Dioxins and dioxin-like compounds

High doses. The symptoms reported to be associated with dioxin toxicity in animal studies are incredibly wide-ranging, both in the scope of the biological systems affected and in the range of dosage needed to bring these about.[4][1][3] Acute effects of single high dose dioxin exposure include reduced feed intake and wasting syndrome, and typically a delayed death of the animal in 1 to 6 weeks.[12] By far most toxicity studies have been performed using 2,3,7,8-tetrachlorodibenzo-p-dioxin.

The LD₅₀ of TCDD varies wildly between species and even strains of the same species, with the most notable disparity being between the seemingly 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.[4] Even between different mouse or rat strains there may be tenfold to thousandfold differences in acute toxicity. Many pathological findings are seen in the liver, thymus, and other organs. Some effects such as thymic atrophy are common in many species, but e.g. liver toxicity is typical in rabbits.[4]

Low doses. Very few signs of toxicity are seen in adult animals after low doses, but developmental effects may occur at low dioxin levels, including foetal, neonatal, and possibly pubescent stages.[24] Well established developmental effects are cleft palate, hydronephrosis, disturbances in tooth development and sexual development, and endocrine effects.[24] Surprisingly, enzyme induction, several developmental effects and aversion to novel foods occur at similar dose levels in animals that respond differently to acute high-dose toxicity. Therefore, it has been suggested that dioxin effects be divided to type I effects (enzyme induction etc.) and type II effects (lethality, liver damage, anorexia, and tumour promotion).[1] The reason may be different requirements of the transactivation domain structure of the AH receptor for different genes. Some of these low-dose effects can in fact be interpreted as protective rather than toxic (enzyme induction, aversion to novel foods).[1]

High doses. Toxicity of dioxins at high doses has been well documented after accidents, deliberate poisonings, food contamination episodes, and high industrial exposures.[1][25] Three women in Vienna, Austria, were poisoned with large doses of TCDD in 1998. The highest concentration of TCDD in fat tissue was 144,000 pg/g, the highest ever reported in human beings. The main feature was chloracne, a serious skin disease. The victim survived, and other symptoms were modest after initial gastrointestinal symptoms and amenorrhea.[26] Another acute incident was the deliberate poisoning of Victor Yushchenko, then presidential candidate of Ukraine, in 2004. TCDD concentration in fat was 108,000 pg/g. Also in this case the most prominent symptom was chloracne after initial stomach pain indicating hepatitis and pancreatitis.[27] These episodes show that a human being is not as sensitive as the most sensitive animals, since the doses must have been up to 25 μg/kg.

Two serious food contamination accidents were caused by PCB oils used in heat exchangers.[1] The PCB oil leaked to rice bran oil consumed by thousands of people in Japan (Yusho disease 1968) and Taiwan (Yu-cheng disease 1979). The toxic effects have been attributed to dioxin-like PCBs and PCDFs. Their daily intake was up to 100,000 times higher than average intake presently.[1] There were many skin problems, chloracne, swelling of eyelids, and hypersecretion of Meibomian glands in the eyes. Babies born to Yusho and Yu-cheng mothers were smaller than normal, they had dark pigmentation and sometimes teeth at birth and tooth deformities. Foetal deaths and miscarriages were common.[28]

Perhaps the best known dioxin accident occurred in Seveso, Italy, in 1976. A tank of chlorophenols released its contents to air including many kilograms of TCDD, and contaminated much of the city. The highest TCDD levels were found in children, up to 56,000 pg/g fat. Acute effects were limited to chloracne, although many animals such as rabbits died after eating contaminated grass.[29] Dental aberrations were found after 25 years in persons exposed as children, and a slightly increased cancer risk was confirmed 35 years later.[1]

In line with animal studies, developmental effects may be much more important than effects in adults. These include disturbances of tooth development,[30] and of sexual development.[31]

