15. Sources and Environmental Impact of PCDD/PCDF
by Dr. Heidelore Fiedler
Polychlorinated dibenzo-p-dioxins (PCDD) and polychlorinated dibenzofurans (PCDF) are environmental contaminants detectable in almost all compartments of the global ecosystem in trace amounts. These compound classes in particular have caused major environmental concern. In contrast to polychlorinated biphenyls (PCB), polychlorinated naphthalenes (PCN), and other polychlorinated pesticides such as DDT, pentachlorophenol (PCP) or others, PCDD/PCDF never were produced intentionally. They are formed as by-products of numerous industrial activities and all combustion processes (Fiedler et al. 1990).
The term dioxins" refers to 75 congeners of polychlorinated dibenzo-p-dioxins (PCDD) and 135 congeners of polychlorinated dibenzofurans (PCDF). Amongst these 210 compounds, 17 congeners can have chlorine atoms at least in the positions 2, 3, 7, an 8 of the parent molecule. These 17 2,3,7,8-substituted congeners are toxic to many laboratory animals, persistent towards chemical, biological, and physical attack, and thus accumulate in the environment and in organisms, such as animals and humans. The 2,3,7,8-TCDD (2,3,7,8-Cl4DD) also named Seveso-dioxin" is considered to be the most toxic man-made compound: Besides the anthropogenic sources, an enzyme-mediated formation of PCDD and PCDF from 2,4,5- and 3,4,5-trichlorophenol has been demonstrated in vitro (Öberg et al. 1990, Wagner et al. 1990).
First risk assessments only focused on the most toxic congener, the 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-Cl4DD = 2,3,7,8-TCDD). Soon it was recognized, though, that all PCDD/PCDF substituted at least in position 2, 3, 7, or 8 are highly toxic and thus, major contributors to the overall toxicity of the dioxin mixture. In addition, despite the complex composition of many PCDD/PCDF containing sources", only congeners with substitutions in the lateral positions of the aromatic ring, namely the carbon atoms 2, 3, 7, and 8, persist in the environment and accumulate in food-chains.
Almost all 210 individual congeners have been identified in emissions from thermal and industrial processes and consequently PCDD/PCDF are found as mixtures of individual congeners in environmental matrices such as soil, sediment, air, and plants and lower animals. PCDD/PCDF, particularly the higher chlorinated, are poorly soluble in water, have a low volatility, and adsorb strongly to particles and surfaces (high KOC). Thus, PCDD/PCDF can hardly be identified in water and are immobile in soils. Especially, the 2,3,7,8-chlorine substituted PCDD/PCDF are extremely stable in the environment and bioaccumulate in fatty tissues (high KOW) of animals and humans.
PCDD and PCDF produce a spectrum of toxic effects in animals; however, most information is available on 2,3,7,8-Cl4DD (TCDD) only. Most toxicity data on TCDD result from high dose oral exposures to animals. There is a wid range of difference in sensitivity to PCDD lethality in animals. The signs and symptoms of poisoning with chemicals contaminated with TCDD in humans are similar to those observed in animals. Dioxin exposures to humans are associated with an increased risk of severe skin lesions (chloracne and hyperpigmentation), altered liver function and lipid metabolism, general weakness associated with drastic weight loss, chnages in activitie of vrious liver enzymes, depression of the immune system, and endocrine and nervous system abnomalities. 2,3,7,8-TCDD is a potent teratogenic and fetotoxic chemical in animals, a potent promoter in rat liver carcinogenesis. TCDD also causes cancers of the liver and other organs in animals.
The most important epidemiological studies for the evaluation of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (2,3,7,8-Cl4DD or 2,3,7,8-TCDD) are four cohort studies of herbicide producers (one each in the United States and the Netherlands, two in Germany). These studies involve the highest exposures to 2,3,7,8- Cl4DD. The cohort of residents in a contaminated area from Seveso, Italy is well known, but the exposures at Seveso were lower and the follow-up shorter than those in the industrial settings. Most of the four industrial cohorts include analyses of sub-cohorts considered to have the highest exposure and/or longest latency. Overall, the strongest evidence for the carcinogenicity of 2,3,7,8-Cl4DD is for all cancers combined, rather than for any specific site. On the basis of theses studies, teh Interantional Agency for Research on Cancer (IARC) concluded that there is limited evidence in humans for the carcinogenicity of 2,3,7,8-Cl4DD. vThere was inadequate evidence in humans for the carcinogenicity of PCDD other than 2,3,7,8- Cl4DD.
