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Dioxin is the common name for the group of compounds classified as polychlorinated dibenzodioxins (PCDDs). PCDDs, which are members of the family of halogenated organic compounds, have been shown to bioaccumulate in humans and wildlife due to their lipophilic properties, and are known teratogens, mutagens, and suspected human carcinogens.
The basic structure of PCDDs comprises two benzene rings joined by a double oxygen bridge. Chlorine atoms are attached to the basic structure at any of 8 different places on the molecule, positions 1–4 and 6–9. There are 75 different types of PCDD congeners (herein, a congener means a related dioxin compound). The toxicity of PCDDs depends on the number and position of the chlorine atoms; only congeners that have chlorines in the 2, 3, 7, and 8 positions have been found to be significantly toxic. Out of the 75 PCDD compounds, only 7 congeners have chlorine atoms in the relevant positions to be considered toxic by the NATO Committee on the Challenges to Modern Society (NATO/CCMS) international toxic equivalent (I-TEQ) scheme.
Concentrations of dioxins in nature prior to industrialization, due to natural combustion and geological processes, were generally about three times lower than today  . The first intentional synthesis of chlorinated dibenzodioxin dates back to 1872. Today, concentrations of dioxins are found in all humans, with higher levels commonly found in persons living in more industrialized countries. The most toxic dioxin, 2,3,7,8 tetrachlorodibenzo-p-dioxin (TCDD), became well known as a contaminant of Agent Orange, a herbicide used in the Vietnam War. Later, dioxins were found in Times Beach, Missouri, USA  and Love Canal, New York, USA  and Seveso, Italy . More recently, dioxin has been in the news with the poisoning of President Viktor Yushchenko of Ukraine, 2004 .
Sources of dioxin
The United States Environmental Protection Agency Dioxin Reassessment Report is possibly the most comprehensive review of dioxin, but other countries now have substantial research. Australia, New Zealand and the United Kingdom all have substantial research into body burdens and sources. Tolerable daily, monthly or annual intakes have been set by the World Health Organization and a number of governments. Dioxin enters the general population almost exclusively from ingestion of food, specifically through the consumption of fish, meat, and dairy products since dioxins are fat-soluble and readily climb the food chain .
Occupational exposure is an issue for some in the chemical industry, or in the application of chemicals, notably herbicides. Inhalation has been a problem for people living near substantial point sources where emissions are not adequately controlled. In many developed nations there are now emissions regulations which have alleviated some concerns, although the lack of constant sampling of dioxin emissions causes concern about the understatement of emissions. In Belgium, through the introduction of a process called AMESA, constant sampling showed that periodic sampling understated emissions by a factor of 30 to 50 times. Few facilities have constant sampling.
Most controversial is the United States Environmental Protection Agency assessment's (draft) finding that any reference dose that were to be set would be far below current average intakes.
Children are passed substantial body burdens by their mothers, and breastfeeding increases the child's body burden. Children's body burdens are often many times above the amount implied by tolerable intakes which are based on body weight. Breast fed children usually have substantially higher dioxin body burdens than non breast fed children until they are about 8 to 10 years old. The WHO still recommends breast feeding for its other benefits.
Dioxins are produced in small concentrations when organic material is burned in the presence of chlorine, whether the chlorine is present as chloride ions or as organochlorine compounds, so they are widely produced in many contexts. According to the most recent US EPA data the major sources of dioxin are:
- Coal fired utilities
- Metal smelting
- Diesel trucks
- Land application of sewage sludge
- Burning treated wood
- Trash burn barrels
These sources together account for nearly 80% of dioxin emissions.
When the original US EPA inventory of dioxin sources was done in 1987, incineration represented over 80% of known dioxin sources. As a result, US EPA implemented new emissions requirements. These regulations have been very successful in reducing dioxin stack emissions from incinerators. Incineration of municipal solid waste, medical waste, sewage sludge, and hazardous waste together now produce less than 3% of all dioxin emissions.
In incineration, dioxins can also reform in the atmosphere above the stack as the exhaust gases cool through a temperature window of 600 to 200°C. The most common method of reducing dioxins reforming or forming de novo is through rapid (30 millisecond) quenching of the exhaust gases through that 400°C window . Incinerator emissions of dioxins have been reduced by over 90% as a result of new emissions control requirements. Incineration is now a very minor contributor to dioxin emissions.