An example of the variation in responses is clearly seen in a study following the Seveso disaster indicating that sperm count and motility were affected in different ways in exposed males, depending on whether they were exposed before, during or after puberty.[32]

In occupational settings many symptoms have been seen, but exposures have always been to a multitude of chemicals including chlorophenols, chlorophenoxy acid herbicides, and solvents. Therefore, definitive proof of dioxins as causative factors has been difficult to obtain. By far the best proven effect is chloracne. The suspected effects in adults are liver damage, and alterations in heme metabolism, serum lipid levels, thyroid functions, as well as diabetes and immunological effects.[29]

Low exposures. Effects after low exposures such as from food have been difficult to prove. Levels of dioxins in contemporary population are 5 to 20 pg/g (TEQ in fat) and 50 to 100 pg in older people[33][34] or at least 1000 times lower than those in poisonings (see above). Tooth deformities have been considered plausible after long breast-feeding, when the dioxin concentrations were high in 1970s and 1980s.[35] When the concentrations decreased during 1990s and 2000s, the effects were no longer seen.[1] According to a study in Russia, sperm counts in 18-19 year old young men were lower when dioxin levels were higher at the age of 8 to 9 years.[36] This was in industrial environments causing relatively high exposures to boys as well as their mothers.[1] The contamination panel of the European Food Safety Agency (EFSA) recommended decreasing tolerable weekly intake (TWI) levels based on the Russian children study.[20] This recommendation can be challenged, because it does not properly consider competing risks following from lost benefits of important and healthy food items such as certain fish.[1] TWI levels are not applied for breast feeding, because benefits of breast milk are judged to be far more important than the remote risks of dioxins.[37] A general conclusion may be that safety margins are not very great concerning developmental effects, but toxic effects are not likely at the present population levels of dioxins.

A number of cross-sectional studies have shown associations between type 2 diabetes and several POP compounds including dioxins.[38] Such observational studies cannot prove causality, i.e. there may be an association which does not prove that one is the cause of the other. The main problem is that similar associations can be found with many quite different POPs, which have only long half-lives and tendency to accumulate in lipids in common. This suggests that they may all be related to diet and obesity which are by far the most common causes of type 2 diabetes.[1]

Over the years there have been speculations on various effects of dioxins on endometriosis, sexual development, liver function, thyroid hormone levels, white blood cell levels, immune functions, and even learning and intelligence. While some of these effects might be possible after heavy exposures (like in the Seveso disaster), these claims are only based on potential exposures of population, not supported by actual measurements of dioxin concentrations.[29] E.g. absorption from bleached tampons claimed to be associated with endometriosis[39] is insignificant compared with daily dioxin intake from food.[33]

Dioxins are well established carcinogens in animal studies, although the precise mechanism is not clear. Dioxins are not mutagenic or genotoxic.[1][22][40] The United States Environmental Protection Agency has categorised dioxin, and the mixture of substances associated with sources of dioxin toxicity as a "likely human carcinogen".[41] The International Agency for Research on Cancer has classified TCDD as a human carcinogen (class 1) on the basis of clear animal carcinogenicity and limited human data,[42] and subsequently also 2,3,4,7,8-PCDF and PCB 126 as class 1 carcinogens.[43] The mechanism is thought to be mainly promotion, i.e. dioxins can accelerate the formation of tumours caused by other factors, and adversely affect the normal mechanisms for inhibiting tumour growth.[22] Some researchers have also proposed that dioxin induces cancer progression through a very different mitochondrial pathway.[44]