For PCDF, two incidents, each involving about 2,000 cases, occurred in which people were exposed to sufficient PCB and PCDF to produce symptoms (Yucheng and Yusho accidents). Fatal liver disease is 2-3 times more frequent than national rates in both cohorts. In teh Yusho cohort from Japan, at 22 years of follow-up, there is a three-fold excess of liver cancer mortality in men, which was already detectable and even higher at 15 years of follow-up. In teh Yucheng cohort, Taiwan, after 12 years of follow-up, there is no excess of liver cancer mortality. Based upon these data, IARC concluded that there is inadequate evidence in humans for the carcinogenicity of PCDF.
PCDD: In a number of experiments with rats and mice in which 2,3,7,8-Cl4DD was administered, increases in the incidence of liver tumours was consistently found in both males and females. vIn addition, tumours were increased at several other sites in rats, mice and Syrian hamsters, but these effects were dependent upon the species, sex and route of administration of 2,3,7,8- Cl4DD. Although the doses resulting in increased tumour incidence in rodents are extremely low, they are very close to doses that are toxic in the same species. These data led to the conclusion that there is sufficient evidence in experimental animals for the carcinogenicity of 2,3,7,8- Cl4DD. Evaluation of much smaller databases led to the conclusion that there is limited evidence in experimental animals for the carcinogenicity of a mixture of 1,2,3,6,7,8- and 1,2,3,7,8,9-Cl6DD and that there was inadequate evidence for the carcinogenicity in experimental animals of 2,7-Cl2DD, 1,2,3,7,8-Cl5DD and 1,2,3,4,6,7,8,-Cl6DD.
PCDF: There are no long-term carcinogenicity studies on PCDF, but some tumour promotion studies were evaluated in which rats and mice were exposed to some of the congeners following short duration exposure to known carcinogens. It was concluded that there is inadequate evidence in experimental animals for the carcinogenicity of 2,3,7,8-Cl4DF, but there is limited evidence in experimental animals for the carcinogenicity of 2,3,4,7,8-Cl5DF and 1,2,3,4,7,8-Cl6DD.
The toxicity of 2,3,7,8-Cl4DD segregates with the cytosolic aryl (aromatic) hydrocarbon receptor (AhR), and the relative toxicities of other PCDD and PCDF congeners is associated with their ability to bind to the receptor, which occurs in all rodent and human tissues. The AhR binding affinities of 2,3,7,8-Cl4DF, 1,2,3,7,8- and 2,3,4,7,8-Cl5DF are in the same order of magnitude as that observed for 2,3,7,8-Cl4DD. PCDD with at least three lateral chlorine atoms bind with some affinity to the AhR. Current evidence is that most, if not all, biological effects of 2,3,7,8-Cl4DD and other PCDD arise from an initial high affinity interaction with the AhR and it appears that the biochemical and toxicological consequences of PCDF exposure are the result of a similar mode of action. The limited carcinogenicity data available for congeners other than 2,3,7,8-Cl4DD indicate that carcinogenic potency is also proportional to AhR affinity. Based on this evidence, all PCDD and PCDF are concluded to act through a similar mechanism and require an initial binding to the AhR. Binding of 2,3,7,8-Cl4DD to the AhR results in transcriptional activation of a battery of 2,3,7,8-Cl4DD-responsive genes, but currently no responsive gene has been proven to have a definitive role in its mechanism of carcinogenesis.
Taking all of the evidence into consideration, the following evaluations were made by IARC:
Many regulatory agencies developed so-called Toxicity Equivalency Factors (TEF) for risk assessment of complex mixtures of PCDD/PCDF (Kutz et al. 1990). The TEF are based on acute toxicity values from in vivo and in vitro studies. This approach is based on the evidence that there is a common, receptor-mediated mechanism of action for these compounds. However, the TEF approach has its limitations due to a number of smplifications. Although the scientific basis cannot be considered as solid, the TEF approach has been developed as an administrative tool and allows to convert quantitative analytical data for individual PCDD/PCDF congeners into a single Toxic Equivalent (TEQ). TEF particularly aid in expressing cumulative toxicities of complex PCDD/PCDF mixtures as one single TEQ value. Today, almost all literature data are reported in I-TEQ.
