Polychlorinated dibenzodioxins
Polychlorinated dibenzodioxins (PCDDs), or simply dioxins, are a group of long-lived polyhalogenated organic compounds that are primarily anthropogenic, and contribute toxic, persistent organic pollution in the environment.[1]
They are commonly but inaccurately referred to as dioxins for simplicity, because every PCDD molecule contains a dibenzo-1,4-dioxin skeletal structure, with 1,4-dioxin as the central ring. Members of the PCDD family bioaccumulate in humans and wildlife because of their lipophilic properties, and may cause developmental disturbances and cancer.
Because dioxins can persist in the environment for more than 100 years, the majority of PCDD pollution today is not the result of recent emissions, but the cumulative result of synthetic processes undertaken since the beginning of the 20th century, including
The word "dioxins" may also refer to other similarly acting chlorinated compounds (see Dioxins and dioxin-like compounds).
Chemical structure of dibenzo-1,4-dioxins
The structure of
In PCDDs, chlorine atoms are attached to this structure at any of 8 different places on the molecule, at positions 1–4 and 6–9. There are 75 different PCDD congeners (that is, related dioxin compounds).[7]
number | formula | name | CAS Number | InChIKey |
---|---|---|---|---|
PCDD-1 | 1-chlorodibenzo-p-dioxin | 39227-53-7 | VGGGRWRBGXENKI-UHFFFAOYSA-N | |
PCDD-2 | 2-chlorodibenzo-p-dioxin | 39227-54-8 | GIUGGRUEPHPVNR-UHFFFAOYSA-N | |
PCDD-12 | 1,2-dichlorodibenzo-p-dioxin | 54536-18-4 | DFGDMWHUCCHXIF-UHFFFAOYSA-N | |
PCDD-13 | 1,3-dichlorodibenzo-p-dioxin | 50585-39-2 | AZYJYMAKTBXNSX-UHFFFAOYSA-N | |
PCDD-14 | 1,4-dichlorodibenzo-p-dioxin | 54536-19-5 | MBMUPQZSDWVPQU-UHFFFAOYSA-N | |
PCDD-16 | 1,6-dichlorodibenzo-p-dioxin | 38178-38-0 | MAWMBEVNJGEDAD-UHFFFAOYSA-N | |
PCDD-17 | 1,7-dichlorodibenzo-p-dioxin | 82291-26-7 | IJUWLAFPPVRYGY-UHFFFAOYSA-N | |
PCDD-18 | 1,8-dichlorodibenzo-p-dioxin | 82291-27-8 | PLZYIHQBHROTFD-UHFFFAOYSA-N | |
PCDD-19 | 1,9-dichlorodibenzo-p-dioxin | 82291-28-9 | JZDVJXBKJDADAY-UHFFFAOYSA-N | |
PCDD-23 | 2,3-dichlorodibenzo-p-dioxin | 29446-15-9 | YCIYTXRUZSDMRZ-UHFFFAOYSA-N | |
PCDD-27 | 2,7-dichlorodibenzo-p-dioxin | 33857-26-0 | NBFMTHWVRBOVPE-UHFFFAOYSA-N | |
PCDD-28 | 2,8-dichlorodibenzo-p-dioxin | 38964-22-6 | WMWJCKBJUQDYLM-UHFFFAOYSA-N | |