As with many toxic endpoints of dioxin, a clear dose–response relationship is difficult to establish. After accidental or high occupational exposures there is evidence on human carcinogenicity.[45][46] Increases in cancer have been modest, in fact reaching statistical significance has been difficult even after high accidental or occupational exposures like in Yusho and Yucheng poisonings, Seveso accident, and combined occupational cohorts.[1] Therefore, controversies on cancer risk at low population levels of dioxins are understandable.[1][21][45][34] The problem with IARC evaluations[43] is that they only assess hazard, i.e. carcinogenicity at any dose. It is likely that there is a practical safe threshold for the non-genotoxic dioxins, and the present population levels do not possess any risk of cancer. There is thus some agreement on that cancer risk is taken care of as well, if daily intake limits are set to protect from developmental effects.[37][1] Among fishermen with high dioxin concentrations in their bodies, cancer deaths were decreased rather than increased.[47] All this means that in case of important beneficial food items and breast feeding a thorough benefit/risk analysis is needed before setting limits, in order to avoid increased other risks or lost benefits.[48]

The uncertainty and variability in the dose–response relationship of dioxins in terms of their toxicity, as well as the ability of dioxins to bioaccumulate, have led WHO experts to recommending very low tolerable daily intake (TDI) of dioxin, 1-4 pg/kg body weight per day, i.e. 7x10⁻¹¹ to 2.8x10⁻¹⁰g per 70-kg person per day, to allow for this uncertainty and ensure public safety in all instances.[37] Authorities have then set weekly or monthly intake levels that equal to TDIs around 2 pg/kg.[1] Because dioxins are eliminated very slowly, the body burden accumulated during the whole lifetime is high compared with daily doses, and occasional modest exceedances of limit values do not change it much. Therefore, long-term intake is much more important than daily intake.[1] Specifically, the TDI has been assessed to guarantee the safety of children born to mothers exposed to such a daily intake of dioxins all their lifetime prior to pregnancy.[37] It is likely that the TDI for other population groups could be higher.

One important cause for differences in different assessments has been carcinogenicity. If the dose-response of TCDD in causing cancer is linear, it might be a true risk. If the dose-response is of a threshold-type or J-shape, there is little or no risk at the present concentrations. Understanding the mechanisms of toxicity better is hoped to increase the reliability of risk assessment.[2][49] Recently also developmental effects have been reassessed by the Contamination Panel of the European Food Safety Agency (EFSA). They propose decreasing the tolerable weekly intake (TWI) from 14 pg/kg to 2 pg/kg.[20] This is likely to cause another controversy before being accepted by European countries.[1] Dioxin intake and levels in breast milk in 1970s and 1980s were 5 to 10 times higher than presently, and very few effects have been found, possibly mild developmental effects on teeth.[1]

All dioxin-like compounds share a common mechanism of action via the aryl hydrocarbon receptor (AHR), but their potencies are very different. This means that similar effects are caused by all of them, but much larger doses of some of them are needed than of TCDD. Binding to the AHR as well as persistence in the environment and in the organism depends on the presence of so-called "lateral chlorines", in case of dioxins and furans, chlorine substitutes in positions 2,3,7, and 8.[3] Each additional non-lateral chlorine decreases the potency, but qualitatively the effects remain similar. Therefore, a simple sum of different dioxin congeners is not a meaningful measure of toxicity. To compare the toxicities of various congeners and to render it possible to make a toxicologically meaningful sum of a mixture, a toxicity equivalency (TEQ) concept was created.[5]

Each congener has been given a toxicity equivalence factor (TEF).[5][50] This indicates its relative toxicity as compared with TCDD. Most TEFs have been extracted from in vivo toxicity data on animals, but if these are missing (e.g. in case of some PCBs), less reliable in vitro data have been used.[5] After multiplying the actual amount or concentration of a congener by its TEF, the product is the virtual amount or concentration of TCDD having effects of the same magnitude as the compound in question. This multiplication is done for all compounds in a mixture, and these "equivalents of TCDD" can then simply be added, resulting in TEQ, the amount or concentration of TCDD toxicologically equivalent to the mixture.

The TEQ conversion makes it possible to use all studies on the best studied TCDD to assess the toxicity of a mixture. This is most useful in regulatory work, but it can also be used in scientific studies.[51] This resembles the common measure of all alcoholic drinks: beer, wine and whiskey can be added together as absolute alcohol, and this sum gives the toxicologically meaningful measure of the total impact.