It should be noted that TEF are interim values and administrative tools. They are based on present state of knowledge and should be revised as new data gets available. Todays most commonly applied TEFs were established by a NATO/CCMS Working Group on Dioxins and Related Compounds as International Toxicity Equivalency Factors (I-TEF). However, in 1997, a WHO/IPCS working group re-evaluated the I-TEFs and established a new scheme. A comparison of the two schemes is shown in Table 1.
Table 1: Toxicity Equivalency Factors for PCDD/PCDF (Kutz et al. 1988, WHO 1997)
Human exposure to background contamination with PCDD/PCDF is possible b several routes:
In 1990, a WHO working group concluded that 90% of the daily dioxin intake (from background contamination) results from ingestion. Especially, foodstuffs of animal origin are rsponsible for the daily intake of approximately 2 pg TEQ/(kg bw·d). All other foodstuffs, especially the non-fatty" ones, are of minor importance in terms of PCDD/PCDF intake. They are either of plant origin or do not have a high potential for bioaccumulation of lipophilic componds. Due to many measures to reduce emissions of PCDD/PCDF into the environment, reduction of PCDD/PCDF contamination in food was observed. As a consequence, the daily intake via food decreased: Whereas in Germany in 1991, the average daily intake was 127.3 pg TEQ/(kg bw·d), the actual daily intake for an average German adult is estimated to 69.6 pg TEQ/(kg bw·d). The strongest decline was observed for fish. In 1991, fish contributed for ca. 30% of the daily intake (same percentage as for dairy and meat products), today only 10% of the daily intake was due to fish.
Although no adverse health effects could be causally linked so far with background exposures of PCDD/PCDF in human milk, for reasons of preventive health care, the relatively high exposure of breast-fed infants must still be considered a matter of concern. Analyses of more than 1,000 individual human milk samplesfrom nursing mothers in Northrhine Westfalia (Germany) revealed that the mean PCDD/PCDF concentration decreased from 34 pg I-TEQ/g milkfat in 1989 to 14.2 pg I-TEQ/g milkfat in 1996. Despite this decline of 60%, the PCDD/PCDF daily intake for babies is 68 pg I-TEQ/kg bw·d), which is almost 70-fold above the TDI of 1 pg TEQ/(kg bw·d) for an adult.
Since the first overview on formation and sources of PCDD/PCDF was published in 1980 (Esposito et al. 1980), several updates are available in the international literature. The findings can be summarized as follows (Hutzinger and Fiedler 1993):
Primary sources of environmental contamination with PCDD/PCDF in the past was due to production and use of chloroorganic chemicals, including the pulp and paper industry. In wet-chemical processes the propensity to generate PCDD/PCDF during synthesis of chemical compounds decreases in the following order:
Chlorophenols < Chlorobenzenes < Aliphatic chlorinated compounds < Inorganic chlorinated compounds
Factors favorable for the formation of PCDD/PCDF are high temperatures, alkaline media, presence of UV-light, and presence of radicals in the reaction mixture/chemical process (Hutzinger and Fiedler 1991, 1993). An overview on dioxin concentrations in chemicals is given in Table 2. As can be seen the concentrations can vary by several orders of magnitude.
Table 2: PCDD/PCDF concentrations in chemical products
|PCP||up to 2320|
|PCP-Na||up to 450|
|PCB - Clophen A 30||11|
|PCB - Clophen A 60||2179|
|Hostaperm Violet RL||1.2|
Changes in the industrial processes resulted in reduction of PCDD/PCDF concentrations in the products: e.g. an estimate for Germany says that until 1990 about 105 g I-TEQ have been introduced through use of the dye pigment Violet 23 (chloranil prodcued by old process as intermediate). Application of a new process via hydroquinone will reduce the annual input to about 3 g I-TEQ (BGA/UBA 1993).
In Germany there exist exclusively sulfite mills which presently do not use molecular chlorine. Dioxin levels detected in German pulp were below 0.1 ng TEQ/kg d.m. (BGA/UBA 1993). The analysis of imported sulfate (Kraft) pulps gave concentrations in the range between 0.2 and 1.3 ng TEQ/kg d.m. Presently the import of Kraft pulp to Germany stands at 3 million tons, so that the total import of dioxins via Kraft pulp is between 0.6 and 3.9 g I-TEQ. Dioxin levels in paper products from fresh fibres generally has less than 1 ng TEQ/kg d.m. In recycling paper, however, average dioxin concentrations are between 5 to 10 ng TEQ/kg.
