not high enough to disturb their reproductive success. 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. due to a multitude of food sources of adult humans exposure is much less averaging at 1 pg teq/kg-day, 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 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. 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. 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". 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. in surface waters, dioxins are bound to organic and inorganic particles. remediation research 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. photocatalysis and other methods have also been tested in attempts to remove dioxins in soils and other environments. because dioxins adsorb tightly to soil particles, and microbial degradation (mostly via dehalogenation, dehalococcoides cbdb1 being an example) of dioxins is very slow, researchers have actively tried to search for mechanisms to increase degradation or to find especially active microbial species for the purposes of bioremediation. by and large, this has not been very successful. in addition, interactions with the animal gut microbiomes are poorly known. sources of human exposure the most important source of human exposure is fatty food of animal origin (see human intake, above), and breast milk. 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. 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. 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. 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. 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). other occupational exposures (working at paper and pulp mills, steel mills and incinerators) have been remarkably lower. 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). 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 dirt. 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. 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. pcbs are also known to flush from industry and land (aka sludge fields) to contaminate fish, 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. there have been several food contamination episodes, one of the best known occurred in belgium in 1999. 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. 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. 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.