The TEQ only applies to dioxin-like effects mediated by the AHR. Some toxic effects (especially of PCBs) may be independent of the AHR, and those are not taken into account by using TEQs.

TEFs are also approximations with certain amount of scientific judgement rather than scientific facts. Therefore, they may be re-evaluated from time to time. There have been several TEF versions since the 1980s. The most recent re-assessment was by an expert group of the World Health organization in 2005.

(T = tetra, Pe = penta, Hx = hexa, Hp = hepta, O = octa)

• The 2,3,7,8-substituted PCDDs[5]
• The 2,3,7,8-substituted PCDFs[5]
• Dioxin-like PCBs[5]

Greenpeace and some other environmental groups have called for the chlorine industry to be phased out.[52][53][54] However, chlorine industry supporters say that "banning chlorine would mean that millions of people in the third world would die from want of disinfected water".[55] Sharon Beder and others have argued that the dioxin controversy has been very political and that large companies have tried to play down the seriousness of the problems of dioxin.[53][54][56] The companies involved have often said that the campaign against dioxin is based on "fear and emotion" and not on science.[57]

Dioxins are absorbed well from the digestive tract if they are dissolved in fats or oils (e.g. in fish or meat).[4] On the other hand, dioxins tend to adsorb tightly to soil particles, and absorption may be quite low: 13.8% of the given dose of TEQs in contaminated soil was absorbed.[67]

The same features causing persistence of dioxins in the environment also cause very slow elimination in humans and animals. Because of low water solubility, kidneys cannot excrete them in urine as such. They must first be metabolised to more-water-soluble metabolites, but that metabolism, especially in humans, is extremely slow. This results in biological half-lives of several years for all dioxins. That of TCDD is estimated to be 7 to 8 years, and for other PCDD/Fs from 1.4 to 13 years, PCDFs on average slightly shorter than PCDDs.[1][3][68]

In mammals, dioxins are found mostly in fat. Concentrations in fat seem to be relatively similar, be it serum fat, adipose tissue fat, or milk fat. This permits measuring dioxin burden by analysing breast milk.[61] Initially, however, at least in laboratory animals, after a single dose, high concentrations are found in the liver, but in a few days, adipose tissue will predominate. In rat liver, however, high doses cause induction of CYP1A2 enzyme, and this binds dioxins. Thus, depending on the dose, the ratio of fat and liver tissue concentrations may vary considerably in rodents.[4]

PCDD/F-compounds were never synthesized for any purpose, except for small quantities for scientific research.[12] Small amounts of PCDD/Fs are formed whenever organics, oxygen and chlorine are available at suitable temperatures.[1] This is augmented by metal catalysts such as copper. The optimal temperature range is 400 °C (752 °F) to 700 °C (1,292 °F). This means that formation is highest when organic material is burned in less-than-optimal conditions such as open fires, building fires, domestic fireplaces, and poorly operated and/or designed solid waste incinerators.[3] Historically, municipal and medical waste incineration was the most important source of PCDD/Fs.

PCB-compounds, always containing low concentrations of dioxin-like PCBs and PCDFs, were synthesized for various technical purposes (see Polychlorinated biphenyls). They have entered the environment through accidents such as fires or leaks from transformers or heat exchangers, or from PCB-containing products in landfills or during incineration. Because PCBs are somewhat volatile, they have also been transported long distances by air leading to global distribution including the Arctic. Only a minor portion of PCBs in mixtures are dioxin-like.[1]

Other sources of PCDD/F include:

• Uncontrolled combustion, particularly open burning of waste ("backyard barrel burning"), accidental fires, wildfires. These are presently the most important sources.[1]
• Metal smelting and refining
• Chlorine bleaching of pulp and paper - historically important source of PCDD/Fs to waterways.[50]
• Synthesis side products of several chemicals, especially PCBs, chlorophenols, chlorophenoxy acid herbicides, and hexachlorophene.[42]
• (Historical) Engines using leaded fuel, which contained the additives 1,2-Dichloroethane and 1,2-Dibromoethane.

