Polychlorinated dibenzodioxins and dibenzofurans

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General structure of dibenzodioxins (see also overview of the group )
General structure of dibenzofurans (see also overview of the group )

Polychlorinated dibenzo- p- dioxins and dibenzofurans ( PCDD / PCDF ) are two groups of chemically similarly structured chlorinated organic compounds . They belong to the oxygen-containing derivatives of halogenated hydrocarbons and are in general usage, sometimes also in the literature, as dioxins - or incorrectly as dioxins (singular).

As persistent organic pollutants , they are hardly broken down in the environment. Traces of polychlorinated dioxins and furans occur all over the world. Dioxins accumulate in living organisms via the food chain , especially in the liver in vertebrates as the detoxification organ of the metabolic cycle. Humans ingest dioxins primarily through animal foods (fish, meat, eggs, dairy products).

Overview of the group

Structural formula of 2,3,7,8-tetrachlorodibenzo- p- dioxin

The most toxic single compound among the dioxins is the so-called "Sevesodioxin" ( 2,3,7,8-Tetrachlorodibenzodioxin , short 2,3,7,8-TCDD). The acute toxicity of the other polychlorinated dibenzodioxins and dibenzofurans is given relative to 2,3,7,8-TCDD. Even small amounts of polychlorinated dioxins and furans can promote the development of cancer from previously damaged cells.

The members of the two groups of substances have either a dibenzodioxin (two benzene rings linked by two oxygen bridges) or a dibenzofuran backbone (two benzene rings are linked via an oxygen atom and directly; this corresponds to a central furan unit). Up to 8 chlorine atoms can be bound to each of these base bodies. The number of chlorine atoms and their position on the benzene rings influence the toxicity , the carcinogenic effect and the degradability of polychlorinated dibenzodioxins and dibenzofurans.

Dibenzo-p-dioxin-numbering-2D-skeletal.png
Dibenzofuran-numbering-2D-skeletal.png


General structure of dibenzodioxins and dibenzofurans with locants
Congeners
Chlorine atoms PCDD isomers PCDF isomers
1 02 004th
2 10 016
3 14th 028
4th 22nd 038
5 14th 028
6th 10 016
7th 02 004th
8th 01 001
Total 75 135

“Dioxins” usually occur as a mixture of different halogenated dibenzodioxins and dibenzofurans. This mixture can have a certain frequency pattern (congener pattern), from which conclusions can be drawn about the causes.

In addition to the polychlorinated dibenzodioxins and dibenzofurans (PCDD / PCDF), there are dioxins with other halogen atoms attached to their benzene rings. The polybrominated dibenzodioxins and furans (PBDD / PBDF) are important. In contrast, polyfluorinated and polyiodinated dibenzodioxins and dibenzofurans are as good as not formed under practical conditions. All of these compounds are grouped under the generic term polyhalogenated dibenzodioxins and dibenzofurans (PXDD / PXDF). If all conceivable combinations are taken into account, the polychlorinated dibenzodioxins 75 and the polychlorinated dibenzofurans 135 comprise different individual substances, so-called congeners . If all possible combinations of congeners mixed with chlorine and bromine atoms are included, there are 1700 different dibenzodioxins and 3320 dibenzofurans.

Spellings

According to IUPAC , the basic structure of dioxins is called dibenzo [ b, e ] [1,4] dioxin, or dibenzo- p- dioxin for short, and that of furans is called dibenzofuran. The positions of the chlorine or halogen atoms (see figures at the top) are introduced to these designations, followed by their number and type (example: 1,2,4,6,8,9-hexachlorodibenzo [ b, e ] [1,4] dioxin).

A simplified notation is based on the IUPAC nomenclature and shortens dibenzo p dioxin with DD, dibenzofuran with DF from. The mixed halogenated 1,3,6,8-tetrabromo-2,7-dichlorodibenzo- p- dioxin is then written in abbreviated form as 1,3,6,8-Br 4 -2,7-Cl 2 -DD. In the literature, the congener 2,3,7,8-Cl 4 DD , which is particularly interesting because of its toxicity, is often abbreviated to 2,3,7,8-TCDD or TCDD.

According to another proposal, chlorinated dioxins (D) and furans (F) can be assigned a consecutive number in ascending order according to the number of their chlorine substituents. Thereafter 2,3,7,8-Cl 4 DD is designated as D 48 , 2,3,7,8-Cl 4 DF as F 83 . The groups with the same number of chlorine atoms ( homolog groups ) can also be named according to this system by adding a number for the degree of chlorination after the D or F. The group of the fourfold chlorinated dioxins becomes D4 (no blank), the group of the fivefold chlorinated furans becomes F5 . This system is sometimes used for labeling tables and chromatograms.

history

The first synthesis of octachlorodibenzodioxin was probably carried out in 1872. In the 1950s, 2,3,7,8-tetrachlorodibenzodioxin was shown to cause chloracne .

During the Vietnam War , the United States Armed Forces used dioxin-contaminated defoliant agents such as Agent Orange , which caused health problems for the Vietnamese people and their own soldiers. Reports of an increased number of malformations in newborns in the Vietnamese population and in the children of Vietnamese veterans, as well as an increased risk of cancer as a result of defoliation actions, are, however, controversial in the scientific literature. A recent analysis of existing studies concluded that parental exposure to Agent Orange did indeed induce malformations in children in a dose-dependent manner. The selection of the studies used there was criticized because many of them were out of date and had not undergone a peer review process. With the exception of spina bifida and anencephaly , no evidence has yet been provided that dioxin leads to congenital malformations .

