Dioxins (the common name for polychlorinated dibenzo-para-dioxins) and furans (polychlorinated dibenzofurans) are two closely related groups of chemical byproducts that are produced throughout the world. Both groups consist of chlorinated compounds that have a range of congeners - members of the same structural group with different configurations. The congeners differ in terms of the number, position, and combination of chlorine atoms on the molecule. There are 75 possible dioxin congeners and 135 possible furan congeners. ^[1] The dioxin and furan congeners thought to be most toxic to humans are the seven dioxins and ten furans with a particular pattern of chlorines known as the 2,3,7,8-congeners. Most studies measuring human exposure to dioxin and furans focus on this group. The term "dioxin" is often used to refer to this group of 17 congeners.

Dioxins and furans are not produced intentionally. They are byproducts from a range of chemical, manufacturing, and combustion processes including: ^[1]

• production of certain pesticides (i.e. chlorophenol, chlorophenoxyacetic acid);
• paper pulp bleaching;
• production of certain dyes and pigments;
• municipal waste incineration;
• sewage-sludge incineration;
• hospital-waste incineration;
• polyvinyl chloride plastic (PVC) production and incineration;
• diesel-engine exhaust;
• accidental fires and explosions of chlorine-containing material;
• metal production; and
• combustion of wood.

Incineration is believed to be the main route by which dioxins and furans are produced and is often the area of focus in pollution-prevention efforts.

Health Effects of Dioxins and Furans

Dioxins and furans are among the most hazardous chemicals known - extremely tiny doses have been shown to cause negative health effects. These chemicals are listed by several governmental agencies as known causes of cancer in humans. Indeed, studies have linked dioxins and furans to many types of cancer, as well as to reproductive problems, abnormalities in fetal development, immune alterations, and disruption of hormones. ^[2] Because dioxins and furans are attracted to fat and are resistant to metabolism, they are notorious for accumulating in the animals humans eat, and by that route accumulating in humans. Within the human body, the highest levels of these chemicals are in fat and breast milk.

Dioxins and Furans in the Body

Some dioxins and furans are extremely persistent in the environment. Once released into the air, dioxins and furans can be transported on air currents to distant places around the globe. International pollution patterns have shown that areas with little or no industry can be contaminated with high dioxin and furan levels. ^[3] For example, people living in remote Inuit villages in the Arctic have significant dioxin levels in their bodies despite their geographic isolation and the lack of dioxin exposure sources in the area. ^[4] Still, higher levels are most commonly associated with industrial areas.

A small share of the dioxins and furans released into the environment are broken down by sunlight, but most persist by attaching to soil particles and sediment in water. Once attached to such particles, they enter the food chain, leading eventually to bioaccumulation in animal fat. ^[3]

Human beings can be exposed to dioxins and furans in a number of ways. Eating contaminated food (primarily meat, dairy products, and fish) is the major path for dioxin exposure, ^[3] but other less common routes of exposure include contact with certain pesticides and herbicides (such as the wood preservative pentachlorophenol, and the phenoxy herbicides), living near hazardous waste sites or incinerators that release dioxins and furans, or working in industries that produce dioxin and furan byproducts. ^[3]

Dietary exposure makes up more than 90 percent of human dioxin and furan intake. ^[5] Fatty foods usually contain more significant levels because they are higher on the food chain and thus have accumulated more dioxin. Figure 30 below shows that the major portion of a person's average dioxin and furan exposure comes from dietary exposure.

Once dioxins and furans have entered animal tissues, they have few avenues of departure, so the chemicals can persist for many years. In lactating women, dioxins and furans may leave the body in breast milk. As with many other persistent chemicals that appear in breast milk, the concentration of dioxins and furans changes with time. ^[6-8]

A number of animal and human studies have looked at the health effects of dioxins and furans on children's health from in utero and postnatal exposure. Health outcomes evaluated have included low birth weight, hormone fluctuation, neurobehavioral function, and altered immune function. Thus far, the studies have not identified any links between these health effects and exposure to dioxins specifically from breast milk. Breast milk contains a mixture of environmental pollutants, many of which may have effects similar to those of dioxin. Moreover, it can be difficult to separate the effects of exposures before birth due to chemicals in the mother's blood, from the effects after birth from breast milk. Thus, it is difficult to link health effects to an individual pollutant in breast milk.

