproductive outcomes among American legionnaires in relation to combat and herbicide exposure in Vietnam. Environ Res 1988; 47:150-174.
- Stevens KM: Agent orange toxicity: a quantitative perspective. Human Toxicol 1981; 1:31-39.
- Stockbauer JW, Hoffman RE, & Schramm WF: Reproductive outcomes of mothers with potential exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin. Am J Epidemiol 1988; 128:410-419.
- Svensson BG, Nilsson A, & Hansson M: Exposure to dioxins and dibenzofurans through the consumption of fish. N Engl J Med 1991; 324:8-12.
- Taylor MJ, Lucier GW, & Mahler JF: Inhibition of acute TCDD toxicity by treatment with anti-tumor necrosis factor antibody or dexamethasone. Toxicol Appl Pharmacol 1992; 117:126-132.
- Thiel R, Koch E, & Ulbrich B: Peri- and postnatal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin: effects on physiological development, reflexes, locomotor activity and learning behavior in Wistar rats. Arch Toxicol 1994; 69:79-86.
- Thiess AM, Fentzel-Beyme R, & Link R: Mortality study of persons exposed to dioxin in a trichlorophenol process accident that occurred in the BASF AG on Nov 17, 1953. Am J Ind Med 1982; 3:179-189.
- Thomke F , Jung D , Besser R , et al: Cranial nerve function in workers exposed to polychlorinated dioxins and furans. Acta Neurol Scand 2002; 106(3):155-158.
- Townsend JC, Bodner KM, & Van Peenen PF: Survey of reproductive events of wives of employees exposed to chlorinated dioxins. Am J Epidemiol 1982; 115:695-713.
- Tritscher AM, Goldstein JA, & Portier CJ: Dose-response relationships for chronic exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin in a rat tumor promotion model: quantification and immunolocalization of CYP1A1 and CYP1A2 in the liver. Cancer Res 1992; 52:3436-3442.
- Tsutsumi O: Effects of endocrine disruptors on preimplantation embryo development. Nippon Rinsho 2000; 58:2464-2468.
- Tucker AN, Vore SJ, & Luster MI: Suppression of B cell differentiation by 2,3,7,8-tetrachlorodibenzo-p-dioxin. Mol Pharmacol 1986; 29:372-377.
- Tullis K, Olsen H, & Bombick DW: TCDD causes stimulation of c-ras expression in the hepatic plasma membranes in vivo and in vitro. J Biochem Toxicol 1992; 7:107-116.
- U.S. Department of Energy, Office of Emergency Management: Protective Action Criteria (PAC) with AEGLs, ERPGs, & TEELs: Rev. 26 for chemicals of concern. U.S. Department of Energy, Office of Emergency Management. Washington, DC. 2010. Available from URL: http://www.hss.doe.gov/HealthSafety/WSHP/Chem_Safety/teel.html. As accessed 2011-06-27.
- U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project : 11th Report on Carcinogens. U.S. Department of Health and Human Services, Public Health Service, National Toxicology Program. Washington, DC. 2005. Available from URL: http://ntp.niehs.nih.gov/INDEXA5E1.HTM?objectid=32BA9724-F1F6-975E-7FCE50709CB4C932. As accessed 2011-06-27.
- U.S. Environmental Protection Agency: Discarded commercial chemical products, off-specification species, container residues, and spill residues thereof. Environmental Protection Agency's (EPA) Resource Conservation and Recovery Act (RCRA); List of hazardous substances and reportable quantities 2010b; 40CFR(261.33, e-f):77-.
- U.S. Environmental Protection Agency: Integrated Risk Information System (IRIS). U.S. Environmental Protection Agency. Washington, DC. 2011. Available from URL: http://cfpub.epa.gov/ncea/iris/index.cfm?fuseaction=iris.showSubstanceList&list_type=date. As accessed 2011-06-21.
- U.S. Environmental Protection Agency: List of Radionuclides. U.S. Environmental Protection Agency. Washington, DC. 2010a. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-sec302-4.pdf. As accessed 2011-06-17.
- U.S. Environmental Protection Agency: List of hazardous substances and reportable quantities. U.S. Environmental Protection Agency. Washington, DC. 2010. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-sec302-4.pdf. As accessed 2011-06-17.