Whereas in the past, the chemical industry and to a lesser extent the pulp and paper industry were considered to be the main source of dioxins and also the cause of today's contaminated sites in Germany, todays dioxin input is due to thermal processes. There is still a considerable focus on waste incineration but based on the requirements set in the 17th Ordinance of the Federal Ambient Air Control Act, the annual input from MSWI via exhaust gases of about 400 g TEQ per year in 1988/89 is reduced to less than 4 g TEQ since 1997.
Table 3. PCDD/PCDF Trends in MWI Emissions
Concentration (ng I-TEQ/m³)
Flux (mg I-TEQ/h)
|MSWI of the 1970s||50||5|
|MSWI around 1990||5||0.5|
The process by which PCDD/PCDF are formed during incineration are not completely understood nor agreed upon. Three possibilities have been proposed to explain the presence of dioxins and furans in incinerator emissions:
From the knowledge gained from MSWIs it can be concluded that PCDD/PCDF can be formed in other thermal processes in which chlorine-containing substances are burnt together with carbon and a suitable catalyst (preferably copper) at temperatures above 300 °C in the presence of excess air or oxygen. Preferentially dioxin formation takes place in the zone when combustion gases cool down from about 450 °C to 250 °C (de novo synthesis). Possible sources of the chlorine input are PVC residues as well as chloroparaffins in waste oils and inorganic chlorine. An overview on combustion sources known to generate and to emit PCDD/PCDF is shown in Table 4.
Table 4: PCDD/PCDF combustion sources
|Waste incineration:||Municipal solid waste, clinical, hazardous waste, sewage sludge|
|Steel industry:||Steel mills, sintering plants, hot-strip mills|
|Recycling plants:||Non-ferrous metals (melting, foundry; Al, Cu, Pb, Zn, Sn),|
|Energy production:||Fossil fuel power plants, wood combustion, landfill gas|
|Traffic:||Automobiles (negative for aircrafts)|
|Home heating:||Coal, oil, gas, wood|
|Accidents:||PCB fires, fires in buildings, forest fires, volcanic eruptions)|
In April 1998, the United States Environmental Agency (US-EPA) published the national dioxin inventory (Table 5). The central estimate for all sources into the atmosphere was 2,745 g I-TEQ of PCDD/PCDF (range: 1,026-7,541 g I-TEQ) with waste incineration as the major sector of dioxin emissions. The USA does not quantify emissions from the ferrous industry which together with the non-ferrous industries are the major dioxin sources in Europe. In Table 6, emissions to land, water and with the products are compiled.
Table 5: PCDD/PCDF inventory to air, USA 1995
|Municipal waste incineration||
|Hazardous waste incineration||
Medical waste/pathological incineration
|Sewage sludge incineration||
|Vehicle fuel combustion unleaded||
|Wood combustion residential||
|Coal combustion industrial/utility||
|Oil combustion industrial/utility||
|Other High Temperature Sources|
|Cement kilns (haz. waste burning)||
|Cement kilns (non-haz. waste burning)||
|Kraft recovery boilers||
|Uncontrolled Comb: Forest, straw||
|Ferrous metal: Sintering, Coke, etc.|
|Non-ferrous metal smelting/refining|
Table 6: PCDD/PCDF to Water, Land and Products, Reference Yr.1995. Concentrations in g TEQ/a (NEG = negligible, NA = Not analyzed)
|Bleached pulp, paper mills||19.5||1.4||24.1|
|Dioxazine dyes+ pigments||NEG||NEG||0.36|
Dioxin reservoirs are present as sewage sludge, compost, and liquid manure which can be used for fertilization in agriculture and gardens. A compilation of German data is given in Table 7. A first survey of German sewage sludges where potentially contaminated sludges should be targetd gave a mean concentration of 202 ng TEQ/kg d.m.; in 1990, most sludges were in the range 50-60 ng TEQ/kg d.m. The legal limit concentration for application on agricultural land is 100 ng I-TEQ/kg d.m. Composting of the total organic fractionfrom municipal waste colection results in a highly contaminated compost, not suitable for application in house gardens or in agriculture (mean concentration: 38 ng TEQ/kg d.m.). Compost from biowaste, kitchen wastes, or green wastes give better qualities in the range of 14 ng I-TEQ/kg d.m. Such a mean value, however, is close to the guideline concentration of 17 ng I-TEQ/kg d.m.