The World Health Organization Working Group on the Assessment of Health Risks for Human Infants from Exposure to PCDDs, PCDFs and PCBs reached two important conclusions ^[5]:

• the incidence of obvious health problems in breast-fed children whose mothers had measurable levels of dioxin in their breast milk was generally within the normal background variation; and
  
  
• they found that the benefits of breastfeeding in terms of neurological measures remained, regardless of dioxin exposure via breast milk.

Several other researchers have reinforced this finding showing that breastfeeding will provide health benefits even if dioxin residues are present in the breast milk. Most scientists have concluded that the benefits of breastfeeding are so great as to outweigh the risks associated with dioxin exposure. Such exposure may diminish the benefits of breastfeeding, but not to the point that women should avoid breastfeeding to avoid exposure. ^[9]

Controlling Exposure: Bans and Restrictions

Unlike pesticides and other POPs that have specific functions, dioxins and furans are unintentional byproducts of industry, making their production difficult to ban or restrict.

Attempting to ban the formation of dioxins and furans would require fundamental changes in industry practice. Environmentalists and activists have called on local, national, and international agencies to reduce dioxin formation. The effort has included local and regional "zero-dioxin" initiatives to force changes in production or the adoption of different methods. Many groups have also called for a halt to all forms of incineration and the phase-out of products whose manufacture and disposal produces dioxin.

Assessing the Extent of Exposure: Limits and Benchmarks

Most chemicals that are either in widespread use or that have caused widespread contamination are subject to national and international benchmark levels, established to protect public health. In the case of dioxins and furans, there is no evidence to show that these benchmarks are protective.

That said, a number of agencies have promulgated a variety of different benchmark values for exposure to dioxins and furans, with little consensus emerging on the questions of which is the most protective and which should be used as a basis for regulation. The U.S. EPA's Dioxin Risk Assessment in 2000 concluded that there is "no 'safe' level of exposure to dioxin."

Separate benchmarks for dioxin and furan levels in breast milk have not been established. Benchmarks set for "dioxin" are sometimes set for the most toxic congener, 2,3,7,8-TCDD, and sometimes for the combined "toxic equivalencies" (TEQs) of numerous dioxin congeners. In keeping with the science indicating toxicity of dioxin at ever lower levels, many successive Tolerable Daily Intake (TDI) levels have been established, and these have tended to go lower and lower over time. Canada and some European countries have set a TDI level of 10 picograms per kilogram of body weight per day (pg/kg/day). (A picogram is one trillionth of a gram.) The Japanese government has set a TDI of 4 pg/kg/day, and the WHO has recommended a TDI of 2 pg/kg/day. In the United States, the Agency for Toxic Substance and Disease Registry (ATSDR) has established a minimal risk level (MRL) of 1 pg/kg/day. The U.S. EPA's new dioxin reassessment could lead to a TDI significantly lower than any of these.

Many of the countries with measured dioxin in breast milk have average residue levels above these "acceptable levels." For instance, a World Health Organization (WHO) study found that the estimated average daily intake of dioxin for a breast-fed infant was significantly higher than most established TDIs. The estimated weight-adjusted intake for infants is approximately 10 to 100 times the estimated intake for adults. ^[10]

Breast-milk monitoring Studies Measuring Dioxin

Dioxins and furans have been measured in the breast milk of women from at least the following countries:

Albania	Faeroe Islands	Kazakhstan	South Africa
Austria	Finland	Lithuania	Spain
Belgium	France	Netherlands	Sweden
Cambodia	Germany	New Zealand	Thailand
Canada	Hungary	Norway	United States
Croatia	India	Pakistan	United Kingdom
Czech Republic	Israel	Poland	Ukraine
Denmark	Japan	Russia	Vietnam
Estonia		Jordan	Slovakia

Much of this data is from the WHO-coordinated studies conducted in 1986-88 and 1992-93. Most countries have not independently measured dioxin in blood or breast milk.

The majority of the data comes from developed nations or countries that have significant industry. However, the paucity of information on dioxin/furan residues in breast milk in African, Latin American, and other nations does not mean that dioxin is not a problem there. Rather, current information about dioxin residues in breast milk only tells us about what has been measured thus far. Based on what we know about the pervasive nature of dioxin contamination in the food chain and its ability to move great distances, dioxin levels in breast milk are likely a worldwide concern.