Improvements and changes have been made to nearly all industrial sources to reduce PCDD/F production. In waste incineration, large amounts of publicity and concern surrounded dioxin-like compounds during the 1980s-1990s continues to pervade the public consciousness, especially when new incineration and waste-to-energy facilities are proposed. As a result of these concerns, incineration processes have been improved with increased combustion temperatures (over 1,000 °C (1,830 °F)), better furnace control, and sufficient residence time allotted to ensure complete oxidation of organic compounds. Ideally, an incineration process oxidizes all carbon to CO₂ and converts all chlorine to HCl or inorganic chlorides prior to the gases passing through the temperature window of 400-700 °C where PCDD/F formation is possible. These substances cannot easily form organic compounds, and HCl is easily and safely neutralized in the scrubber while CO₂ is vented to the atmosphere. Inorganic chlorides are incorporated into the ash.

Scrubber and particulate removal systems manage to capture some of the PCDD/F which forms even in sophisticated incineration plants. These PCDD/Fs are generally not destroyed but moved into the fly ash. Catalytic systems have been designed which destroy vapor-phase PCDD/Fs at relatively low temperatures. This technology is often combined with the baghouse or SCR system at the tail end of an incineration plant.

The European Union limit for concentration of dioxin-like compounds in the discharged flue gas is 0.1 ng/Nm³ TEQ.[73][74]

Both in Europe[75] and in U.S.A.,[76] the emissions have decreased dramatically since the 1980s, by even 90% (see Figure). This has also led to decreases in human body burdens, which is neatly demonstrated by the decrease of dioxin concentrations in breast milk.[61] With the substantial decrease of emissions from municipal waste incinerators, other potentially large sources of dioxin-like compounds, for example from forest and wild fires, have increased relative to industrial sources.[77] They are however not included in the total inventory due to uncertainties in available data.[78] A more recent study on the environmental effects of accidental fires, including forest fires, estimated the emissions from dioxins (PCDD/Fs) to be about equivalent to those from traffic and municipal waste combustion.[79]

Open burning of waste (backyard barrel burning) has not decreased effectively, and in the U.S. it is now the most important source of dioxins. Total U.S. annual emissions decreased from 14 kilograms (31 lb) in 1987 to 1.4 kilograms (3.1 lb) in 2000. However, backyard barrel burning decreased only modestly from 0.6 kilograms (1.3 lb) to 0.5 kilograms (1.1 lb), resulting in over one third of all dioxins in the year 2000 from backyard burning alone.[76]

Low concentrations of dioxins have been found in some soils without any anthropogenic contamination. A puzzling case of milk contamination was detected in Germany. The source was found to be kaolin added to animal feed. Dioxins have been repeatedly detected in clays from Europe and USA since 1996, with contamination of clay assumed to be the result of ancient forest fires or similar natural events with concentration of the PCDD/F during clay sedimentation.[80]

In sugarcane cultivation, the remaining bagasse after extraction of sugar is used in large amounts for energy production (both process heat and electric energy for use both in the sugar factory itself and for other consumers), and locally it has been thought to be a remarkable source of dioxins.[81] This basically indicates that burning biomass produces dioxins and it should be done at high enough temperatures and there should be proper filtering of flue gases. For the treatment of gases and pollutants, sugarcane industries often use wet gas scrubbers, such as the Venturi type. In addition, other treatment systems also used are electrostatic precipitators and bag filters.[82] These methods may be insufficient[81][82][83] Improperly burned biomass, which undergoes only low temperature incomplete combustion, is responsible for much of the negative health effects of indoor air pollution and is a particular problem in the Global South where biomass like wood or cowdung are often the only commonly available fuels for cooking and home heating. In addition to dioxins, other harmful products of incomplete combustion - such as carbon monoxide - are also released when biomass is burned in low oxygen conditions. Using plastic, particularly chlorine-containing plastics such as polyvinyl chloride, as a fuel or firestarter further increases dioxin emissions.

