Dioxin

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Space-filling model of 2,3,7,8- tetrachlorodibenzo-p-dioxin
Space-filling model of 2,3,7,8- tetrachlorodibenzo-p-dioxin
Structure of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)
Structure of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)

Dioxin is the popular name for the family of halogenated organic compounds, the most common consisting of polychlorinated dibenzofurans (PCDFs) and polychlorinated dibenzodioxins (PCDDs). PCDD/PCDFs (PCDD/Fs) have been shown to bioaccumulate in humans and wildlife due to their lipophilic properties. Recently, polybrominated dibenzofurans and dibenzodioxins have been discovered as impurities in brominated flame retardants, such as polybrominated diphenyl ethers.

Contents

[edit] Chemical structure

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

The basic structure of PCDD/Fs comprises two benzene rings joined by either a single (furan) or a double oxygen bridge (dioxin). Although the first synthesis goes back to the year 1872 the structure of 2,3,7,8-tetrachlorodibenzo-p-dioxin was unknown until 1957.[1] 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 210 different types of PCDD/F congeners (herein, a congener means a related dioxin compound) comprising of 75 PCDDs and 135 PCDFs. The toxicity of PCDD/Fs depends on the number and position of the chlorine atoms; only congeners that have chlorines in the 2, 3, 7, and 8 positions have any observable toxicity. Out of the 210 PCDD/F compounds in total, only 17 congeners (7 PCDDs and 10 PCDFs) 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.

[edit] Toxicity

Dioxins are a carcinogen in higher amounts, and cause developmental and reproductive problems. They are absorbed primarily through dietary intake of fat, as this is where they accumulate in animals, including humans.

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. [2][3] Many other compounds may also have dioxin-like properties, particularly non-ortho PCBs, some of which can have TEFs as high as 0.1.

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.

[edit] 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.[4]

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 US EPA 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 breast feeding 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.

Dioxins are also in smoke from typical cigarettes, those with chlorine-bleached paper and residues of many chlorine pesticides. 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 is "anthropogenic" (man-made, "not likely in nature"). Dioxin cannot come from the tobacco or any natural plant. Since then, the USA classified dioxin as a Known Human Carcinogen, and the USA signed the Stockholm Convention on Persistent Organic Pollutants(POPs) to globally phase out dioxin and 11 other of the worst industrial pollutants, though the treaty has not been ratified by the Senate. Nevertheless, chlorine tobacco pesticides and chlorine-bleached cigarette papers remain legal, with no warning required to consumers.

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.[5] 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.
A chart illustrating how much dioxin the average American consumes per day.

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. [6]

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 modern 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 if 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 other scientists. Summaries of the primary dietary sources are in the following two graphics (note pg = picogram, or one trillionth of a gram, or 10−12, or 0.000000000001 g). [7]

[edit] Health effects

Dioxins build up primarily in fatty tissues over time (bioaccumulate), so even small exposures may eventually reach dangerous levels. TCDD, the most toxic of the dibenzodioxins, has a half-life of approximately 7 years in humans, but at high concentrations, the elimination rate is enhanced by metabolism [8][9]. The health effects of dioxins are mediated by their action on a cellular receptor, the Aryl Hydrocarbon Receptor (AhR). [10] [11][12]

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 [4]. Other effects may include:

[edit] 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. 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 Center for Disease Control found that dioxin levels in Vietnam veterans[17] 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.

[edit] 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 EPA 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/per cubic meter of air, or nearly six times the highest dioxin level ever recorded in the U.S. Dioxin levels in the rubble of the World Trade Centers was 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,[22] 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 [23].
  • 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 recognised the symptoms of chloracne while viewing television news coverage of his condition. [24]
  • 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.

[edit] Incineration and dioxin emissions

It is claimed that modern waste incinerators—like Texas Industries' cement plant in Midlothian, Texas—are equipped with pollution control equipment which reduces dioxin emissions to insignificant levels. (However, the emissions from TXI's Midlothian plant have increased.[25][26]) Incineration of municipal solid waste, medical waste, sewage sludge, and hazardous waste together produce less than 3% of all 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.