Limitations of Studies Measuring Dioxin in Breast Milk

Dioxins and furans rarely occur independently. Rather, they are produced as complex mixtures. Because of this, they are usually combined in measurement. Often, values of combined furan and dioxin congeners are simply referred to as "dioxins" or "dioxin."

It is often difficult to draw conclusions about national and international trends in dioxin contamination because of the numerous factors affecting levels and limitations in the way the data is reported. Some of these challenges include:

• Toxic Equivalencies. Unlike many other chemicals, whose toxicity is expressed in terms of a measured concentration, the potential toxicity of dioxins and furans in human tissues is often expressed in terms of "toxic equivalencies" (TEQs). The concept of TEQs was developed to aid in the interpretation and comparison of mixtures of dioxins and furans. A TEQ is calculated by evaluating the relative toxicity of each individual dioxin and furan congener and comparing it to the most toxic dioxin congener - 2,3,7,8-tetrachlorinated dibenzo-para-dioxin (TCDD). A congener's relative toxicity is multiplied by the detected concentration to get a TEQ value. The final reported value, referred to as the dioxin TEQ, is the sum of all individual TEQs. It is this final sum that is used in the comparison of dioxin and furan values in breast milk. ^[1]

Several different conventions have been devised for conversion to toxic equivalencies, put forward by Nordic, the U.S. EPA and WHO. The most common is WHO's International TEQ, or I-TEQ. ^[1] But some studies use other toxic equivalency calculation schemes. In such cases, it is difficult to compare these with studies using I-TEQs.

• Congener Detection. Another problem in comparing studies of dioxin/furan levels in breast milk is the different methods of detection. TCDD is considered the most toxic of the dioxins and is almost always measured. However, different researchers may measure different assortments of the remaining 16 dioxins and furans. For WHO-coordinated studies, all 17 must be measured so that data are comparable. Other researchers, however, may not follow the WHO protocol.

Related to this are regional variations in common dioxin congeners. Because different industrial processes produce different mixtures of dioxins and furans, dioxin pollution patterns are not uniform. ^[11] As a result, it can be difficult to compare regions with exposure to different pollution sources since their congener patterns will differ.

• Separating Out Specific Congener Trends. When values are simply given as an I-TEQ value, another set of challenges can occur. Analyzing only the sum I-TEQ values may give a general idea of the total level of contamination, but data trends seen in the summed values may be different if the data is separated into specific trends for different dioxin congeners. Changes in the congener composition of the contamination may not be noticed if only the summed value is available. Such changes can be important because they could be the result of changes in industrial practices and pollution patterns and may therefore have different implications, depending on the toxicity and longevity of the increasing congeners.
  
  
• Pooling Samples. Because of the expense of the analytical techniques and the relatively large quantities of breast milk needed for detecting dioxins and furans in breast milk, most studies look at only pooled samples. That is, a group of women may all donate samples that are then combined into one sample for analysis. This means that individual levels, and the variability (range) of dioxin levels, may not be known. Not knowing the range can be problematic because outliers (extremely high or low values) can indicate unique exposure scenarios.
  
  
• Number of Studies. Relatively few studies measuring dioxins in breast milk have been performed over time, so it is not possible in most cases to draw definitive time trends or make conclusions about how levels are changing. Instead, with only two or three measurements in most countries, conclusions must be narrower.

Some Important Examples of Dioxin in Breast Milk

Because of their persistence, dioxins and furans are found throughout the environment, making human intake, and their presence in breast milk, extremely common. Dioxins/furans have been found in breast milk in every country tested, and are likely present in countries that have yet to be tested.

The general time trend in many countries seems to be toward a slight decrease of dioxin levels in breast milk over the past decade. In some countries, the decrease has been quite dramatic, with levels reduced by as much as 50 percent. ^[4] However, despite this downward trend in some countries, trend lines elsewhere may be going up. ^[12]

A report on dioxin in breast milk in the European Union showed that between 1988 and 1993, average levels among women in European Union nations decreased. Some regional differences emerged, but the average decrease was approximately 35 percent. ^[12]

Dioxins in Breast Milk in the European Union

	1988	1993	Change
Rural	28.2	17.7	37% decrease
Urban	29.5	19.2	35% decrease
Industrial	35.9	24	33% decrease

As would be expected, industrial areas generally have higher levels. ^[12] Populations exposed to such local sources of dioxin emission as waste incinerators may have even higher values. Data illustrating trends in breast milk dioxin levels as well as unique exposure situations are presented below.