- U.S. Environmental Protection Agency: The list of extremely hazardous substances and their threshold planning quantities (CAS Number Order). U.S. Environmental Protection Agency. Washington, DC. 2010c. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-part355.pdf. As accessed 2011-06-17.
- U.S. Occupational Safety and Health Administration: Part 1910 - Occupational safety and health standards (continued) Occupational Safety, and Health Administration's (OSHA) list of highly hazardous chemicals, toxics and reactives. Subpart Z - toxic and hazardous substances. CFR 2010 2010; Vol6(SEC1910):7-.
- U.S. Occupational Safety, and Health Administration (OSHA): Process safety management of highly hazardous chemicals. 29 CFR 2010 2010; 29(1910.119):348-.
- Umbreit TH, Hesse EJ, & Gallo MA: Bioavailability of dioxin in soil from a 2,4,5-T manufacturing site. Science 1986; 232:497-499.
- United States Environmental Protection Agency Office of Pollution Prevention and Toxics: Acute Exposure Guideline Levels (AEGLs) for Vinyl Acetate (Proposed). United States Environmental Protection Agency. Washington, DC. 2006. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6af&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
- Vale JA, Kulig K, American Academy of Clinical Toxicology, et al: Position paper: Gastric lavage. J Toxicol Clin Toxicol 2004; 42:933-943.
- Vale JA: Position Statement: gastric lavage. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol 1997; 35:711-719.
- VanMiller JP, Lalich JJ, & Allen JR: Increased incidence of neoplasms in rats exposed to low levels of 2,3,7,8-tetrachlorodibenzo-p-dioxin. Chemosphere 1977; 6:537-544.
- Verger P, Cordier S, & Thuy LTB: Correlation between dioxin levels in adipose tissue and estimated exposure to Agent Orange in South Vietnamese residents. Environ Res 1994; 65:226-242.
- Verschueren K: Handbook of Environmental Data on Organic Chemicals. 4th ed. CD-ROM version. Wiley-Interscience. Hoboken, NJ. 2001.
- Wahba ZZ, Lawson TA, & Stohs SJ: Induction of hepatic DNA single strand breaks in rats by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Cancer Lett 1988; 39:281-286.
- Walsh RJ, Donovan JW, & Adena MA: Case control study of congenital anomalies and Vietnam service (birth defect study). Report to the Minister for Veterans Affairs, Australian Government Publishing Service, Canberra, Australia, 1983.
- Wendling JM & Orth RG: Determination of (3H)-2,3,7,8-tetrachlorodibenzo-p-dioxin in human feces to ascertain its relative metabolism in man. Anal Chem 1990; 62:796-800.
- Wolfe WH, Michalek JE, & Miner JC: Paternal serum dioxin and reproductive outcomes among veterans of Operation Ranch Hand. Epidemiol 1995; 6:17-22.
- Wolfle D & Marquardt H: Antioxidants inhibit the enhancement of malignant cell transformation induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin. Carcinogenesis 1996; 17:1273-1278.
- Xu Yh, Dragan YP, & Maronpot RR: Criteria, mechanisms, and potency evaluation for tumor promoters: Dioxin as a model. Chemosphere 1992; 25:227-230.
- Young AL, Calcagni JA & Thalken CE et al: The toxicology, environmental fate, and human risk of herbicide orange and its associated dioxin. USAF OEHL Technical Report TR-78-92, Brooks Air Force Base, Texas, 1978.
- Zack JA & Suskind RR: The mortality experience of workers exposed to tetrachlorodibenzodioxin in a trichlorophenol process accident. J Occup Med 1980; 22:11-14.
- Zahm SH, Weisenburger DD, & Babbitt PA: A case-control study of non-Hodgkin's lymphoma and the herbicide 2,4-dichlorophenoxyacetic acid (2,4-D) in eastern Nebraska. Epidemiology 1990; 1:349-356.
- Zenz C: Occupational Medicine, 3rd ed, Mosby Year Book, Inc, St Louis, MO, 1994.
- Zober A, Messerer P, & Huber P: Thirty-four year follow-up of BASF employees exposed to 2,3,7,8-TCDD after the 1953 accident. Int Arch Occup Environ Health 1990; 62:138-157.
- de Mesquita HBB & Doornbos G: Occupational exposure to phenoxy herbicides and chlorophenols and cancer mortality in the Netherlands. Am J Ind Med 1993; 23:289-300.
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