PCDD-123 | 1,2,3-trichlorodibenzo-p-dioxin | 54536-17-3 | SKMFBGZVVNDVFR-UHFFFAOYSA-N | |
PCDD-124 | 1,2,4-trichlorodibenzo-p-dioxin | 39227-58-2 | HRVUKLBFRPWXPJ-UHFFFAOYSA-N | |
PCDD-126 | 1,2,6-trichlorodibenzo-p-dioxin | 69760-96-9 | XQBPVWBIUBCJJO-UHFFFAOYSA-N | |
PCDD-127 | 1,2,7-trichlorodibenzo-p-dioxin | 82291-30-3 | TXJMXDWFPQSYEQ-UHFFFAOYSA-N | |
PCDD-128 | 1,2,8-trichlorodibenzo-p-dioxin | 82291-31-4 | QBEOCKSANJLBAE-UHFFFAOYSA-N | |
PCDD-129 | 1,2,9-trichlorodibenzo-p-dioxin | 82291-32-5 | DQLRDBDQLSIOIX-UHFFFAOYSA-N | |
PCDD-136 | 1,3,6-trichlorodibenzo-p-dioxin | 82291-33-6 | LNPVMVSAUXUGHH-UHFFFAOYSA-N | |
PCDD-137 | 1,3,7-trichlorodibenzo-p-dioxin | 67028-17-5 | RPKWIXFZKMDPMH-UHFFFAOYSA-N | |
PCDD-138 | 1,3,8-trichlorodibenzo-p-dioxin | 82306-61-4 | FJAKCOBYQSEWMT-UHFFFAOYSA-N | |
PCDD-139 | 1,3,9-trichlorodibenzo-p-dioxin | 82306-62-5 | DGDADRUTFAIIQQ-UHFFFAOYSA-N | |
PCDD-146 | 1,4,6-trichlorodibenzo-p-dioxin | 82306-63-6 | UTTYFTWIJLRXKB-UHFFFAOYSA-N | |
PCDD-147 | 1,4,7-trichlorodibenzo-p-dioxin | 82306-64-7 | NBWAQBGJBSYXHV-UHFFFAOYSA-N | |
PCDD-178 | 1,7,8-trichlorodibenzo-p-dioxin | 82306-65-8 | CAPCTZJHYADFNX-UHFFFAOYSA-N | |
PCDD-237 | 2,3,7-trichlorodibenzo-p-dioxin | 33857-28-2 | ZSIZNEVHVVRPFF-UHFFFAOYSA-N | |
PCDD-1234 | 1,2,3,4-tetrachlorodibenzo-p-dioxin | 30746-58-8 | DJHHDLMTUOLVHY-UHFFFAOYSA-N | |
PCDD-1236 | 1,2,3,6-tetrachlorodibenzo-p-dioxin | 71669-25-5 | XEZBZSVTUSXISZ-UHFFFAOYSA-N | |
PCDD-1237 | 1,2,3,7-tetrachlorodibenzo-p-dioxin | 67028-18-6 | SKGXYFVQZVPEFP-UHFFFAOYSA-N | |
PCDD-1238 | 1,2,3,8-tetrachlorodibenzo-p-dioxin | 53555-02-5 | BXKLTNKYLCZOHF-UHFFFAOYSA-N | |
PCDD-1239 | 1,2,3,9-tetrachlorodibenzo-p-dioxin | 71669-26-6 | CMVHZKSHSHQJHS-UHFFFAOYSA-N | |
PCDD-1246 | 1,2,4,6-tetrachlorodibenzo-p-dioxin | 71669-27-7 | KQNBZUDHTCXCNA-UHFFFAOYSA-N | |
PCDD-1247 | 1,2,4,7-tetrachlorodibenzo-p-dioxin | 71669-28-8 | SMPHQCMJQUBTFZ-UHFFFAOYSA-N | |
PCDD-1248 | 1,2,4,8-tetrachlorodibenzo-p-dioxin | 71669-29-9 | XGIKODBWQSAEFQ-UHFFFAOYSA-N | |
PCDD-1249 | 1,2,4,9-tetrachlorodibenzo-p-dioxin | 71665-99-1 | WDAHVJCSSYOALR-UHFFFAOYSA-N | |
PCDD-1267 | 1,2,6,7-tetrachlorodibenzo-p-dioxin | 40581-90-6 | SAMLAWFHXZIRMP-UHFFFAOYSA-N | |
PCDD-1268 | 1,2,6,8-tetrachlorodibenzo-p-dioxin | 67323-56-2 | YYUFYZDSYHKVDP-UHFFFAOYSA-N | |