Mass poisoning ( Yushō disease ) from rice oil contaminated with polychlorinated dibenzofurans and PCBs occurred in 1968 in Japan (Yusho) and 1979 in Taiwan (Yucheng).

With the escape of 2,3,7,8-tetrachlorodibenzodioxin from a reactor of the chemical plant Icmesa in Seveso, Italy on July 10, 1976 ( Sevesounglück ), the group of substances of dioxins became well known. The cause of the accident was overpressure in the production system caused by overheating. Days after the accident, birds and small animals died in the vicinity. Cases of chloracne were found in around 190 exposed persons . As a result of the accident, the houses of 40 families had to be demolished. After 25 years, an increased risk of death from some types of cancer and from diabetes in women was observed among those affected , while no increase has so far been ascertained for any type of cancer or the overall risk.

In the USA, the toxic waste scandals of Love Canal (from 1978) and Times Beach (from 1982) caused a sensation in the media.

Before 1968, more than 400,000 tons of slag from copper extraction were used under the trade name Kieselrot as a covering for sports fields and playgrounds in Germany. It was not until 1991 that it was discovered that silica red is heavily contaminated with polychlorinated dibenzodioxins and furans. Sports areas with a pebble red top layer may have been significant sources of dioxin for the surrounding area.

After the Stockholm Convention came into force in 2004, the emission of PCDD / PCDF into the environment must be reduced or prevented as far as possible by applying the best available techniques .

In June 1998 two employees of the Vienna Textile Research Institute were diagnosed with severe dioxin poisoning, and three other employees had elevated dioxin concentrations in their blood. The circumstances of the incident have not yet been clarified. In September 2004 the Ukrainian opposition politician Viktor Yushchenko was a victim of dioxin poisoning.

The DIOXIN Conference , an international scientific congress on dioxins and other long-lived organohalogens, has been held annually since 1980 .

properties

Dome model of the 2,3,7,8-TCDD

Dioxin and furan molecules are almost perfectly planar . In the case of the 2,3,7,8-substituted dioxins, the molecule resembles a flat, elongated rectangle with a length of 10  Å and a width of 3 Å. With the exception of the hydrogen atoms, no atom in 2,3,7,8-Cl 4 DD protrudes more than 0.018 Å from the molecular plane.

At room temperature, dioxins are colorless, crystalline solids. They are of low volatility, the saturation vapor pressure falling even further the more halogen atoms are contained in the molecule. Their solubility in water is extremely low; it decreases with increasing degree of halogenation and increases with increasing temperature. Dioxins dissolve reasonably well in organic solvents such as benzene , anisole and xylene . They are lipophilic (fat-soluble) substances and, due to their high octanol-water partition coefficient (K OW ), accumulate in adipose tissue, but also in sediments and soils. Their chemical persistence , for example against acids and bases, is very high.

Physical and chemical properties of selected dioxins
1-Cl 1 DD 2-Cl 1 DD 2,3-Cl 2 DD 2,3,7,8-Cl 4 DD Cl 8 DD
Melting point 105 ° C   163 ° C 305 ° C 330 ° C
boiling point 315 ° C   358 ° C 447 ° C 510 ° C
Saturation vapor pressure above the supercooled melt (25 ° C) 1.0 · 10 −1 Pa   9.3 · 10 −3 Pa 1.2 · 10 −4 Pa 2.8 · 10 −7 or 1.2 · 10 −7 Pa
Water solubility (25 ° C)   278,000-318,000 ng / L   8-200 or 690 ng / l 0.074 or 0.4 (20 ° C) ng / l
log K OW   5.00 5.60 6.80 and 6.64, respectively 8.20 and 8.60, respectively

Emergence

Except for research and analysis, dioxins are not specifically produced. There is no technical use of dioxins.

They arise as by-products in a large number of thermal processes, in the production of organochlorine chemicals or in any oxidation reactions of hydrocarbon compounds in the presence of chlorine compounds (e.g. sodium chloride NaCl). When organic (carbon-containing) compounds are burned in the presence of organic or inorganic chlorine compounds in a temperature range of 300–600 ° C (“dioxin window”, limited at the bottom by the association of the dioxin molecules, at the top by their dissociation ), dioxins can form. Incineration processes with possible dioxin formation are, for example, cremation in crematoria and waste incineration , which was one of the main causes of dioxin production until the 1980s. Technical measures, for example the installation of filters in waste incineration plants and post-combustion in the exhaust gas streams , can significantly reduce PCDD / PCDF emissions. However, the prevalence of such measures differs from country to country. In Germany, the emissions are regulated in the Federal Immission Control Act or the resulting ordinances for the implementation of the Federal Immission Control Act (BImSchV). With the ordinance on incineration plants for waste and similar flammable substances and the ordinance on cremation facilities , new limit values ​​have been introduced for industrial incineration plants and crematoriums. Compared to emissions from private furnaces , the dioxin pollution from newly approved waste incineration and cremation plants has therefore decreased significantly.

