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dioxin

  (dī-ŏk'sĭn) pronunciation
n.

Any of several carcinogenic or teratogenic heterocyclic hydrocarbons that occur as impurities in petroleum-derived herbicides.

[DI–1 + OX(O)– + –IN.]


 
 
Encyclopedia of Public Health: Dioxins

Dioxins are a class of halogenated aryl hydrocarbons, formed during chemical synthesis when chlorophenols are used in the starting material. The three most widely studied sources of dioxins are the manufacturing of the herbicide Agent Orange, the manufacturing of the microbicide hexachlorphene, and the chlorine bleaching of wood pulp. Other sources include combustion of wastes that contain chlorine residues in plastics, and combustion in engines where a chlorinated product has been used as a fuel additive.

2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is the prototype for the toxicity of this chemical class, which also includes chlorinated dibenzofurans. TCDD is one of the most highly toxic chemicals tested in several laboratory animal species. The acute LD50 (the lethal dose that will kill 50 percent of test animals) in guinea pigs (the most susceptible species) is in the microgram per kilogram range; the toxicity in rodents varies by species and strain of animal. The reason for this variation is that TCDD operates through a specific protein called the aryl hydrocarbon receptor (AhR), and the level of this protein and its ancillary proteins varies across species. TCDD is teratogenic in mice and carcinogenic in rats and mice, and is classified as a probable human carcinogen based on animal data and epidemiological studies. The most common human finding observed in high level occupational and accidental exposures is chloracne, a skin disorder. Several epidemiology studies have been conducted in worker cohorts, and in veterans and residents of Vietnam, with inconsistent results. However, it is generally accepted that TCDD has the potential to be a human carcinogen and teratogen, and exposures should be reduced to an absolute minimum.

The controversy surrounding this class of compounds stems from five areas. First, TCDD is highly toxic having carcinogenic, teratogenic, immunotoxic, and endocrine modulation properties. Second, there are over 200 analogs and congeners of the dioxins and benzofurans, with varying qualitative and/or qualitative toxicity. Toxic Equivalent Factors (TEFs) have been developed based on the ability of the analogs and congeners to bind to the AhR and induce a family of enzymes in a manner similar to TCDD. Third, TCDD is very persistent in soil and in animal tissues (including humans). Half-life estimates range from months to several years. Dioxins also bioaccumulate in the food chain. Hence, the potential is there for the compounds to accumulate in human tissue. Fourth, the extent of toxicity in humans has not been well defined. Fifth, dioxins are produced as combustion products when chlorine is available in the burning process. This area is of particular importance because of the incineration of municipal waste that contains bottles made from chlorinated plastics.

A great deal of research has gone into the generation and control of dioxin emissions from incinerators. One confounding factor is that incinerators may not be the only point source for dioxins, and fewer chemical plants are using starting materials that will lead to major releases of dioxins as in the past. Wood pulp and paper bleaching in the United States and Canada has minimized or eliminated the use of chlorine bleaches, but the contamination that exists is very persistent. The search for other sources of dioxins continues.

Some polychlorinated biphenyls (PCBs), another class of chlorinated hydrocarbons, mimic the biological activity of dioxins.

(SEE ALSO: Carcinogen; Carcinogenesis; Endocrine Disrupters; PCBs; Persistent Organic Pollutants [POPs]; Pollution; Toxicology)

— MICHAEL GALLO


 
US Military Dictionary: dioxin

n.a highly toxic compound produced as a by-product in some manufacturing processes, notably herbicide production (especially Agent Orange) and paper bleaching. It is a serious and persistent environmental pollutant.

See the Introduction, Abbreviations and Pronunciation for further details.

 
Britannica Concise Encyclopedia: dioxin

Aromatic compound, any of a group of contaminants produced in making herbicides (e.g., Agent Orange), disinfectants, and other agents. Their basic chemical structure consists of two benzene rings connected by a pair of oxygen atoms; when substituents on the rings are chlorine atoms, the molecules are particularly toxic. The best-known, usually called simply dioxin, is 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD). It is extremely stable chemically; it does not dissolve in water but dissolves in oils (and thus accumulates in body fat). The extent of its human toxicity is disputed and the subject of continuing research.

For more information on dioxin, visit Britannica.com.

 
Food & Culture Encyclopedia: Dioxin

Endocrine disruptor. Causes birth defects, developmental problems, and cancer.

 
Science Dictionary: dioxin
(deye-ok-sin)

A group of pollutants created as by-products in many industrial processes. Dioxins accumulate in human tissue and affect human metabolism. They are carcinogens. Eliminating dioxins is an important goal of environmental policy.

 
Veterinary Dictionary: dioxin

A highly toxic and teratogenic chlorinated hydrocarbon that is a trace contaminant in the herbicide 2,4,5-T. Acute poisoning causes vomiting, abortion, anestrus. Chronic poisoning causes liver damage, especially in dogs. Congenital defects caused include cranio-facial deformity and anasarca. It is excreted in the milk.

 
Wikipedia: dioxin

Dioxin in its original usage denoted the organochemical heterocyclic compound with the general chemical formula C4H4O2 in which two CH groups of a benzene ring were replaced (endocyclic substitution) by oxygen atoms, of which two isomers were possible, the ortho (o) and the para (p) variety: 1,2-dioxin and 1,4-dioxin. This name then extended to the family of compounds derivable from the parent compounds by exocyclic substitution, and especially to the dibenzo substitution of the para variety.

Dioxin in current usage 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.