PCDD-1269 | 1,2,6,9-tetrachlorodibenzo-p-dioxin | 40581-91-7 | ZKMXKYXNLFLUCD-UHFFFAOYSA-N | |
PCDD-1278 | 1,2,7,8-tetrachlorodibenzo-p-dioxin | 34816-53-0 | YDZCLBKUTXYYKS-UHFFFAOYSA-N | |
PCDD-1279 | 1,2,7,9-tetrachlorodibenzo-p-dioxin | 71669-23-3 | QIKHBBZEUNSCAF-UHFFFAOYSA-N | |
PCDD-1289 | 1,2,8,9-tetrachlorodibenzo-p-dioxin | 62470-54-6 | WELWFAGPAZKSBG-UHFFFAOYSA-N | |
PCDD-1368 | 1,3,6,8-tetrachlorodibenzo-p-dioxin | 33423-92-6 | OTQFXRBLGNEOGH-UHFFFAOYSA-N | |
PCDD-1369 | 1,3,6,9-tetrachlorodibenzo-p-dioxin | 71669-24-4 | QAUIRDIJIUMMEP-UHFFFAOYSA-N | |
PCDD-1378 | 1,3,7,8-tetrachlorodibenzo-p-dioxin | 50585-46-1 | VPTDIAYLYJBYQG-UHFFFAOYSA-N | |
PCDD-1379 | 1,3,7,9-tetrachlorodibenzo-p-dioxin | 62470-53-5 | JMGYHLJVDHUACM-UHFFFAOYSA-N | |
PCDD-1469 | 1,4,6,9-tetrachlorodibenzo-p-dioxin | 40581-93-9 | QTIIAIRUSSSOHT-UHFFFAOYSA-N | |
PCDD-1478 | 1,4,7,8-tetrachlorodibenzo-p-dioxin | 40581-94-0 | FCRXUTCUWCJZJI-UHFFFAOYSA-N | |
PCDD-2378 (TCDD) | 2,3,7,8-tetrachlorodibenzo-p-dioxin | 1746-01-6 | HGUFODBRKLSHSI-UHFFFAOYSA-N | |
PCDD-12346 | 1,2,3,4,6-pentachlorodibenzo-p-dioxin | 67028-19-7 | LNWDBNKKBLRAMH-UHFFFAOYSA-N | |
PCDD-12347 | 1,2,3,4,7-pentachlorodibenzo-p-dioxin | 39227-61-7 | WRNGAZFESPEMCN-UHFFFAOYSA-N | |
PCDD-12367 | 1,2,3,6,7-pentachlorodibenzo-p-dioxin | 71925-15-0 | RLGWDUHOIIWPGN-UHFFFAOYSA-N | |
PCDD-12368 | 1,2,3,6,8-pentachlorodibenzo-p-dioxin | 71925-16-1 | VKDGHBBUEIIEHL-UHFFFAOYSA-N | |
PCDD-12369 (PCDD-14678) | 1,2,3,6,9-pentachlorodibenzo-p-dioxin | 82291-34-7 | NWKWRHSKKNELND-UHFFFAOYSA-N | |
PCDD-12378 | 1,2,3,7,8-pentachlorodibenzo-p-dioxin | 40321-76-4 | FSPZPQQWDODWAU-UHFFFAOYSA-N | |
PCDD-12379 (PCDD-23468) | 1,2,3,7,9-pentachlorodibenzo-p-dioxin | 71925-17-2 | UAOYHTXYVWEPIB-UHFFFAOYSA-N | |
PCDD-12389 (PCDD-23467) | 1,2,3,8,9-pentachlorodibenzo-p-dioxin | 71925-18-3 | VUMZAVNIADYKFC-UHFFFAOYSA-N | |
PCDD-12467 | 1,2,4,6,7-pentachlorodibenzo-p-dioxin | 82291-35-8 | SEKDDGLKEYEVQK-UHFFFAOYSA-N | |
PCDD-12468 | 1,2,4,6,8-pentachlorodibenzo-p-dioxin | 71998-76-0 | SJJWALZHAWITMS-UHFFFAOYSA-N | |
PCDD-12469 | 1,2,4,6,9-pentachlorodibenzo-p-dioxin | 82291-36-9 | GNQVSAMSAKZLKE-UHFFFAOYSA-N | |
PCDD-12478 | 1,2,4,7,8-pentachlorodibenzo-p-dioxin | 58802-08-7 | QUPLGUUISJOUPJ-UHFFFAOYSA-N | |