However, there is debate over how "clean" this has made incineration, since the process of removing dioxin from stack emissions transfers dioxin residues to filter cake, slag and fly ash, toxic waste which still has to be disposed of safely.

[edit] References

  1. ^ Sandermann, W., Stockmann, H., Casten, R. (1957). "Pyrolysis of pentachlorophenol". Chemische Berichte 90: 690—692. 
  2. ^ M. Van den Berg, L. S. Birnbaum, M. Denison, M. De Vito, W. Farland, M. Feeley, H. Fiedler, H. Hakansson, A. Hanberg, L. Haws, Martin Rose, S. Safe, D. Schrenk, C. Tohyama, A. Tritscher, J. Tuomisto, M. Tysklind, N. Walker, Richard E. Peterson (2006). "The 2005 World Health Organization Reevaluation of Human and Mammalian Toxic Equivalency Factors for Dioxins and Dioxin-Like Compounds". Toxicology Science 93: 223–241. DOI:10.1093/toxsci/kfl055. 
  3. ^ [1]
  4. ^ http://www.ejnet.org/dioxin/dioxininfood.pdf
  5. ^ Gordon McKay (2002). "Dioxin, formation and minimisation during municipal solid waste (MSW) incineration: review". Chemical Engineering Journal 86: 343–368. DOI:10.1016/S1385-8947(01)00228-5. 
  6. ^ Latch D. E., Packer J. L., Stender B. L., VanOverbeke J., Arnold W. A., McNeill K. (2005). "Aqueous photochemistry of triclosan: formation of 2,4-dichlorophenol, 2,8-dichlorodibenzo-p-dioxin, and oligomerization products". Environmental toxicology and chemistry 24 (3): 517–525. DOI:10.1897/04-243R.1. 
  7. ^ "Levels of Dioxin in U.S. Food Supply (1995)" from May 2001 study by Arnold Schecter et. al., Journal of Toxicology and Environmental Health, Part A, 63:1–18.
  8. ^ Arch Toxicol. (2002) 76(5-6):316–25
  9. ^ J Expo Anal Environ Epidemiol. (2005) 15(1):51–65.
  10. ^ Biochim Biophys Acta. 2003 Feb 17;1619(3):263–8
  11. ^ J Comp Physiol [B]. 2005 May;175(4):221–30.
  12. ^ Biochem Pharmacol. 2006 Aug 14;72(4):393–404
  13. ^ http://ehp.niehs.nih.gov/docs/2004/6920/abstract.html
  14. ^ Peterson R. E., Theobald H. M., Kimmel G. L. (1993). "Developmental and reproductive toxicity of dioxins and related compounds: cross-species comparisons". Critical Review in Toxicology 23: 283–335. 
  15. ^ http://ehp.niehs.nih.gov/docs/2002/110p1169-1173baccarelli/abstract.html
  16. ^ Kociba RJ, Keyes DG, Beyer JE, et al. 1978. Results of a two-year chronic toxicity and oncogenicity study of 2,3,7,8-TCDD in rats. Toxicol Appl Pharmacol 46:281–287
  17. ^ http://www.cdc.gov/nceh/veterans/vet_hlth_actvy.pdf
  18. ^ Zack, J. A., Suskind, R. R. (1980). "The mortality experience of workers exposed to tetrachlorodibenzodioxin in a trichlorophenol process accident". J. Occup. Med. 22: 11–14. 
  19. ^ http://www.roche.com/com_his_sev-e.pdf
  20. ^ http://www.hse.gov.uk/comah/sragtech/caseseveso76.htm
  21. ^ http://www.chm.bris.ac.uk/motm/245t/245th/seveso.htm
  22. ^ http://ehp.niehs.nih.gov/members/2001/109p865-869geusau/geusau-full.html
  23. ^ Lancet (1999) 354(9186):1266–7
  24. ^ http://www.nature.com/news/2004/041122//pf/041122-8_pf.html
  25. ^ TECQ monitoring station [2]
  26. ^ latest US EPA report [3]
  • Law & Order: Criminal Intent. "Beast" (2005) - A woman dies from dioxin poisoning.

[edit] External links

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