Chemical structure

The skeletal formula and substituent numbering scheme of the parent compound dibenzo-p-dioxin
Enlarge
The skeletal formula and substituent numbering scheme of the parent compound dibenzo-p-dioxin

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.

Historical perspective

Concentrations of dioxins in nature prior to industrialization, due to natural combustion and geological processes, were generally about three times lower than today [1] [2]. 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[3]. Later, dioxins were found in Times Beach, Missouri, USA [4] and Love Canal, New York, USA [5] and Seveso, Italy [6]. More recently, dioxin has been in the news with the poisoning of President Viktor Yushchenko of Ukraine, 2004 [7].

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 [8].

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[citation needed]. 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 [9]. 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.

A chart illustrating how much dioxin the average American consumes per day. (Note: pg = picogram, or one trillionth of a gram, or 10−12 g) [8].
Enlarge
A chart illustrating how much dioxin the average American consumes per day. (Note: pg = picogram, or one trillionth of a gram, or 10−12 g) [8].

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 [10].

Dioxins are also in typical cigarette smoke[citation needed]. 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[citation needed].

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.[citation needed] Such materials include tampons, and a wide variety of food packaging substances[citation needed]. The use of these materials means that all Western humans receive at least a very small daily dose of dioxin[citation needed]—however, it is disputed whether such exceptionally tiny exposures have any clinical relevance[citation needed]. 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[citation needed].

Dietary sources of dioxin in the United States have been analyzed by the EPA and scientists from other organizations.

Toxicity

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 [11].

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.[citation needed] The oxidized dioxins can then be more readily excreted rather than stored for long time.[citation needed]

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 [12]. 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 [13]. The health effects of dioxins are mediated by their action on a cellular receptor, the aryl hydrocarbon receptor (AhR) [14].

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 [15]. Other effects in humans may include:

  • Central and Peripheral Nervous System pathology[18]
  • Thyroid disorders[19]

Recent studies have shown that exposure to dioxin changes the ratio of male to female births among a population such that more females are born than males.[23]

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 [24]. 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:

In rodents, including rats [25], mice [26], hamsters and guinea pigs [27]; birds [28]; and fish [29].
In rodents [25] [30] and fish [31]
  • Hepatotoxicity (liver toxicity)
In rodents [30]; chickens [32]; and fish [33]
  • Endocrine disruption
In rodents[citation needed] and fish [34]
  • Immunosuppression
In rodents[35] and fish[36].

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 [37].

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 [38] 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 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.
  • 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 [15], 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 [45].
  • 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 [46].
  • 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.
  • DuPont is being sued by 1,995 people who claim dioxin emissions from DuPont's plant in DeLisle, Mississippi, 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.

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  41. ^ Icmesa chemical company, Seveso, Italy. 9th July 1976. Retrieved on 2007-06-04.
  42. ^ Seveso. Retrieved on 2007-06-04.
  43. ^ AROUND THE NATION; Times Beach, Mo., Board Moves to Seal Off Town - New York Times. Retrieved on 2007-06-04.
  44. ^ AROUND THE NATION; Times Beach, Mo., Votes Itself Out of Existence - New York Times. Retrieved on 2007-06-04.
  45. ^ 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. 
  46. ^ Yushchenko's acne points to dioxin poisoning. Retrieved on 2007-06-04.

External links

  • "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.

This entry is from Wikipedia, the leading user-contributed encyclopedia. It may not have been reviewed by professional editors (see full disclaimer)

 
Translations: Translations for: Dioxin

Dansk (Danish)
n. - dioxin

Nederlands (Dutch)
dioxine

Français (French)
n. - dioxine

Deutsch (German)
n. - (chem.) Dioxin

Ελληνική (Greek)
n. - (χημ.) διοξίνη

Italiano (Italian)
diossina

Português (Portuguese)
n. - dioxina (f) (Quím.)

Русский (Russian)
разлагающее вещество в гербициде

Español (Spanish)
n. - dioxina

Svenska (Swedish)
n. - dioxin

中文（简体） (Chinese (Simplified))
戴奥辛

中文（繁體） (Chinese (Traditional))
n. - 戴奧辛

한국어 (Korean)
n. - 다이옥신

日本語 (Japanese)
n. - ダイオキシン

العربيه (Arabic)
‏(الاسم) مادة ملوثه و سامه‏

עברית (Hebrew)
n. - ‮דיוקסין (כימיקל)‬

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Dictionary. The American Heritage® Dictionary of the English Language, Fourth Edition Copyright © 2007, 2000 by Houghton Mifflin Company. Updated in 2007. Published by Houghton Mifflin Company. All rights reserved.  Read more
Encyclopedia of Public Health. Encyclopedia of Public Health. Copyright © 2002 by The Gale Group, Inc. All rights reserved.  Read more
US Military Dictionary. The Oxford Essential Dictionary of the U.S. Military. Copyright © 2001, 2002 by Oxford University Press, Inc. All rights reserved.  Read more
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Science Dictionary. The New Dictionary of Cultural Literacy, Third Edition Edited by E.D. Hirsch, Jr., Joseph F. Kett, and James Trefil. Copyright © 2002 by Houghton Mifflin Company. Published by Houghton Mifflin. All rights reserved.  Read more
Veterinary Dictionary. Saunders Comprehensive Veterinary Dictionary 3rd Edition. Copyright © 2007 by D.C. Blood, V.P. Studdert and C.C. Gay, Elsevier. All rights reserved.  Read more
Wikipedia. This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Dioxin".  Read more
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