PCDD-12479 (PCDD-13468) | 1,2,4,7,9-pentachlorodibenzo-p-dioxin | 82291-37-0 | QLBBXWPVEFJZEC-UHFFFAOYSA-N | |
PCDD-12489 (PCDD-13467) | 1,2,4,8,9-pentachlorodibenzo-p-dioxin | 82291-38-1 | KLLFLRKEOJCTGC-UHFFFAOYSA-N | |
PCDD-123467 | 1,2,3,4,6,7-hexachlorodibenzo-p-dioxin | 58200-66-1 | NLBQVWJHLWAFGJ-UHFFFAOYSA-N | |
PCDD-123468 | 1,2,3,4,6,8-hexachlorodibenzo-p-dioxin | 58200-67-2 | IMALTUQZEIFHJW-UHFFFAOYSA-N | |
PCDD-123469 | 1,2,3,4,6,9-hexachlorodibenzo-p-dioxin | 58200-68-3 | UDYXCMRDCOVQLG-UHFFFAOYSA-N | |
PCDD-123478 | 1,2,3,4,7,8-hexachlorodibenzo-p-dioxin | 39227-28-6 | WCYYQNSQJHPVMG-UHFFFAOYSA-N | |
PCDD-123678 | 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin | 57653-85-7 | YCLUIPQDHHPDJJ-UHFFFAOYSA-N | |
PCDD-123679 (PCDD-124678) | 1,2,3,6,7,9-hexachlorodibenzo-p-dioxin | 64461-98-9 | BQOHWGKNRKCEFT-UHFFFAOYSA-N | |
PCDD-123689 (PCDD-134678) | 1,2,3,6,8,9-hexachlorodibenzo-p-dioxin | 58200-69-4 | GZRQZUFXVFRKBI-UHFFFAOYSA-N | |
PCDD-123789 (PCDD-234678) | 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin | 19408-74-3 | LGIRBUBHIWTVCK-UHFFFAOYSA-N | |
PCDD-124679 | 1,2,4,6,7,9-hexachlorodibenzo-p-dioxin | 39227-62-8 | BSJDQMWAWFTDGD-UHFFFAOYSA-N | |
PCDD-124689 (PCDD-134679) | 1,2,4,6,8,9-hexachlorodibenzo-p-dioxin | 58802-09-8 | URELDHWUZUWPIU-UHFFFAOYSA-N | |
PCDD-1234678 | 1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin | 35822-46-9 | WCLNVRQZUKYVAI-UHFFFAOYSA-N | |
PCDD-1234679 | 1,2,3,4,6,7,9-heptachlorodibenzo-p-dioxin | 58200-70-7 | KTJJIBIRZGQFQZ-UHFFFAOYSA-N | |
PCDD-12346789 | octachlorodibenzo-p-dioxin | 3268-87-9 | FOIBFBMSLDGNHL-UHFFFAOYSA-N |
The toxicity of PCDDs depends on the number and positions of the chlorine atoms. Congeners that have chlorine in the 2, 3, 7, and 8 positions have been found to be significantly toxic. In fact, 7 congeners have chlorine atoms in the relevant positions which were considered toxic by the World Health Organization toxic equivalent (WHO-TEQ) scheme.[8]
Historical perspective
Low concentrations of dioxins existed in nature prior to
Sources of dioxins
The United States Environmental Protection Agency inventory of sources of dioxin-like compounds is possibly the most comprehensive review of the sources and releases of dioxins,[18] but other countries now have substantial research as well.