Dioxins are also generated in reactions that do not involve burning — such as bleaching fibers for paper or textiles, and in the manufacture of chlorinated phenols, particularly when reaction temperature is not well controlled. Affected compounds include the wood preservative pentachlorophenol, and also herbicides such as 2,4-dichlorophenoxyacetic acid (or 2,4-D) and 2,4,5-trichlorophenoxyacetic acid (2,4,5-T). Higher levels of chlorination require higher reaction temperatures and greater dioxin production. See Agent Orange for more on contamination problems in the 1960s. Dioxins may also be formed during the photochemical breakdown of the common antimicrobial compound triclosan .
Dioxins are also in typical cigarette smoke. Dioxin in cigarette smoke was noted as "understudied" by the US EPA in its "Re-Evaluating Dioxin" (1995). In that same document, the US EPA acknowledged that dioxin in cigarettes is "anthropogenic" (man-made, "not likely in nature"). Nevertheless, the use of chlorine-containing tobacco pesticides and chlorine-bleached cigarette papers remains legal.
Dioxins are present in minuscule amounts in a wide range of materials used by humans — including practically all substances manufactured using plastics, resins, or bleaches. Such materials include tampons, and a wide variety of food packaging substances. The use of these materials means that all Western humans receive at least a very small daily dose of dioxin—however, it is disputed whether such exceptionally tiny exposures have any clinical relevance. It is even controversially discussed whether dioxins might have a non-linear dose-response curve with beneficial health effects in a certain lower dose range, a phenomenon called hormesis.
Dietary sources of dioxin in the United States have been analyzed by the EPA and scientists from other organizations.
Dioxins are absorbed primarily through dietary intake of fat, as this is where they accumulate in animals and humans. In humans, the highly chlorinated dioxins are stored in fatty tissues and are neither readily metabolized nor excreted. The estimated elimination half-life for highly clorinated dioxins (4-8 chlorine atoms) in humans ranges from 7.8 to 132 years .
The persistence of a particular dioxin congener in an animal is thought to be a consequence of its structure. It is believed that dioxins with few chlorines, which thus contain hydrogen atoms on adjacent pairs of carbons, can more readily be oxidized by cytochromes P450. The oxidized dioxins can then be more readily excreted rather than stored for long time.
2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is the most toxic of the congeners. Other dioxin congeners (or mixtures thereof) are given a toxicity rating from 0 to 1, where TCDD = 1. This toxicity rating is called the Toxic Equivalence Factor, or TEF. TEFs are consensus values and, because of the strong species dependence for toxicity, are listed separately for mammals, fish, and birds. TEFs for mammalian species are generally applicable to human risk calculations. The TEFs have been developed from detailed assessment of literature data to facilitate both risk assessment and regulatory control . Many other compounds may also have dioxin-like properties, particularly non-ortho PCBs, some of which can have TEFs as high as 0.1.
The total dioxin toxic equivalence (TEQ) value expresses the toxicity as if the mixture were pure TCDD. The TEQ approach and current TEFs have been adopted internationally as the most appropriate way to estimate the potential health risks of mixture of dioxins. Recent data suggest that this type of linear scaling factor may not be the most appropriate treatment for complex mixtures of dioxins; further research into non-linear toxicity models is required to substantiate this hypothesis.
Dioxins and other persistent organic pollutants (POPs) are subject to the Stockholm Convention. The treaty obliges signatories to take measures to eliminate where possible, and minimize where not possible to eliminate, all sources of dioxin.
Health effects in humans
Dioxins build up primarily in fatty tissues over time (bioaccumulate), so even small exposures may eventually reach dangerous levels. In 1994, EPA reported that dioxin is a probable carcinogen, but notes that non-cancer effects (reproduction and sexual development, immune system) may pose an even greater threat to human health. TCDD, the most toxic of the dibenzodioxins, has a half-life of approximately 8 years in humans, but at high concentrations, the elimination rate is enhanced by metabolism . The health effects of dioxins are mediated by their action on a cellular receptor, the aryl hydrocarbon receptor (AhR) .
Dioxins also accumulate in food chains in a fashion similar to other chlorinated compounds (bioaccumulate). This means that even small concentrations in contaminated water can be concentrated up a food chain to dangerous levels due to the long biological half life and low solubility of dioxins.
Exposure to high levels of dioxin in humans causes a severe form of persistent acne, known as chloracne . Other effects in humans may include:
- Central and Peripheral Nervous System pathology
- Thyroid disorders
- Damage to the Immune systems .