Up until the early 1990s, the exhaust gases from gasoline engines in motor vehicles and aircraft also contained polychlorinated (but also other polyhalogenated) dibenzodioxins and dibenzofurans. This was due to the leaded petrol added Verflüchtigungszusätze based on 1,2-dichloroethane or 1,2-dibromoethane , the lead deposits in the engine ( "bridging" of the spark plug ) through which, upon the combustion of the lead alkyls resulting lead oxides should prevent. It was not until the 19th ordinance on the Federal Immission Control Act (19th BImSchV) of January 17, 1992 that this source of dioxins was eliminated by prohibiting the addition of chlorine and bromine compounds as fuel additives.

Other industrial processes that can produce dioxins include:

The heat effect on polychlorinated phenols is particularly critical. These condense particularly easily in the presence of alkali via the phenolates to dioxin, as in the example of the Seveso poison 2,3,7,8-TCDD, formed from the sodium salt of 2,4,5-trichlorophenol (2,4,5- TCP):

Reaction scheme for the formation of 2,3,7,8-tetrachlorodibenzodioxin

Natural processes can also lead to the formation of dioxins, for example forest or steppe fires caused by lightning strikes, as well as microbial activities or volcanic eruptions. It is estimated that a forest fire produces around 20 ng of toxicity equivalents of dioxins per kg of biomass. Compared to anthropogenic emissions, natural sources only contribute to a small extent to the dioxin pollution of the environment.

During the microbial degradation of the wood builder lignin and humic acids , chlorinated phenols are formed, which can condense to dioxins under the decomposition conditions as well as in the event of fire.

In various house and industrial fires, too, PCDD / PCDF were found in the soot to such an extent that extensive renovation of the affected buildings was necessary. In these cases dioxin precursors, such as PCBs, or larger amounts of other potential precursors, for example PVC cable jackets, were present in the fire load. The concentration and congener distribution of the PCDD / PCDF in the soot varied depending on the fire conditions and the starting materials.

Emissions

Dioxins escape into the air from plants in the metal industry, from waste incineration plants and private chimneys. However, emissions have decreased significantly in recent years. This success is mainly due to the improved exhaust gas cleaning in the waste incineration plants. The - illegal - waste incineration in the chimney or in the garden accounts for the largest share of dioxin emissions today. The wild burning of one kilogram of waste pollutes the environment as much as the disposal of ten tons in a modern waste incineration plant.

Atmospheric emissions of dioxins and furans from industrial processes in the EU25
process Emissions proportion of
2004 2008
Metal industry and roasting or sintering plants for metal ore, plants for the extraction of ferrous and non-ferrous metals 575 g / year 47%
Manufacture and processing of metals 361 g
Organic chemical raw materials 202 g / year 17%
Chemical industry 6.6 g
Systems for the disposal or recycling of hazardous waste or municipal waste 178 g / year 15%
Waste and sewage management 52.9 g
Incinerators 163 g / year 13%
Energy sector 661 g
Plants for the production of cement clinker, lime, glass, minerals or ceramic products 63 g / year  5%
Mineral processing industry 42.6 g
Others  38 g / year 66.3 g  3%
total  1219 g / year 1190.4 g  100%

Improper recycling of electrical appliances can lead to significant emissions of dioxins. In Guiyu , the largest electronic waste recycling area in China, the highest dioxin concentrations ever measured were found in the atmosphere with up to 2765  pg / m 3 or 48.9 pg  TEQ / m 3 .

Emission reduction

Essential measures to reduce emissions of dioxins and furans are thermal decomposition at temperatures of over 850 ° C and a residence time of over two seconds, as well as preventing new formation ( de novo synthesis ) in the exhaust gas. Another primary measure is the best possible exhaust gas burnout, whereby the possibility of adsorption of the dioxins and furans on carbon-containing dusts is limited. Higher sulfur dioxide concentrations in the exhaust gas also prevent the formation of dioxins and furans, but are undesirable from the point of view of immission control.

Secondary measures to reduce emissions of dioxins and furans aim at their destruction or removal from the exhaust gas. Catalysts and catalytically active surface filters are used to destroy dioxins. It is separated from the exhaust gas by means of adsorbents and dust separation.

Gas scrubbers are at best conditionally suitable for separating dioxins and furans. Scrubber components and seals made of plastic can lead to the entrainment of dioxins and furans through adsorption and desorption ; permanent separation does not take place. If there are gas scrubbers in a multi-stage exhaust gas cleaning system, the devices for reducing dioxins and furans must already be in operation when starting up.

Environmental behavior

Course of concentration of PCDD in a sediment core of Esthwaite Water in Cumbria
Course of concentration of PCDF in a sediment core of Esthwaite Water in Cumbria

Dioxins are persistent (long-lived) and are mainly distributed in the environment via the air path, bound to dust particles . They can be detected ubiquitously , i.e. they occur all over the world in soils, bodies of water, sediments , plants, animals, people, etc.

The entry of dioxins and furans into the atmosphere occurs primarily with the smoke from combustion processes. The evaporation of molecules attached ( adsorbed ) or dissolved in water also plays a role. Dioxins and furans are distributed over a large area through the atmosphere ( long-distance transport ) so that they can even be found in environmental samples from remote regions. Low halogenated dioxins predominantly occur in the atmosphere in the gas phase, higher halogenated dioxins are mostly bound to aerosol particles. The quantitative ratio of gaseous to particle-bound molecules is given as 13 for Cl 4 DF and 0.05 for Cl 8 DF.

