Information About

Dioxins





CHEMICAL STRUCTURE


and Substituent numbering scheme of the parent compound dibenzo-''p''-dioxin]]

The basic structure of PCDDs comprises two Benzene Ring s 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 Congener s (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 War3. 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 Burden s 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 Herbicide s. 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 Ion s or as Organochlorine Compound s, 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.

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 Herbicide s 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 11.

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 Pesticide s 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 Plastic s, Resin s, or Bleach es. Such materials include Tampon s, 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.


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 12.

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.

(TCDD)]]

2,3,7,8-tetrachlorodibenzo-''p''-dioxin (TCDD) is the most toxic of the Congener s. 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 13. 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 Pollutant s (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 14. The health effects of dioxins are mediated by their action on a cellular receptor, the Aryl Hydrocarbon Receptor (AhR) 15.

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 16. Other effects in humans may include:


  • Central and Peripheral Nervous System pathology19


  • Thyroid disorders20






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 30 31 and fish 32

  • Hepatotoxicity (liver toxicity)


: In rodents 33; chickens 34; and fish 35

  • Endocrine disruption


: In rodents and fish 36

  • Immunosuppression


: In rodents37 and fish38.

  • Learning 39



STUDIES OF DIOXIN'S EFFECTS IN VIETNAM


US veterans' groups and Vietnam ese 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 40.

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 41 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 1976 , large amounts of dioxin were released in an industrial Accident At Seveso , although no immediate human fatalities or birth defects occurred 43 44 45.



  • 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 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." 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 48, 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 49.


  • 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 50.


  • 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.



REFERENCES



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.