Health effects in other animals
While it has been difficult to prove that dioxins cause specific health effects in humans due to the lack of controlled dose experiments, studies in animals have shown that dioxin causes a wide variety of toxic effects. In particular, TCDD has been shown to be teratogenic, mutagenic, carcinogenic, immunotoxic, and hepatotoxic. Furthermore, alterations in multiple endocrine and growth factor systems have been reported. The most sensitive effects, observed in multiple species, appear to be developmental, including effects on the developing immune, nervous, and reproductive systems . These effects are caused at body burdens close to those reported in humans.
Among the animals for which TCDD toxicity has been studied, there is strong evidence for the following effects:
- Birth defects (teratogenicity)
- In rodents, including rats , mice , hamsters and guinea pigs ; birds ; and fish .
- Cancer (including neoplasms in the mammalian lung, oral/nasal cavities, thyroid and adrenal glands, and liver, squamous cell carcinoma, and various animal hepatocarcinomas)
- Hepatotoxicity (liver toxicity)
- Endocrine disruption
- In rodents and fish 
- Learning 
Studies of dioxin's effects in Vietnam
US veterans' groups and Vietnamese groups, including the Vietnamese government, have convened scientific studies to explore their belief that dioxins were responsible for a host of disorders, including tens of thousands of birth defects in children, amongst Vietnam veterans as well as an estimated one million Vietnamese, through their exposure to Agent Orange during the Vietnam War, which was found to be highly contaminated with TCDD. Several exposure studies showed that some US Vietnam Veterans who were exposed to Agent Orange had serum TCDD levels up to 600 ppt (parts per trillion) many years after they left Vietnam, compared to general population levels of approximately 1 to 2 ppt of TCDD. In Vietnam, TCDD levels up to 1,000,000 ppt have been found in soil and sediments from Agent Orange contaminated areas 3 to 4 decades after spraying. In addition, elevated levels have been measured in food and wildlife in Vietnam .
The most recent study, paid for by the National Academy of Sciences, was released in an April 2003 report. This report is currently (March 2007) being revised for release again later in 2007.
The Centers for Disease Control found that dioxin levels in Vietnam veterans  were in no way atypical when compared against the rest of the population. The only exception existed for those who directly handled Agent Orange. These were members of Operation Ranch Hand. Long-term studies of the members of Ranch Hand have thus far uncovered a possibility of elevated risks of diabetes.
Dioxin exposure incidents
- In 1949, in herbicide production plant for 2,4,5-T in Nitro, West Virginia, 240 people were affected when a relief valve opened .
- In 1963, a dioxin cloud escapes after an explosion in a Philips-Duphar plant (now Solvay Group) near Amsterdam. In the 1960s, Philips-Duphar produced 2250 tonnes of 'Agent Orange' for the US Army.
- In 1976, large amounts of dioxin were released in an industrial accident at Seveso, although no immediate human fatalities or birth defects occurred   .
- In 1978, dioxin was one of the contaminants that forced the evacuation of the Love Canal neighborhood of Niagara Falls, New York. Dioxin also caused the 1983 evacuation of Times Beach, Missouri.
- In the 1960s, parts of the Spolana chemical plant in Neratovice, Czechoslovakia, were heavily contaminated by dioxins, when the herbicide 2,4,5-T (also a component of Agent Orange) was produced there. Workers in this factory were exposed to high concentrations of dioxins at that time. Dozens of them fell seriously ill. A possibly large amount of dioxins was flushed from the factory into the Labe river during the 2002 European flood. No direct consequences of this incident have thus far been recorded.
- From 1982 through to 1985, Times Beach, Missouri, was bought out and evacuated under order of the United States Environmental Protection Agency due to high levels of dioxin in the soil . The town eventually disincorporated .
- In December 1991, an electrical explosion caused dioxin (created from the oxidation of polychlorinated biphenyl) to spread through four residence halls and two other buildings on the college campus of SUNY New Paltz.
- In May 1999, there was a dioxin crisis in Belgium: quantities of dioxin had entered the food chain through contaminated animal feed. 7,000,000 chickens and 60,000 pigs had to be slaughtered. This scandal was followed by a landslide change in government in the elections one month later.