Degradation in the atmosphere only takes place in the case of gaseous dioxins and furans. Direct photolysis occurs through UV rays , and reactions with hydroxyl radicals are also important. The atmospheric degradation reactions are mainly subject to PCDDs substituted at the peri positions (1,4,6,9) and PCDFs substituted at positions 1 and 9. On the other hand, with increasing degree of halogenation, the susceptibility to these degradation mechanisms decreases.

As a discharge route from the atmosphere, dry deposition by settling (fall out) of particles predominates compared to wet deposition in a ratio of about 5: 1. In the case of wet deposition, rain out (particle scavenging) outweighs washing out (gas scavenging) .

Dioxins and furans find their way into bodies of water mainly through deposition from the atmosphere and with sewage . As lipophilic compounds, they are largely attached to colloids dissolved in the water such as humic substances , to organic particles floating (suspended) in the water, or to the lipophilic skin on the water. PCDD / PCDF freely dissolved in water can volatilize into the atmosphere, degradation by photolysis takes place directly on the water surface. Dioxins and furans bound to particles are mostly deposited in the sediments. Conclusions about historical emissions can be made on the basis of trends in concentrations in dated sediment cores over time. However, it must be noted that the congener pattern can change through various degradation processes (e.g. reductive dehalogenation ). The proportion of low-chlorinated PCDD / PCDF can therefore increase over longer periods of time. Nevertheless, on the basis of the low chlorinated PCDD that dominated before 1900, it can be concluded that during this period there was a large input from the dimerization of 2,4-dichlorophenol . Since around the 1960s, the inputs of PCDD and PCDF into Esthwaite Water in northern England have been declining (see graphics on the right). This is mainly due to technical measures in industry and in waste incineration.

The pollution of the soil is mainly due to atmospheric deposition, on meadows and fields the spreading of sewage sludge or pesticides may also have contributed. Dioxins and furans adsorb on the soil organic matter and are largely retained there. They are mainly found in the top five centimeters, and due to the low water solubility there is hardly any shifting into the depth. In addition to sediments, soils are the most important sink for PCDD / PCDF. The half-lives in the soil range from years to decades. Discharge or degradation processes, such as volatilization, photolysis on the soil surface, degradation by microorganisms and fungi or absorption in plants, are very slow. In laboratory tests, for example, the Dehalococcoides strain CBDB1 degraded 60% of 1,2,3-trichlorodibenzodioxin to 2-monochlorodibenzodioxin in 56 days, but this is not achieved in the environment. Due to soil erosion , adsorbed dioxins can be carried away to a significant extent.

Dioxins and furans get into or on plants mainly via the air, by diffusion from the gas phase or the mechanisms of dry and wet deposition already mentioned. They are mainly found in the leaves and needles. Herbivorous animals ingest dioxins through their food. Since they often eat small amounts of the soil particles, which are usually more heavily polluted than the plants, this can make a noticeable contribution to the total intake. Dioxins and furans are mainly stored in the liver and adipose tissue and accumulate more and more in the course of the food chain. In water, dissolved dioxins or dioxins bound to suspended matter are particularly readily available to small organisms , which is why they accumulate strongly in the food chains.

Exposure to individual foods and breast milk

Hens in free range to take dioxins and furans mainly by the pecking of soil particles. In eggs, due to their solubility in fat, these substances occur predominantly in the yolk , one third of which is fat. Since January 2005, applies to eggs EU a dioxin limit of 3 -wide pg TEQ dioxins / g fat or 6 pg TEQ / g fat for dioxins and dioxin-like PCBs. In random samples, eggs from free-range hens were usually more contaminated with dioxins than eggs from floor or cage systems. The limit values ​​are occasionally exceeded when kept outdoors.

In addition, farm animals can ingest dioxins through contaminated feed . In May 2010, several laying hen farms in Germany had to be closed after contaminated maize was processed into organic feed. In December 2010 contaminated samples of eggs and poultry meat were found again. The source of the dioxin contamination turned out to be the feed producer Harles und Jentzsch , who had used technical fats from biodiesel production for the production of animal feed fats . According to estimates by the Federal Government, up to 3000 tons of contaminated animal feed fat were produced and fed to laying hens, fattening pigs and fattening poultry.

The fat content in fish has a great influence on the load with lipophilic pollutants

Fish are often heavily contaminated with dioxins, especially fish with a high fat content. The EU limit values ​​(4 pg TEQ dioxins / g fresh weight or 8 pg TEQ the sum of dioxins and dioxin-like PCBs) are exceeded particularly frequently in fish from the Baltic Sea area. In Sweden and Finland with a derogation, after salmon , herring , river lamprey , trout , char and roe of vendace may be placed on the market, even if they exceed the EU dioxin limit values. Consumers need to be informed about the associated health risk. In addition, it must be ensured that the goods do not end up in other countries.

Since dioxins are very lipophilic (fat-soluble), they accumulate in humans and animals, especially in adipose tissue. Breast milk is often examined as an indicator for the dioxin exposure of humans , because due to the high fat content dioxins accumulate in it and samples are easy to get. Swedish scientists were able to detect dioxins in breast milk for the first time in 1984, and the Kiel Federal Institute for Milk Research found in 1985 that the dioxin guide values ​​for cow milk were often exceeded in breast milk. It was recommended that infants be breast-fed for no more than six months. As a result of legal regulations and the resulting technical measures, the overall exposure to dioxins has decreased significantly in Central Europe.