Occupational exposure is an issue for some in the
Dioxins are produced in small concentrations when organic material is
- Combustion sources, e.g. incineratorsand private backyard barrel burning
- Metal smelting
- Refining and process sources
- Chemical manufacturing sources
- Natural sources
- Environmental reservoirs
When first carried out in 1987, the original US EPA inventory of dioxin sources revealed that incineration represented more than 80% of known dioxin sources. As a result, US EPA implemented new emissions requirements. These regulations succeeded in reducing dioxin stack emissions from incinerators. Incineration of
In incineration, dioxins can also reform or form de novo in the
Dioxins are also generated in reactions that do not involve burning — such as
Sources of human intake
Tolerable daily, monthly or annual intakes have been set by the World Health Organization and a number of governments. Dioxins enter 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.[22][23]
Children are passed substantial body burdens by their mothers, and breastfeeding increases the child's body burden.[24] Dioxin exposure can also occur from contact with Pentachlorophenol (Penta) treated lumber as Pentachlorophenol often contains dioxins as a contaminant. Children's daily intakes during breast feeding are often many times above the intakes of adults based on body weight. This is why the WHO consultation group assessed the tolerable intake so as to prevent a woman from accumulating harmful body burdens before her first pregnancy.[25] Breast fed children usually still have higher dioxin body burdens than non breast fed children. The WHO still recommends breast feeding for its other benefits.[26] In many countries dioxins in breast milk have decreased by even 90% during the two last decades.[27]
Dioxins are present in cigarette smoke.[28] 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").
Metabolism
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 chlorinated dioxins (4–8 chlorine atoms) in humans ranges from 4.9 to 13.1 years.[29]
The persistence of a particular dioxin congener in an animal is thought to be a consequence of its structure. Dioxins with no lateral (2, 3, 7, and 8) chlorines, which thus contain hydrogen atoms on adjacent pairs of carbons, can more readily be oxidized by cytochromes P450.[30] The oxidized dioxins can then be more readily excreted rather than stored for a long time.[citation needed]
Toxicity
2,3,7,8-Tetrachlorodibenzodioxin (TCDD) is considered the most toxic of the congeners (for the mechanism of action, see 2,3,7,8-Tetrachlorodibenzodioxin and Aryl hydrocarbon receptor). Other dioxin congeners including PCDFs and PCBs with dioxin-like toxicity, are given a toxicity rating from 0 to 1, where TCDD = 1 (see Dioxins and dioxin-like compounds). This toxicity rating is called the Toxic Equivalence Factor concept, 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.[8] Many other compounds may also have dioxin-like properties, particularly non-ortho PCBs, one of which has a TEF 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 simple scaling factor may not be the most appropriate treatment for complex mixtures of dioxins; both transfer from the source and absorption and elimination vary among different congeners, and the TEF value is not able to accurately reflect this.[31]
Dioxins and other
Health effects in humans
Dioxins build up primarily in fatty tissues over time (bioaccumulation), so even small exposures may eventually reach dangerous levels. In 1994, the US EPA reported that dioxins are a probable carcinogen, but noted that non-cancer effects (reproduction and sexual development, immune system) may pose a greater threat to human health. TCDD, the most toxic of the dibenzodioxins, is classified as a Group 1 carcinogen by the International Agency for Research on Cancer (IARC). TCDD has a half-life of approximately 8 years in humans, although at high concentrations, the elimination rate is enhanced by metabolism.[32] The health effects of dioxins are mediated by their action on a cellular receptor, the aryl hydrocarbon receptor (AhR).[33]
Exposure to high levels of dioxins in humans causes a severe form of persistent
- Developmental abnormalities in the
- Central and peripheral nervous system pathology[38]
- Thyroid disorders[39]
- Damage to the immune systems[40]
- Endometriosis[41]
- Diabetes[42]
Recent studies have shown that high exposure to dioxins changes the ratio of male to female births among a population such that more females are born than males.[43]
Dioxins accumulate in food chains in a fashion similar to other chlorinated compounds (bioaccumulation). This means that even small concentrations in contaminated water can be concentrated up a food chain to dangerous levels because of the long biological half life and low water solubility of dioxins.