- On September 11, 2001, explosions released massive amounts of dust into the air. The air was measured for dioxin from September 23, 2001, to November 21, 2001, and reported to be "likely the highest ambient concentration that have ever been reported." [in history]. The United States Environmental Protection Agency report dated October 2002 and released in December of 2002 titled "Exposure and Human Health Evaluation of Airborne Pollution from the World Trade Center Disaster" authored by the EPA Office of Research and Development in Washington states that dioxin levels recorded at a monitoring station on Park Row near City Hall Park in New York between October 12 and 29, 2001, averaged 5.6 parts per trillion, or nearly six times the highest dioxin level ever recorded in the U.S. Dioxin levels in the rubble of the World Trade Centers were much higher with concentrations ranging from 10 to 170 parts per trillion. The report did no measuring of the toxicity of indoor air.
- In a 2001 case study , physicians reported clinical changes in a 30 year old woman who had been exposed to a massive dosage (144,000 pg/g blood fat) of dioxin equal to 16,000 times the normal body level; the highest dose of dioxin ever recorded in a human. She suffered from chloracne, nausea, vomiting, epigastric pain, loss of appetite, leukocytosis, anemia, amenorrhoea and thrombocytopenia. However, other notable laboratory tests, such as immune function tests, were relatively normal. The same study also covered a second subject who had received a dosage equivalent to 2,900 times the normal level, who apparently suffered no notable negative effects other than chloracne. These patients were provided with olestra to accelerate dioxin elimination .
- In 2004, a notable individual case of dioxin poisoning, Ukrainian politician Viktor Yushchenko was exposed to the second-largest measured dose of dioxins, according to the reports of the physicians responsible for diagnosing him. This is the first known case of a single high dose of TCDD dioxin poisoning, and was diagnosed only after a toxicologist recognized the symptoms of chloracne while viewing television news coverage of his condition .
- In the early 2000s, residents of the city of New Plymouth, New Zealand, report many illnesses of people living around and working at the Dow Chemical plant. This plant ceased production of 2,4,5-T in 1987.
- 1,995 people are suing DuPont, claiming dioxin emissions from its plant in DeLisle, Mississppi, caused their cancers, illnesses or loved one's death. In August 2005, Glenn Strong, an oyster fisherman with the rare blood cancer multiple myeloma, was awarded $14 million from DuPont. In another case, parents claim dioxin from pollution caused the death of their 8 year old daughter; the trial is expected to begin May 2007. DuPont's DeLisle plant is one of three titanium dioxide facilities (including Edgemoor, DE, and New Johnsonville, TN) that are the largest producers of dioxin in the country, according to the US EPA's Toxic Release Inventory.
- ↑ "Compilation of EU Dioxin Exposure and Health Data" (PDF). Retrieved 2007-06-04.
- ↑ "FDA/CFSAN - Questions and Answers about Dioxins". Retrieved 2007-06-04.
- ↑ Schecter A, Birnbaum L, Ryan JJ, Constable JD (2006). "Dioxins: an overview". Environ. Res. 101 (3): 419–28. doi:10.1016/j.envres.2005.12.003. PMID 16445906.
- ↑ "Times Beach Record of Decision Signed". United States Environmental Protection Agency. Retrieved 2007-06-04. Text " EPA History " ignored (help)
- ↑ "Love Canal Record of Decision Signed". United States Environmental Protection Agency. Retrieved 2007-06-04. Text " EPA History " ignored (help)
- ↑ "4 Seveso: A paradoxical classic disaster". Retrieved 2007-06-04.
- ↑ "Yushchenko's acne points to dioxin poisoning". Retrieved 2007-06-04.
- ↑ 8.0 8.1 Schecter A, Cramer P, Boggess K; et al. (2001). "Intake of dioxins and related compounds from food in the U.S. population". J. Toxicol. Environ. Health Part A. 63 (1): 1–18. PMID 11346131.
- ↑ Cheung WH, Lee VK, McKay G (2007). "Minimizing dioxin emissions from integrated MSW thermal treatment". Environ. Sci. Technol. 41 (6): 2001–7. PMID 17410797.
- ↑ Latch DE, Packer JL, Stender BL, VanOverbeke J, Arnold WA, McNeill K (2005). "Aqueous photochemistry of triclosan: formation of 2,4-dichlorophenol, 2,8-dichlorodibenzo-p-dioxin, and oligomerization products". Environ. Toxicol. Chem. 24 (3): 517–25. PMID 15779749.
- ↑ Geyer HJ, Schramm KW, Feicht EA; et al. (2002). "Half-lives of tetra-, penta-, hexa-, hepta-, and octachlorodibenzo-p-dioxin in rats, monkeys, and humans--a critical review". Chemosphere. 48 (6): 631–44. PMID 12143938.