In 1988, the average PCDD / PCDF load in breast milk in urban areas of the EU was 29.5 pg I-TEQ per gram of milk fat . By 1993, exposure had dropped by a third to 19.2 pg I-TEQ per gram of milk fat. The Federal Institute for Risk Assessment (BfR) has published even more recent data for Germany: According to this, the average dioxin content in Germany in 1986 was 35.7 pg and fell to 6.3 pg WHO-PCDD / F-TEQ / g milk fat by 2009 . Although this value for infants also exceeds the daily intake value (TDI) calculated by the World Health Organization (WHO), WHO, BfR and the National Breastfeeding Commission advise breastfeeding without restrictions. At the same time, the Breastfeeding Commission recommends further reducing the pollutant content of breast milk.

toxicology

Intake and metabolism

Since dioxins are ubiquitous, their ingestion cannot be avoided. In humans, 90–95% of the absorption of dioxins occurs through food, especially through fatty animal foods such as dairy products, meat and fish, but also vegetables. In Switzerland, almost two thirds of this intake ( including PCBs ) is obtained through the consumption of dairy products and meat. In Sweden, the dietary intake is around 100 pg I-TEQ / day, half of which is due to the consumption of fish and seafood. The average dioxin intake of Americans today is around 1 pg TEQ / kg body weight and day in the same range. Infants ingest on average 35–53 pg TEQ / kg body weight per day. Thanks to a higher excretion rate and due to their growth, the dioxin levels in the tissue of infants are only about three times higher than in adults.

Dioxins can be absorbed through the lungs, especially if they are bound to fine dust . Humans typically ingest 2–6 pg I-TEQ daily, about 5% of total intake. When smoking a cigarette, about 0.1 pg I-TEQ PCDD / PCDF are produced, which is why heavy smokers absorb a little more through the lungs . Although absorption through the skin is possible, it only plays a role in the event of exceptionally high levels of dioxin.

In the body, absorbed dioxins and furans are attached to the lipids and lipoproteins of the blood and distributed further. They mainly accumulate in adipose tissue and in the liver . In humans, adipose tissue contains about 30 ng I-TEQ / kg. Dioxins stored in fat are biologically inactive, they are only released again when the fat is broken down. This is particularly important for the exposure of infants through breast milk.

The metabolism of dioxins in the liver occurs through reductive dehalogenation or as hydroxylation by the cytochrome P450 enzyme complex . Halogen atoms are split off via epoxidic intermediate stages and hydroxyl groups are introduced into the dioxin molecule. In a further step, glucuronic acid, for example, can be attached to a hydroxy radical . The degradation rate is lowest in the 2,3,7,8-substituted congeners , which increases their relative proportion in the body. Congeners with three or more halogen atoms per phenyl ring are also hardly degraded. Metabolized and unmetabolized dioxins are excreted in the faeces. The biological half-lives can vary greatly from species to species; for 2,3,7,8-Cl 4 DD they are 17–31 days in rats and 6–10 years in humans.

Recommendations and limit values

The determination of maximum levels is not based directly on toxicity, but "essentially on the unavoidable pollution of food by dioxins from the environment, the so-called background pollution ".

NOAEL values ​​were determined on the basis of animal experiments , from which various states and organizations have derived recommendations for the tolerable daily intake (TDI) of dioxins , taking into account a safety factor . In 1991 the World Health Organization recommended a TDI of 1 to 10 pg I-TEQ / kg body weight and day; in 1998 the recommended TDI was reduced to 1–4 pg I-TEQ / kg. A committee working on behalf of the EU Commission published a tolerable weekly intake (TWI) of 14 pg TEQ / kg in 2001, which corresponds to the lowered WHO TDI. In Germany, the intake of dioxins corresponds to the permissible intake: The Federal Institute for Risk Assessment assumes “a daily intake of 1–2 picograms WHO-PCDD / F-PCB-TEQ per kg body weight through food”.

Since 2006, the limit values ​​in individual foods have been set in the EU both as toxicity equivalents for dioxins and for the sum of the TEQ from dioxins and dioxin-like PCBs. The limit values ​​apply per gram of fat content (for fish per gram of muscle meat) and have therefore been since 2012:

  • 1 pg for pork
  • 1.75 pg for poultry
  • 2.5 pg for dairy products, chicken eggs, cattle and sheep
  • 3.5 pg for fish
  • 4.5 pg for liver

With a fat content in the egg yolk of 32% and an assumed yolk weight of 30 g, one should ingest up to 125 pg of dioxin with five eggs - as well as with almost 40 g of fish.

acute toxicity

Polychlorinated dibenzodioxins and -furans are very toxic, the 2,3,7,8-TCDD is sometimes referred to as "the most toxic compound produced by humans". In mice, the dose at which 50% of the animals die (so-called LD 50 ) is around 100 µg 2,3,7,8-TCDD / kg body weight. However, the toxic effects of TCDD can be very different, even for closely related animals; in hamsters only around 1,000 µg / kg are lethal, while it is extremely toxic for guinea pigs at around 1 µg / kg. The deadly limit dose for humans is not known, but it is significantly higher than for guinea pigs. In the chemical accident in Seveso, Italy in 1976, only birds and small animals died from the 2,3,7,8-tetrachlorodibenzo-p-dioxin (since then called "Sevesodioxin"). Chloracne , a severe form of chronic acne that can occur with acute dioxin poisoning, has been identified in around 190 people . Sevesodioxin levels in blood serum were up to 56  ppb . The highest value to date of 144 ppb was measured in the blood fat of a woman in Austria. When Viktor Yushchenko a concentration of 100 ppb was detected.