Table 7: PCDD/PCDF in sewage sludge and compost
|Sewage Sludge:||Limit value:||
100 ng I-TEQ/kg dm
202 ng I-TEQ/kg dm
50-60 ng I-TEQ/kg dm
17 ng I-TEQ/kg dm
38±22 ng I-TEQ/kg dm
14±9 ng I-TEQ/kg dm
So far, hardly any country did a reservoir inventory for PCDD/PCDF. First attempts, see Table 6. In other words, there is almost no knowledge about the total amounts of PCDD/PCDF present in sinks such as sediments of harbors, rivers, lakes, and oceans, landfills, contaminated soils from (chemical) production sites. Although these reservoirs may be highly contaminated with PCDD/PCDF, the chemical-physical properties of these compounds imply that dioxins and furans will stay absorbed to organic carbon of soils or other particles. On the other hand, mobilisation can occur in the presence of lipophilic solvents (Þ leaching into deeper layers of soils and/or groundwater) or in cases of erosion or run-off by rain from topsoil (Þ translocation into the neighborhood). Experience has shown that PCDD/PCDF transport due to soil erosion and run-off does not play a major role for environmental contamination and human exposure (Fiedler 1995).
Other reservoirs include the former use of PCDD/PCDF-contaminated products such as 2,4,5-T (2,4,5-trichlorophenoxyacetic acid), polychlorinated biphenyls (PCB), and pentachlorophenol/-phenate (PCP/PCP-Na). Although there are estimates of the total amount of these compounds produced for various purposes, it seems to be impossible to deduce from these numbers a quantitative impact of PCDD/PCDF to the environment or humans (Fiedler 1995).
During the last years there is a growing recognition of the importance of aerial transport of PCDD/PCDF. Ambient air data from Germany, the United Kingdom and Japan showed that PCDD/PCDF exhibit seasonal trends with higher concentrations in the winter months and lower levels during summer. Comparative measurements by Wallenhorst et al. (1995) have shown that in terms of I-TEQ approximately the same amount of PCDD/PCDF is found in the gas-phase and bound to particles.
Many current combustion processes are significant sources of polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans (PCDD/PCDF) in the environment. Once emitted into the air, PCDD/PCDF can be transported long distances via the atmosphere and, thus, can be detected in remote areas with no known major point sources. Ambient air concentrations and deposition data for Germany are shown in Table 8 and Table 9. It can be seen that measures to reduce dioxin emissions from e.g. municipal solid waste incinerators as required by law significantly reduced the PCDD/PCDF concentrations in ambient air.
Table 8: PCDD/PCDF Ambient Air Concentrations - Germany 1993
Ambient Air (fg TEQ/m³)
Deposition (pg TEQ/m²·d)
|Close to point source||
Up to 1,000
Table 9: Ambient Air - Northrhine Westfalia 1987/88 vs. 1993/94 (NRW 1995)
Concentration (fg I-TEQ/m³)
Ambient air levels of PCDD/PCDF were determined from a total of 223 ambient air samples during a 2½ year period in two networks in southern Bavaria, Germany. A clear seasonal trend was identified in both sampling campaigns with lower PCDD/PCDF concentrations in summer and higher levels in winter. A graphical sketch of the results is shown in Figure 1. The opposite trend is found for PCB where generally the higher concentrations were found in summer.
Figure 1: Ambient air concentrations of PCDD/PCDF and PCB in two networks in southern Bavaria, Germany (AGB = Augsburg; BKI = Burgkirchen)
This chapter briefly summarizes German regulations and guidelines addressing polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans (PCDD/PCDF).
The first laws addressed the ban of chemicals known to be contaminated with PCDD/PCDF (ppb to ppm-range I-TEQ): Ban of polychlorinated biphenyls (PCB) of July 18, 1989 (PCB 1989) and the ban of the production and use of pentachlorophenol (PCP) of December 12, 1989 (PCP 1989).
The First Ordinance on the Prohibition of Certain Chemicals (amended in 1994 and 1996, ChemVerbotsV 1996) sets limit values for all seventeen 2,3,7,8-chlorine substituted congeners (and eight 2,3,7,8-bromine substituted dibenzo-p-dioxins and dibenzofurans, PBDD/PBDF). According to the law, substances, preparations and/or articles are not allowed to be placed on the market:
Table 10: Limit values of PCDD/PCDF as given by the Chemicals Law
Note: the concentrations given in Table 10 are absolute values, not I-TEQ!
|Congeners||Substances, preparations and/or articles are not allowed to be placed on the market if concentrations exceed the following limit values|
|Congeners in column 1 No.1:
|Congeners in column 1 Nos. 1 and 2:
|Congeners in column 1 Nos. 1, 2 and 3:
On December 1, 1990, the Ordinance on Waste Incineration Plants (17th BImSchV 1990) entered into force setting a limit value of 0.1 ng TEQ/m³ for PCDD/PCDF emissions from incinerators for waste and similar combustible materials. According to this Ordinance, new plants had to comply with the emission limit of 0.1 ng TEQ/m³ immediately, existing plants by 1994 or 1996 at the latest.