All groups of dioxin-like compounds are persistent in the environment. Very few soil microbes nor animals can break down the PCDD/Fs with lateral chlorines (positions 2,3,7, and 8).[84] Lipophilicity (tendency to seek for fat-like environments) and very poor water solubility make these compounds move from water environment to living organisms having lipid cell structures. This is called bioaccumulation. Increase in chlorination increases both stability and lipophilicity. The compounds with the very highest chlorine numbers (e.g. octachlorodibenzo-p-dioxin) are, however, so poorly soluble that this hinders their bioaccumulation.[84] Bioaccumulation is followed by biomagnification. Lipid-soluble compounds are first accumulated to microscopic organisms such as phytoplankton (plankton of plant character, e.g. algae). Phytoplankton is consumed by animal plankton, this by invertebrates such as insects, these by small fish, and further by large fish and seals. At every stage or trophic level, the concentration is higher, because the persistent chemicals are not "burned off" when the higher organism uses the fat of the prey organism to produce energy.

Due to bioaccumulation and biomagnification, the species at the top of the trophic pyramid are most vulnerable to dioxin-like compounds. In Europe, the white-tailed eagle and some species of seals have approached extinction due to poisoning by persistent organic pollutants.[85] Likewise, in America, the population of bald eagles declined because of POPs causing thinning of eggshells and other reproductive problems.[86] Usually, the failure has been attributed mostly to DDT, but dioxins are also a possible cause of reproductive effects. Both in America and in Europe, many waterfowl have high concentrations of dioxins, but usually not high enough to disturb their reproductive success.[85][87] Due to supplementary winter feeding and other measures also, the white-tailed eagle is recovering (see White-tailed eagle). Also, ringed seals in the Baltic Sea are recovering.

Humans are also at the top of the trophic pyramid, particularly newborns. Exclusively breastfed newborns were estimated to be exposed to a total of 800 pg TEQ/day, leading to an estimated body weight-based dose of 242 pg TEQ/kg/day.[88] Due to a multitude of food sources of adult humans exposure is much less averaging at 1 pg TEQ/kg-day,[88] and dioxin concentrations in adults are much less at 10-100 pg/g, compared with 9000 to 340,000 pg/g (TEQ in lipid) in eagles[85] or seals feeding almost exclusively on fish.

Because of different physicochemical properties, not all congeners of dioxin-like compounds find their routes to human beings equally well. Measured as TEQs, the dominant congeners in human tissues are 2,3,7,8-TCDD, 1,2,3,7,8-PeCDD, 1,2,3,6,7,8-HxCDD and 2,3,4,7,8-PeCDF.[3] This is very different from most sources where hepta- and octa-congeners may predominate. The WHO panel re-evaluating the TEF values in 2005 expressed their concern that emissions should not be uncritically measured as TEQs, because all congeners are not equally important.[5] They stated that "when a human risk assessment is to be done from abiotic matrices, factors such as fate, transport, and bioavailability from each matrix be specifically considered".[5]

All POPs are poorly water-soluble, especially dioxins. Therefore, ground water contamination has not been a problem, even in cases of severe contamination due to the main chemicals such as chlorophenols.[89] In surface waters, dioxins are bound to organic and inorganic particles.