The toxic effect of dioxins is based on their binding to a cell protein that is widespread in animals and humans, the aryl hydrocarbon receptor (AhR). The dioxin binds to this receptor in the cell, the enzyme-substrate complex attaches itself to the DNA and thus triggers the increased formation of enzymes that break down foreign substances, in particular of cytochrome P450 monooxygenases. The strength of the bond and thus the toxicity of the substance depends on the particular dioxin or furan (number and position of the halogen atoms). The tendency to bind to the Ah receptor is greatest with the 2,3,7,8-substituted dioxins and furans.

Further mechanisms of action of dioxins and furans were discussed: their binding to the receptor for the epidermal growth factor (EGF), their agonistic effect on thyroid hormones and effects on the vitamin A metabolism .

Viktor Yushchenko with chloracne due to a poison attack

In humans, chloracne is the leading symptom of severe acute dioxin poisoning. It is triggered by skin contact with dioxins or by dioxin concentrations in the blood serum of more than 800 ng / kg. Damage to the liver disrupts the metabolism, which increases the levels of lipids, cholesterol and transaminases in the blood. In animal experiments, dioxins and furans lead to persistent nausea, vomiting and loss of appetite. There is severe weight loss, the " wasting syndrome ". In terms of neurological disorders, they can cause nausea, sleep disorders, headaches, irritability, depression and a general change in the psyche. At higher doses, changes in the thyroid can trigger immunotoxic effects, to which humans appear to be less susceptible than some mammals.

Chronic toxicity

The chronic toxicity of lower PCDD / PCDF concentrations includes their foetotoxic and teratogenic ( teratogenic ) effects. In mice, even very low doses of 1 ng / kg body weight / day lead to the formation of cleft palates or damage to the kidney and thyroid. No teratogenic effects occurred in monkeys at this dose, but the number of miscarriages was increased. An increase in the concentration of certain enzymes ( enzyme induction ) through binding to the Ah receptor is possible in rodents even at low doses. Dioxins and furans have no direct genotoxic effects. They can accelerate the development of cancer from a previously damaged cell (tumor-promoting effect). The 2,3,7,8-TCDD is considered to be one of the most potent tumor-promoting substances. In rats, dioxins can cause liver cancer as well as carcinomas of the lungs, thyroid and adrenal glands. It has not been conclusively established whether dioxins can cause cancer in humans. Various studies found an increased incidence of leukemia , tumors of the respiratory organs and the gall bladder, and soft tissue sarcoma in highly exposed persons . The case numbers of the individual studies were too small for a statistically reliable statement, and the effects of other chemicals and smoking were not taken into account. Expert committees of the World Health Organization (WHO), the American health authorities and the US Environmental Protection Agency (EPA) classify 2,3,7,8-TCDD as carcinogenic to humans. Recent studies on the eggs of quail ( Coturnix japonica), pheasants and white leghorn chickens demonstrate the very different species-dependent toxicity of TCDD, 2,3,4,7,8-pentachlorodibenzofuran (PeCDF) and TCDF.

Toxicity equivalents

Since the toxicity of the individual dioxin and furan congeners is different, the system of toxicity equivalents (TEQ) was introduced to better assess the hazardousness of “dioxin mixtures”. The concept was developed in the 1980s in order to be able to assess the pollution of a New York office building contaminated with PCDD, PCDF and PCB after a transformer fire. The toxicity of 2,3,7,8-TCDD, the most toxic compound among the polychlorinated dibenzodioxins, is arbitrarily set as 1. The other congeners receive, depending on their toxicity and the applied calculation model, toxicity equivalence factors (TEF) between 0.0001 and 1. A dioxin / furan with a toxicity equivalent of 0.5 is regarded as half as toxic as the 2,3,7,8 -TCDD.

2,3,7,8-substituted PCDD.svg
2,3,7,8-substituted PCDF.svg


Structures of 2,3,7,8-substituted PCDD and PCDF
Toxicity Equivalence Factors (TEF) according to different systems
Congener BGA 1985 NATO (I-TEF) 1988 WHO 1998 WHO 2005
2,3,7,8-Cl 4 DD 1 1 1 1
1,2,3,7,8-Cl 5 DD 0.1 0.5 1 1
2,3,7,8-subst. Cl 6 DD 0.1 0.1 0.1 0.1
1,2,3,4,6,7,8-Cl 7 DD 0.01 0.01 0.01 0.01
Cl 8 DD 0.001 0.001 0.0001 0.0003
2,3,7,8-Cl 4 DF 0.1 0.1 0.1 0.1
1,2,3,7,8-Cl 5 DF k. A. 0.05 0.05 0.03
2,3,4,7,8-Cl 5 DF 0.01 0.5 0.5 0.3
2,3,7,8-subst. Cl 6 DF 0.01 0.1 0.1 0.1
2,3,7,8-subst. Cl 7 DF 0.01 0.01 0.01 0.01
other Cl 7 DF 0.001 0 0 0
Cl 8 DF 0.001 0.001 0.0001 0.0003
other PCDD and PCDF 0.01 0 0 0

The total TEQ value of a mixture of dioxins and furans is calculated by multiplying the concentrations of the individual PCDD or PCDF congeners by their toxicity equivalence factor (TEF). The values ​​obtained in this way are added up to form the TEQ value.