In 1997, a dioxin limit value of 0.1 ng I-TEQ/m³ and a minimum temperature of 850 °C for crematories was set by law (27th BImSchV 1997).
Presently, there is ongoing work to evaluate if the limit value for waste incinerators of 0.1 ng TEQ/m³ can also apply to other thermal plants, e.g. plants for metallurgical treatment of iron ore, melting plants of secondary aluminum, and others.
To stop the impact of dioxins into the environment from use of so-called scavengers, e.g. dichloroethane or dibromoethane as additives, in leaded gasoline, a ban of the use scavengers was passed in 1992 (19th BImSchV 1992).
The Ordinance on Sewage Sludge (AbfKlärV 1992) set a limit value of 100 ng I-TEQ/kg dry matter for sewage sludges used as fertilizer in agriculture, horticulture or forestry. In addition, the law sets a freight limit for 5 tons of dry matter of sewage sludge per hectare once within three years. Application of sewage sludge on pasture is forbidden by law. Similarly, there exists a recommendation for use of compost. The limit value is 17 ng I-TEQ/kg d.m. In the State of Baden-Württemberg, this limit value is confirmed in a law.
In Germany, a Joint Working Group on Dioxins was established whcih deriveed guideline concentrations for soil and milk. Still today, all the proposed measures are recommendations for action, but they are not legally binding. Nevertheless, they are a basis for political decisions to protect men and the environment. In some cases, e.g. accidents such as a fire at a plastic store, these recommendations for actions were taken for decision making. The proposed limit concentrations are shown in Table 11 and Table 12.
Table 11: Recommendation values and action levels for PCDD/PCDF in soil.
(Concentrations in ng I-TEQ/kg d.m.)
The recommendations have been translated into governmental decrees in a number of Länder (Federal States in Germany).
|Control of products if dioxin transfer|
|Restriction to crops with minimum dioxin transfer|
|Soil exchange on children playgrounds|
|Soil exchange in residential areas|
|Soil exchange independent of the location|
Table 12: Recommendation values and action levels for PCDD/PCDF in milk and milk products. (Concentrations in ng I-TEQ/kg Milk fat)
|Target concentration (Minimum of dioxin input)|
|1. Identification and reduction of sources.
If not possible within a short time ® stop dairy farming
2. Recommendation not to market milk to end-user
|Milk and milk products are not allowed to be marketed|
The possibility of the formation of dioxins and furans in the pulp industry during chlorine bleaching is known. Based on the knowledge of the migration of PCDD/PCDF from filter paper into coffee and from paperboard into milk, the paper manufacturers reduced the dioxin levels in paperboard cartons to less than 1 ppt TEQ.
AbfKlärV: Klärschlammverordnung (AbfKlärV) vom 15.04.1992. Bundesgesetzblatt, Jahrgang 1992, Teil 1, 912-934 (Sewage Sludge Ordinance)
BImSchV (1990): 17. Verordnung zur Durchführung des Bundesimmissionsschutzgesetzes vom 23.1.1990 (Verordnung über Verbrennungsanlagen für Abfälle und ähnliche brennbare Stoffe - 17. BImSchV). Bundesgesetzblatt Teil I, Jahrgang 1990, 2832. (Ordinance for waste incinerators)
BImSchV (1992): 19. Verordnung zur Durchführung des Bundesimmissionsschutzgesetzes vom 24.07.1992 (Verordnung über Chlor- und Bromverbindungen als Kraftstoffzusatz-19. BImSchV). Bundesgesetzblatt Teil 1, Jahrgang 1992, 75 (Ordinance on ban of halogenated scavengers)
BImSchV (1997): Siebenundzwanzigste Verordnung zur Durchführung des Bundes-Immissionsschutzgesetzes (Verordnung über Anlagen zur Feuerbestattung - 27. BImSchV) vom 19. März 1997. BGBl. I, S. 545. (Ordinance for crematories)
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