- ↑ Van den Berg M, Birnbaum LS, Denison M; et al. (2006). "The 2005 World Health Organization reevaluation of human and Mammalian toxic equivalency factors for dioxins and dioxin-like compounds". Toxicol. Sci. 93 (2): 223–41. doi:10.1093/toxsci/kfl055. PMID 16829543.
- ↑ Geusau A, Schmaldienst S, Derfler K, Päpke O, Abraham K (2002). "Severe 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD) intoxication: kinetics and trials to enhance elimination in two patients". Arch. Toxicol. 76 (5–6): 316–25. doi:10.1007/s00204-002-0345-7. PMID 12107649.
- ↑ Bock KW, Köhle C (2006). "Ah receptor: dioxin-mediated toxic responses as hints to deregulated physiologic functions". Biochem. Pharmacol. 72 (4): 393–404. doi:10.1016/j.bcp.2006.01.017. PMID 16545780.
- ↑ 15.0 15.1 Geusau A, Abraham K, Geissler K, Sator MO, Stingl G, Tschachler E (2001). "Severe 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) intoxication: clinical and laboratory effects". Environ. Health Perspect. 109 (8): 865–9. PMID 11564625.
- ↑ Alaluusua S, Calderara P, Gerthoux PM; et al. (2004). "Developmental dental aberrations after the dioxin accident in Seveso". Environ. Health Perspect. 112 (13): 1313–8. PMID 15345345.
- ↑ Peterson RE, Theobald HM, Kimmel GL (1993). "Developmental and reproductive toxicity of dioxins and related compounds: cross-species comparisons". Crit. Rev. Toxicol. 23 (3): 283–335. PMID 8260069.
- ↑ Pelclová D, Urban P, Preiss J; et al. (2006). "Adverse health effects in humans exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)". Reviews on environmental health. 21 (2): 119–38. PMID 16898675.
- ↑ Pavuk M, Schecter AJ, Akhtar FZ, Michalek JE (2003). "Serum 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) levels and thyroid function in Air Force veterans of the Vietnam War". Annals of epidemiology. 13 (5): 335–43. PMID 12821272.
- ↑ Baccarelli A, Mocarelli P, Patterson DG; et al. (2002). "Immunologic effects of dioxin: new results from Seveso and comparison with other studies". Environ. Health Perspect. 110 (12): 1169–73. PMID 12460794.
- ↑ Eskenazi B, Mocarelli P, Warner M; et al. (2002). "Serum dioxin concentrations and endometriosis: a cohort study in Seveso, Italy". Environ. Health Perspect. 110 (7): 629–34. PMID 12117638.
- ↑ Arisawa K, Takeda H, Mikasa H (2005). "Background exposure to PCDDs/PCDFs/PCBs and its potential health effects: a review of epidemiologic studies". J. Med. Invest. 52 (1–2): 10–21. PMID 15751269.
- ↑ 23.0 23.1 Birnbaum LS, Tuomisto J (2000). "Non-carcinogenic effects of TCDD in animals". Food additives and contaminants. 17 (4): 275–88. PMID 10912242.
- ↑ 24.0 24.1 "NTP technical report on the toxicology and carcinogenesis studies of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (CAS No. 1746-01-6) in female Harlan Sprague-Dawley rats (Gavage Studies)". National Toxicology Program technical report series (521): 4–232. 2006. PMID 16835633.
- ↑ Peters JM, Narotsky MG, Elizondo G, Fernandez-Salguero PM, Gonzalez FJ, Abbott BD (1999). "Amelioration of TCDD-induced teratogenesis in aryl hydrocarbon receptor (AhR)-null mice". Toxicol. Sci. 47 (1): 86–92. PMID 10048156.
- ↑ Kransler KM, McGarrigle BP, Olson JR (2007). "Comparative developmental toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin in the hamster, rat and guinea pig". Toxicology. 229 (3): 214–25. doi:10.1016/j.tox.2006.10.019. PMID 17126467.
- ↑ Bruggeman V, Swennen Q, De Ketelaere B, Onagbesan O, Tona K, Decuypere E (2003). "Embryonic exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin in chickens: effects of dose and embryonic stage on hatchability and growth". Comp. Biochem. Physiol. C Toxicol. Pharmacol. 136 (1): 17–28. PMID 14522596.