Historically, different toxicity equivalence factors exist. The values ​​of the NATO research group Committee on the Challenges of Modern Society (I-TEF) are the most widespread and, for example, prescribed in the European Union for the calculation of dioxins and furans from waste incineration plants and waste co-incineration plants. In Germany, dioxins and furans must also be determined in power plants with I-TEF values ​​if the power plants use solid or liquid fuels.

The latest classification comes from the WHO in 2005. The Federal Institute for Risk Assessment warned against adopting the WHO-TEF from 2005, as these are not based on any new toxicological findings and the lowering of several factors would result in a higher limit value if the limit value remained unchanged Dioxins and furans in food would be permitted. In addition, it would no longer be possible to compare measured values ​​with historical series of measurements. Since 2012, the maximum levels in food have been based on the WHO-TEF from 2005, with the TEQ being adjusted.

The system of toxicity equivalents is only used for PCDD / PCDF and for some PCBs which are stereochemically similar to 2,3,7,8-TCDD (“dioxin-like”, dl-PCBs). In the case of bromine-containing or mixed halogenated congeners, there is still too little data for their classification. In terms of their toxicity, they are comparable to chlorinated dioxins and furans. They belong to the dioxin-like compounds (DLC), i.e. the dioxin-like compounds for which a relative potency (REP) proves the danger in relation to 2,3,7,8-TCDD. The DLC also includes representatives of polychlorinated naphthalenes ( PCN ), methyl-substituted PCDD / PCDF or polycyclic aromatic hydrocarbons ( PAH ).

In the case of biological samples, only the 2,3,7,8-substituted PCDD / PCDF (17 congeners) are usually taken into account for the calculation of the TEQ. In the international calculation methods, the undetectable congeners are sometimes also taken into account with the value of half their detection limit and the total value is given as ITEQ (½ NWG). In addition to specifying the concentration in TEQ, another method of determination is used in which the total sum of all detected four to eightfold chlorinated dioxins and furans is calculated. In both calculations (TEQ and total sums), the monochlorinated to triple chlorinated dioxins and furans are not taken into account, as their toxicological mechanism of action is not comparable with that of the more highly chlorinated dioxins. As a rule, these connections are therefore not determined.

A study by the European Commission on improvements to the directive on the incineration and co-incineration of waste (2000/76 / EC) recommended in 2007:

  • to introduce a measurement specification for dioxin-like PCBs in order to derive a suitable limit value from the results;
  • to introduce a uniform rule for the inclusion of measured values ​​that are below the limit of quantification;
  • to consider a switch from I-TEF (1988) to WHO-TEF (2005), provided that the calculation factors must always be specified and taking into account the resulting lower measured values ​​and the fact that they are no longer comparable with previous measured values.

The European Commission has made in converting the waste incineration and Abfallmitverbrennungsrichtlinie in the industrial emissions directive (2010/75 / EU) no changes to the existing requirement to apply NATO (I-TEF) values in the year of 2010. The German Federal Council has proposed in place of the previously valid NATO (I-TEF) values on 14 December 2012 in power plants, waste incinerators and garbage mitverbrennenden cement and lime plants, WHO-TEF 2005 and the factors for twelve dioxin-like future PCB introduce.

treatment

In the case of acute poisoning, there is no known possibility of rapid detoxification. Because they are stored in the body's adipose tissue, they cannot be eliminated or can only be eliminated slowly, even through blood washing. Even for the administration of paraffin oil and medical alcohol proposed in the medical literature, there is so far no proof of success, but more recent findings and comparisons with other pollutants and poisons make this approach appear promising. Successful therapy would therefore be possible by administering certain fat substitutes , such as. B. Olestra . These fat substitutes are not absorbed by the intestine, but when they pass through the intestine they dissolve some of the dioxins present in the body, which are also eliminated.

Data and measuring programs

The Federal Environment Agency (UBA) operates the federal and state dioxin database in collaboration with the Federal Institute for Risk Assessment (BfR) and the Federal Office for Consumer Protection and Food Safety (BVL). The measurement programs are divided into compartments, which can be divided into the following categories: soil, air, biota, water, waste, food and human samples. As far as possible, statements about the current state of contamination of “material” with dioxins and PCBs are to be made based on the compartment and location. Measurement programs have also been carried out in Austria (cow's milk) and Switzerland (soil) in recent years. Between 2004 and 2007, the EU project MONARPOP (of the Alpine countries Germany, Italy, Austria and Slovenia and Switzerland Mon nitoring N etwork in the A lpine R egion for P ersistent and other O rganic P ollutants) performed. For PCDD / PCDF and other substances from the dirty dozen, the long-distance transport to remote alpine regions, the primary source areas, the extent of pollution in the alpine region and the accumulated deposits in mountain forests as well as the biological effects of the measured pollution were examined.

