General structure of PCDDs where n and m can range from 0 to 4
General structure of PCDDs where n and m can range from 0 to 4

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 organochloride-related manufacturing, incineration of chlorine-containing substances such as polyvinyl chloride (PVC), and chlorine bleaching of paper.[2][3] Forest fires and volcanic eruptions have also been cited as an airborne source, although their contribution to the current levels of PCDD accumulation are minor in comparison.[4][5] Incidents of dioxin poisoning resulting from industrial emissions and accidents were first recorded as early as the mid 19th century during the Industrial Revolution.[6]

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 skeletal formula and substituent numbering scheme of the parent compound dibenzo-1,4-dioxin
The skeletal formula and substituent numbering scheme of the parent compound dibenzo-1,4-dioxin

The structure of dibenzo-1,4-dioxin consists of two benzene rings joined by two oxygen bridges. This makes the compound an aromatic diether. The name dioxin formally refers to the central dioxygenated ring, which is stabilized by the two flanking benzene rings.

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

Structure of 2,3,7,8-tetrachlorodibenzodioxin (TCDD)
Structure of 2,3,7,8-tetrachlorodibenzodioxin (TCDD)

Low concentrations of dioxins existed in nature prior to industrialization as a result of natural combustion and geological processes.[9][10] Dioxins were first unintentionally produced as by-products from 1848 onwards as Leblanc process plants started operating in Germany.[6] The first intentional synthesis of chlorinated dibenzodioxin was in 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-tetrachlorodibenzodioxin (TCDD), became well known as a contaminant of Agent Orange, a herbicide used in the Malayan Emergency and the Vietnam War.[11] Later, dioxins were found in Times Beach, Missouri[12] and Love Canal, New York[13] and Seveso, Italy.[14] More recently, dioxins have been in the news with the poisoning of President Viktor Yushchenko of Ukraine in 2004,[15] the Naples Mozzarella Crisis,[16] the 2008 Irish pork crisis, and the German feed incident of 2010.[17]

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.

Concentration profile of PCDD in a dated sediment core from Esthwaite Water, Cumbria, UK
Concentration profile of PCDD in a dated sediment core from Esthwaite Water, Cumbria, UK

Occupational exposure is an issue for some in the chemical industries, historically for those making chlorophenols or chlorophenoxy acid herbicides or in the application of chemicals, notably herbicides. In many developed nations there are now emissions regulations which have dramatically decreased the emissions[18] and thus alleviated some concerns, although the lack of continuous sampling of dioxin emissions causes concern about the understatement of emissions. In Belgium, through the introduction of a process called AMESA, continuous sampling showed that periodic sampling understated emissions by a factor of 30 to 50 times. Few facilities have continuous sampling.

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 dioxins are broadly in the following types:[18]

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 municipal solid waste, medical waste, sewage sludge, and hazardous waste together now produce less than 3% of all dioxin emissions. Since 1987, however, backyard barrel burning has showed almost no decrease, and is now the largest source of dioxin emissions, producing about one third of the total output.[18]

In incineration, dioxins can also reform or form de novo 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 the quantity of dioxins reforming or forming de novo is through rapid (30 millisecond) quenching of the exhaust gases through that 400 °C window.[19] Incinerator emissions of dioxins have been reduced by over 90% as a result of new emissions control requirements. Incineration in developed countries is now a very minor contributor to dioxin emissions.

Dioxins are also generated in reactions that do not involve burning — such as chlorine bleaching fibers for paper or textiles, and in the manufacture of chlorinated phenols, particularly when reaction temperature is not well controlled.[20] Compounds involved 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. Dioxins may also be formed during the photochemical breakdown of the common antimicrobial compound triclosan.[21]

Sources of human intake

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).[22]
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).[22]

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

Toxicity

Space-filling model of 2,3,7,8-tetrachlorodibenzodioxin
Space-filling model of 2,3,7,8-tetrachlorodibenzodioxin

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.[30]

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

Chloracne on the ear and neck of a herbicide production worker
Chloracne on the ear and neck of a herbicide production worker

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.[31] The health effects of dioxins are mediated by their action on a cellular receptor, the aryl hydrocarbon receptor (AhR).[32]

Exposure to high levels of dioxins in humans causes a severe form of persistent acne, known as chloracne.[33] High occupational or accidental levels of exposures to dioxins have been shown by epidemiological studies to lead to an increased risk of tumors at all sites.[34] Other effects in humans (at high dose levels) may include:

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.[42]

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.[43] 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.[44] The most sensitive effects are caused at body burdens relatively 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,[45] mice,[46] hamsters and guinea pigs,[47] birds,[48] and fish.[49]
In rodents[45][50] and fish.[51]
In rodents,[50] chickens,[52] and fish.[53]
In rodents[44] and fish.[54]
In rodents[55] and fish.[56]

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.[43]

Agent Orange

U.S. Army Huey helicopter spraying Agent Orange over Vietnamese agricultural land
U.S. Army Huey helicopter spraying Agent Orange over Vietnamese agricultural land

Main article: Agent Orange

Agent Orange was the code name for one of the herbicides and defoliants the U.S. military used as part of its herbicidal warfare program, Operation Ranch Hand, during the Vietnam War from 1961 to 1971. It was a mixture of 2,4,5-T and 2,4-D. The 2,4,5-T used was contaminated with 2,3,7,8-tetrachlorodibenzodioxin (TCDD), an extremely toxic dioxin compound.

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.[57]

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.[58] In South Vietnam alone, an estimated 10 million hectares of agricultural land were ultimately destroyed.[59] In some areas, TCDD concentrations in soil and water were hundreds of times greater than the levels considered safe by the U.S. Environmental Protection Agency.[60][61]

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 birth defects.[62] The Red Cross of Vietnam estimates that up to 1 million people are disabled or have health problems due to Agent Orange contamination.[63] The United States government has challenged these figures as being unreliable and unrealistically high.[64][65]

Dioxin exposure incidents

See also: Dioxin controversy

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.[90]

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.[91]

See also

References

  1. ^ Weber, Roland; Tysklind, Mats; Gaus, Caroline (2008-03-01). "Dioxin - contemporary and future challenges of historical legacies". Environmental Science and Pollution Research. 15 (2): 96–100. doi:10.1065/espr2008.01.473. ISSN 1614-7499. PMID 18380226. S2CID 36662487.
  2. ^ Beychok, Milton R. (January 1987). "A data base for dioxin and furan emissions from refuse incinerators". Atmospheric Environment. 21 (1): 29–36. Bibcode:1987AtmEn..21...29B. doi:10.1016/0004-6981(87)90267-8.
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