TCDD has been long known to be sensitive to photochemical dechlorination. If exposed to direct sunlight or UV-radiation, it will decompose in a matter of hours.[90] Photocatalysis and other methods have also been tested in attempts to remove dioxins in soils and other environments.[91][92] Because dioxins adsorb tightly to soil particles, and microbial degradation (mostly via dehalogenation, Dehalococcoides CBDB1 being an example)[93][94] of dioxins is very slow, researchers have actively tried to search for mechanisms to increase degradation[95] or to find especially active microbial species for the purposes of bioremediation.[96][91][92] By and large, this has not been very successful. In addition, interactions with the animal gut microbiomes are poorly known.[97]

The most important source of human exposure is fatty food of animal origin (see Human intake, above),[33] and breast milk.[88] There is much variation between different countries as to the most important items. In U.S. and Central Europe, milk, dairy products and meat have been by far the most important sources. In some countries, notably in Finland and to some extent in Sweden, fish is important due to contaminated Baltic fish and very low intake from any other sources.[3] In most countries, a significant decrease of dioxin intake has occurred due to stricter controls during the last 20 years.

Historically, occupational exposure to dioxins has been a major problem.[42] Dioxins are formed as important toxic side products in the production of PCBs, chlorophenols, chlorophenoxy acid herbicides, and other chlorinated organic chemicals. This caused very high exposures to workers in poorly controlled hygienic conditions. Many workers had chloracne. In a NIOSH study in the U.S., the average concentration of TCDD in exposed persons was 233 ng/kg (in serum lipid) while it was 7 ng/kg in unexposed workers, even though the exposure had been 15–37 years earlier.[42] This indicates a huge previous exposure. In fact the exact back-calculation is debated, and the concentrations may have been even several times higher than originally estimated.[98]

Handling and spraying of chlorophenoxy acid herbicides may also cause quite high exposures, as clearly demonstrated by the users of Agent Orange in the Malayan Emergency and in the Vietnam War. The highest concentrations were detected in nonflying enlisted personnel (e.g. filling the tanks of planes), although the variation was huge, 0 to 618 ng/kg TCDD (mean 23.6 ng/kg).[42] Other occupational exposures (working at paper and pulp mills, steel mills and incinerators) have been remarkably lower.[42]

Accidental exposures have been huge in some cases. The highest concentrations in people after the Seveso accident were 56,000 ng/kg, and the highest exposure ever recorded was found in Austria in 1998, 144,000 ng/kg (see TCDD).[26] This is equivalent to a dose of 20 to 30 μg/kg TCDD, a dose that would be lethal to guinea pigs and some rat strains.

Exposure from contaminated soil is possible when dioxins are blown up in dust, or children eat soil. Inhalation was clearly demonstrated in Missouri in the 1970s, when waste oils were used as dust suppressant in horse arenas. Many horses and other animals were killed due to poisoning.[99] Dioxins are neither volatile nor water-soluble, and therefore exposure of human beings depends on direct eating of soil or production of dust which carries the chemical. Contamination of ground water or breathing vapour of the chemical are not likely to cause a significant exposure. Currently, in the US, there are 126 Superfund sites with a completed exposure pathway contaminated with dioxins.

Further, PCBs are known to pass through treatment plants and accumulate in sludge which is used on farm fields in certain countries. In 2011 in South Carolina, SCDHEC enacted emergency sludge regulations after PCBs were found to have been discharged to a waste treatment plant.[100]

PCBs are also known to flush from industry and land (aka sludge fields) to contaminate fish,[101] as they have up and down the Catawba River in North and South Carolina. State authorities have posted fish consumption advisories due to accumulation of PCBs in fish tissue.[102]

There have been several food contamination episodes, one of the best known occurred in Belgium in 1999.[1] A tank of recycled fats collected for animal feed production was contaminated by PCB oil containing about 1 g of dioxins and 2 g of DL-PCBs. This caused a major alarm in the European Union, but due to relatively fast response and slow accumulation of dioxins in humans there were no health impacts.[1] There was a similar incidence in Ireland in 2008. In 2008, Chile experienced a pork crisis caused by high dioxin concentrations in their pork exports. The contamination was found to be due to zinc oxide used in pork feed, and caused reputational and financial losses for the country, as well as leading to the introduction of new food safety regulations.[103] These episodes emphasize the importance of food control, and early detection guarantees that very slowly accumulating dioxins do not increase in humans to levels causing toxic effects.