Toxic effects in animals
While it has been difficult to establish 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.
Among the animals for which TCDD toxicity has been studied, there is strong evidence for the following effects:
- Birth defects (teratogenicity)
- Cancer (including squamous cell carcinoma, and various animal hepatocarcinomas)
- Hepatotoxicity (liver toxicity)
- Endocrine disruption
- Immunosuppression
The LD50 of dioxin also varies wildly between species with the most notable disparity being between the ostensibly similar species of hamster and guinea pig. The oral LD50 for guinea pigs is as low as 0.5 to 2 μg/kg body weight, whereas the oral LD50 for hamsters can be as high as 1 to 5 mg/kg body weight, a difference of as much as thousandfold or more, and even among rat strains there may be thousandfold differences.[44]
Agent Orange
Agent Orange was the code name for one of the
During the Vietnam war, between 1962 and 1971, the United States military sprayed 20,000,000 U.S. gallons (76,000,000 L) of chemical herbicides and defoliants in Vietnam, eastern Laos and parts of Cambodia, as part of Operation Ranch Hand.[58]
By 1971, 12% of the total area of South Vietnam had been sprayed with defoliating chemicals, which were often applied at rates that were 13 times as high as the legal USDA limit.
According to Vietnamese Ministry of Foreign Affairs, 4.8 million Vietnamese people were exposed to Agent Orange, resulting in 400,000 people being killed or maimed, and 500,000 children born with
Dioxin exposure incidents
- In 1949, in a Monsanto herbicide production plant for 2,4,5-T in Nitro, West Virginia, 240 people were affected when a relief valve opened.[67]
- In 1963, a dioxin cloud escaped after an explosion in a
- Also during 1965 through 1968, Dr. Albert M. Kligman was contracted by the Dow Chemical Company to perform threshold tests for TCDD on inmates at Holmesburg Prison in Philadelphia after Dow studies revealed adverse effects on workers at Dow's Midland, Michigan, plant were likely due to TCDD. A subsequent test by Dow in rabbit ear models when exposed to 4–8μg usually caused a severe response. The human studies carried out in Holmesburg failed to follow Dow's original protocol and lacked proper informed consent by the participants. As a result of poor study design and subsequent destruction of records, the tests were virtually worthless even though ten inmates were exposed to 7,500μg of TCDD.[76]
- In 1976, large amounts of dioxins were released in an industrial accident at Seveso, Italy, although no immediate human fatalities or birth defects occurred.[77][78][79]
- In 1978, dioxins were some of the contaminants that forced the evacuation of the Love Canal neighborhood of Niagara Falls, New York.
- 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 dioxins in the soil caused by applications of contaminated oil meant to control dust on the town's dirt roads.[80] The town eventually disincorporated.[81]
- In the spring of 1990, a chemical plant Khimprom in Ufa, Russia released phenol into the water tributaries. An investigation revealed previously classified disposal of dioxin in manufacturing 2,4,5-Trichlorophenoxyacetic acid. The accident affected 670,000 people. Dioxin was found in tap water. It was assumed that it resulted from chlorophenol produced by a reaction with chlorine in water purification.[82]
- In December 1991, an electrical explosion caused dioxins (created from the oxidation of SUNY New Paltz.