- ↑ Carney SA, Prasch AL, Heideman W, Peterson RE (2006). "Understanding dioxin developmental toxicity using the zebrafish model". Birth Defects Res. Part A Clin. Mol. Teratol. 76 (1): 7–18. doi:10.1002/bdra.20216. PMID 16333842.
- ↑ 29.0 29.1 Mann PC (1997). "Selected lesions of dioxin in laboratory rodents". Toxicologic pathology. 25 (1): 72–9. PMID 9061855.
- ↑ Grinwis GC, Vethaak AD, Wester PW, Vos JG (2000). "Toxicology of environmental chemicals in the flounder (Platichthys flesus) with emphasis on the immune system: field, semi-field (mesocosm) and laboratory studies". Toxicol. Lett. 112-113: 289–301. PMID 10720744.
- ↑ El-Sabeawy F, Enan E, Lasley B (2001). "Biochemical and toxic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin in immature male and female chickens". Comp. Biochem. Physiol. C Toxicol. Pharmacol. 129 (4): 317–27. PMID 11489429.
- ↑ Zodrow JM, Stegeman JJ, Tanguay RL (2004). "Histological analysis of acute toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in zebrafish". Aquat. Toxicol. 66 (1): 25–38. PMID 14687977.
- ↑ Heiden TK, Carvan MJ, Hutz RJ (2006). "Inhibition of follicular development, vitellogenesis, and serum 17beta-estradiol concentrations in zebrafish following chronic, sublethal dietary exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin". Toxicol. Sci. 90 (2): 490–9. doi:10.1093/toxsci/kfj085. PMID 16387744.
- ↑ Holladay SD (1999). "Prenatal immunotoxicant exposure and postnatal autoimmune disease". Environ. Health Perspect. 107 Suppl 5: 687–91. PMID 10502532.
- ↑ Spitsbergen JM, Schat KA, Kleeman JM, Peterson RE (1986). "Interactions of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) with immune responses of rainbow trout". Vet. Immunol. Immunopathol. 12 (1–4): 263–80. PMID 3765346.
- ↑ Schecter A, Dai LC, Thuy LT; et al. (1995). "Agent Orange and the Vietnamese: the persistence of elevated dioxin levels in human tissues". American journal of public health. 85 (4): 516–22. PMID 7702115.
- ↑ "Veterans Health - Vietnam Studies" (PDF). Retrieved 2007-06-04.
- ↑ Collins JJ, Strauss ME, Levinskas GJ, Conner PR (1993). "The mortality experience of workers exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin in a trichlorophenol process accident". Epidemiology (Cambridge, Mass.). 4 (1): 7–13. PMID 8420584.
- ↑ "Seveso – 30 Years After" (PDF). Retrieved 2007-06-04.
- ↑ "Icmesa chemical company, Seveso, Italy. 9th July 1976". Retrieved 2007-06-04.
- ↑ "Seveso". Retrieved 2007-06-04.
- ↑ "AROUND THE NATION; Times Beach, Mo., Board Moves to Seal Off Town - New York Times". Retrieved 2007-06-04.
- ↑ "AROUND THE NATION; Times Beach, Mo., Votes Itself Out of Existence - New York Times". Retrieved 2007-06-04.
- ↑ Geusau A, Tschachler E, Meixner M; et al. (1999). "Olestra increases faecal excretion of 2,3,7,8-tetrachlorodibenzo-p-dioxin". Lancet. 354 (9186): 1266–7. PMID 10520643.
- ↑ "Yushchenko's acne points to dioxin poisoning". Retrieved 2007-06-04.
- "EPA: Exposure and Human Health Reassessment of 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) and Related Compounds National Academy Sciences (NAS) Review Draft"
- "Dioxins and Dioxin-like Compounds in the Food Supply: Strategies to Decrease Exposure", a 2003 report by the National Academy of Sciences
- "Rhodes Remediation" Website about remediation of dioxin contaminated Homebush Bay and land in Rhodes, a suburb of Sydney, NSW, Australia. Union Carbide was the polluter.
- "Researcher Dispels Myth of Dioxins and Plastic Water Bottles" Johns Hopkins Researcher explains the facts about Dioxin
- "Health Risks from Dioxin and Related Compounds: Evaluation of the EPA Reassessment" Includes discussion of methods of evaluating risk of low concentrations, and Toxic Equivalency
- "Assessment of the Health Risks of Dioxins", a 1998 report by the World Health Organisation.
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