Analytics

The trace analysis of the dioxins is complex and is carried out by specialized analysis laboratories. Sampling and processing depend on the type of sample examined. The dioxin content can be determined in food and animal feed, but also in air, exhaust gas, ash, water, sewage sludge, soil, plants, blood, fatty tissue and textiles. The EU regulations 278/2012 (animal feed) and 252/2012 (food) describe the complex trace analysis determination of dioxins. A distinction is made here between two analytical methods. On the one hand, the classically used capillary gas chromatography can be carried out. The examination with this method used to take usually between 2 and 3 weeks and was accordingly expensive. Today the processing time in routine laboratories is approx. 2-3 working days. The price of the analysis has fallen significantly due to the optimization of the method and is in the order of magnitude between 250 and 450 € / sample. The screening method using bioassays is somewhat cheaper, although it cannot differentiate between the individual congeners. Positive samples from the bioassay screening must therefore always be confirmed again using a reference method.

Gas chromatography

When preparing and extracting samples for gas chromatography, a distinction is made between liquid / liquid distribution and solid / liquid extraction. For the latter, Soxhlet extraction has long been used. Extraction with supercritical fluids (SFE) has gained in importance in recent years . For the dioxin extraction, mainly carbon dioxide or nitrous oxide is used at pressures of several hundred bar .

In order to separate co-extracted substances that would interfere with further analysis, a matrix separation (clean-up) is often necessary before the actual determination . To do this, the extract can be purified using a liquid chromatography column, gel permeation chromatography is also used for this purpose. With the help of capillary gas chromatography , the individual congeners of the PCDD and PCDF can be separated from one another. These then have to be multiplied by the respective toxicity equivalence factors (TEF) in order to be able to evaluate the total exposure of the sample. A mass spectrometer is used as standard for detection . High resolution mass spectrometers should preferably be used for reliable identification. Also ion trap systems that operate in MS / MS mode, can provide reliable information. In any case, certification of the laboratory analysis through regular participation in round robin tests for quality assurance is required. Electron capture detectors (ECD) or flame ionization detectors (FID) can only be used for initial, orienting overview analyzes. Isotope- labeled 13 C -dioxin congeners are often used as internal standards for reliable quantification . They are added to the samples in a known amount as early as possible in the work-up process, go through further work-up and appear in the chromatogram at the same time as the dioxins to be analyzed.

Bioassay

This is a cell-based in vitro test, such as B. the so-called CALUX ® -Assay. CALUX represents c hemically a ctivated lu ciferase generic e x pression. This assay is based on a Ah receptor ( a romatic h ydrocarbon) -mediated expression of a luciferase -Genes in genetically modified rat hepatoma cells. If dioxins or dioxin-like substances get into the cell, they bind to the Ah receptor. This complex migrates into the cell nucleus and binds there to the DNA. This enables the luciferase gene to be read and thus the luciferase to be formed. After adding the substrate luciferin , the cells begin to glow. Highly toxic compounds such as 2,3,7,8-tetrachlorodibenzodioxin (TCDD) bind more strongly to the receptor and thus trigger a stronger cell response. The light intensity measured with a luminometer is therefore directly parallel to the toxicity of the dioxins contained in the sample. Since the bioassay reacts specifically to dioxins / furans and dioxin-like PCBs, complex sample preparation is not necessary. Usually a simple liquid / liquid extraction with hydrophobic solvents and a subsequent solid phase extraction are carried out. Positive tests always require confirmation via a recognized reference method (e.g. HR-GC-MS, GC-MS / MS ).

literature

  • Karlheinz Ballschmiter , Reiner Bacher: Dioxins: chemistry, analysis, occurrence, environmental behavior and toxicology of halogenated dibenzo-p-dioxins and dibenzofurans VCH, Weinheim / New York / Basel / Cambridge / Tokyo 1996, ISBN 3-527-28768-X .
  • Otto Hutzinger , Margot Fink, Heinz Thoma: PCDD and PCDF: Danger to humans and the environment? In: Chemistry in Our Time . tape 20 , no. 5 , October 1986, p. 165–170 , doi : 10.1002 / ciuz.19860200505 .
  • Heidelore Fiedler: Existing dioxin inventories worldwide and new methodology for creating comparable and complete emissions inventories . In: Environmental sciences and pollutant research . tape 13 , no. 2 , March 2001, p. 88-94 , doi : 10.1007 / BF03038644 .
  • Heinz Köser: Dioxins - a task for environmental technology . In: Chemical Engineer Technology . tape 70 , no. December 12 , 1998, pp. 1517-1525 , doi : 10.1002 / cite.330701205 .
  • Dieter Lenoir, Stefan Leichsenring: Concepts and methods of environmental protection: the example of dioxins . In: Chemistry in Our Time . tape 30 , no. 4 , August 1996, p. 182-191 , doi : 10.1002 / ciuz.19960300404 .
  • Peter Luthardt: Dioxin inventories In: WLB water, air and soil. 6/2002, pp. 60-62.
  • Karl-Heinz van Pée: Dehalogenation of polyhalogenated dioxins . In: Angewandte Chemie . tape 115 , no. 32 , August 2003, p. 3846-3848 , doi : 10.1002 / anie.200301662 .
  • Dieter Schrenk: Toxicity of Dioxins. Ultra poisons or scare tactics? In: Biology in Our Time . tape 41 , no. 3 , June 2011, p. 174–180 , doi : 10.1002 / biuz.201110449 .

Web links

Commons : Polychlorinated Dibenzodioxins  - Collection of Pictures, Videos and Audio Files
Commons : Polychlorinated Dibenzofurans  - Collection of Pictures, Videos and Audio Files

Individual evidence

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