- In May 1999, there was a 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.[83]
- Explosions resulting from the terrorist attacks on the US on 11 September 2001, released massive amounts of dust into the air. The air was measured for dioxins from 23 September 2001, to 21 November 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 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 12 and 29 October 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,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.[84]
- In 2004, in 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.[15]
- In the early 2000s, residents of the city of New Plymouth, New Zealand, reported 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 has been sued by 1,995 people who claim dioxin emissions from DuPont's plant in DeLisle, Mississippi, caused their cancers, illnesses or loved ones' deaths; of these only 850 were pending as of June 2008. In August 2005, Glen Strong, an oyster fisherman with the rare blood cancer multiple myeloma, was awarded $14 million from DuPont, but the ruling was overturned 5 June 2008, by a Mississippi jury who found DuPont's plant had no connection to Mr. Strong's disease.[85] In another case, parents claimed dioxin from pollution caused the death of their 8-year-old daughter; the trial took place in the summer of 2007, and a jury wholly rejected the family's claims, as no scientific connection could be proven between DuPont and the family's tragic loss.[86] DuPont's DeLisle plant is one of three titanium dioxide facilities (including Edgemoor, Delaware, and New Johnsonville, Tennessee) that are the largest producers of dioxin in the country, according to the US EPA's Toxic Release Inventory. DuPont maintains its operations are safe and environmentally responsible.
- In 2007, thousands of tonnes of foul-smelling refuse were piled up in Naples, Italy and its surrounding villages, defacing entire neighbourhoods. Authorities discovered that polychlorinated dibenzodioxins levels in buffalo milk used by 29 mozzarella makers exceeded permitted limits; after further investigation they impounded milk from 66 farms. Authorities suspected the source of the contamination was from waste illegally disposed of on land grazed by buffalo. Prosecutors in Naples placed 109 people under investigation on suspicion of fraud and food poisoning. Sales of Mozzarella cheese fell by 50% in Italy.[87]
- In December 2008 in polychlorinated biphenyls, and the contribution from actual polychlorinated dibenzodioxins was relatively low. It is thought that the incident resulted from the contamination of fuel oil used in a drying burner at a single feed processor, with PCBs. The resulting combustion produced a highly toxic mixture of PCBs, dioxins and furans, which was included in the feed produced and subsequently fed to a large number of pigs.[88]
- According to data in 2009,[89] in 2005 the production of dioxin by the steel industry ILVA in Taranto (Italy) accounted for 90.3 per cent of the overall Italian emissions, and 8.8 per cent of the European emissions.
- German dioxin incident: In January 2011 about 4700 German farms were banned from making deliveries after self-checking of an animal feed producer had showed levels of dioxin above maximum levels. This incident appeared to involve PCDDs and not PCBs.[17] Dioxins were found in animal feed and eggs in many farms. The maximum values were exceeded twofold in feed and maximally fourfold in some individual eggs.[17] Thus the incident was minor as compared with the Belgian crisis in 1999, and delivery bans were rapidly cleared.[90]
Dioxin testing
The analyses used to determine these compounds' relative toxicity share common elements that differ from methods used for more traditional analytical determinations. The preferred methods for dioxins and related analyses use high resolution gas chromatography/mass spectrometry (HRGC/HRMS). Concentrations are determined by measuring the ratio of the analyte to the appropriate isotopically labeled internal standard.[91]
Also novel bio-assays like DR CALUX are nowadays used in identification of dioxins and dioxin-like compounds. The advantage in respect to HRGC/HRMS is that it is able to scan many samples at lower costs. Also it is able to detect all compounds that interact with the Ah-receptor which is responsible for carcinogenic effects.[92]
See also
- Dioxins and dioxin-like compounds
- toxic equivalentscheme for the purposes of assessing dioxin levels.
- Chemetco – this former copper smelter is cited in an academic study as one of the 10 highest ranking sources of dioxin pollution reaching Nunavut in the Canadian Arctic
- toxic equivalentscheme when measuring dioxin levels.
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External links
- NIEHS dioxin fact sheet
- "Dioxins and Dioxin-like Compounds in the Food Supply: Strategies to Decrease Exposure" Archived 2004-12-25 at the National Academy of Sciences
- "Assessment of the Health Risks of Dioxins", a 1998 report by the World Health Organization.