Time Trends

Coordinated WHO studies in Europe have provided data over the seven-year period from 1986 to 1993. During this period, average dioxin levels appear to have decreased in many countries. ^[13-16] Figure 31 reflects this data.

Scientists gathered extensive data measuring dioxin in breast milk in Sweden. The research, presented in Figure 32, shows a downward trend in average breast-milk levels over the last 25 years. ^{[17, 18]}

In many other countries, it has been difficult to make a national assessment of whether levels are going down because different regions have shown different trends. For instance, in Croatia, average breast-milk levels of dioxin in Krk decreased between 1986 and 1988, while in Zagreb, they increased. ^{[6, 13]} Similarly, findings in Finland and Kazakhstan showed different trend lines for different regions. ^{[6, 13, 26-28]}

Unique Exposure Scenarios: The Effect of Diet

In many of the studies, diet emerges as the single most important factor in dioxin exposure. ^[5] But the effects of life-long accumulation of dioxin must be considered, not just recent exposures. Usually, the levels of dioxin found in breast milk that come from diet are a combination of all of the exposures a woman has had over her lifetime.

A study in South Africa demonstrated the point. The study looked at dioxin in breast milk in both black and white women, and found that white women had higher levels of dioxin. Industrial pollution in South Africa is pervasive, so the disparity could not have been the product of location alone. Eventually, the difference was attributed to diet: the white women in the study were from a higher socioeconomic class than the black women, and were therefore more likely to eat meat, milk, eggs, cheese, and fish. ^[11] Black women were more likely to eat grains and vegetables than meat and dairy products. Foods derived from animals or animal products have been shown to be much higher in dioxin content. Thus, exposure was much higher for the white women in this study population.

Similarly, researchers have found lower levels of dioxin in breast milk in vegetarian mothers in Germany compared to those women who ate a diet rich in meat. ^[29] Vegetarians consume only 2 percent of the dioxin load of the general population because their diet is dominated by foods low on the food chain. ^[10]

In many areas of the world, people's diets include foods produced in a number of locations - the result of international trade. But in places where diets consist completely or significantly of locally produced foods, diet-influenced differences in dioxin concentration may exist. A study conducted in Jordan showed extreme differences in breast-milk dioxin concentrations depending on location. In addition to significant differences in average levels, local differences in concentrations of specific dioxin and furan congeners emerged. The town with the most notably different results was one in which people's diets consisted almost completely of locally produced food. The public bakeries in this town used diesel and/or a mixture of diesel and motor oil for heating the ovens in which they bake bread. Thus, the bread served as a major local exposure pathway for dioxin. ^[8]

Sometimes congener patterns of dioxins in breast milk can help to identify the source of exposure. In Finland, significant differences in the congener make-up of dioxins in breast milk emerged in different regions of the country. The researchers eventually traced the differences to the types of fish consumed in these regions. Different species of fish were contaminated with different congener combinations. ^[30]

Other unique exposure scenarios have turned up, as well. In Vietnam, concentrations of dioxin in breast milk were especially high after intensive aerial spraying of Agent Orange during the Vietnam War. ^[31] Agent Orange was highly contaminated with dioxin. Especially high levels of dioxin in breast milk as a result of Agent Orange exposure have also been an issue in Kazakhstan. ^[27] In Kazakhstan, women in one geographic region were found to have some of the highest levels in the world of the most toxic form of dioxin (2,3,7,8-TCDD) in their breast milk. The levels were most likely related to the use of Agent Orange to control weeds in the rice fields. The dioxin contaminants ran off into the lake and accumulated in fish, the dietary staple in the region.

Related Site on the Web

The Center for Health, Environment and Justice has posted this dioxin home page. It describes a nationwide campaign focused on eliminating all sources of dioxin discharge. This site provides general information about dioxin and information about the U.S. campaign to eliminate this toxic substance.

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Notes

1. IARC. Polychlorinated Dibenzo-para-dioxins and Polychlorinated Dibenzofurans, IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, ed. W.H.O.I.A.f.R.o., Cancer, Vol. 69. 1997, Lyon.

2. U.S. EPA. Exposure and Human Health Reassessment of 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) and Related Compounds, 2000, U.S. Environmental Protection Agency: Washington DC.

3. ATSDR. ToxFAQs for Chlorinated Dibenzo-p-Dioxins (CDDs), 1999, ATSDR.

4. Dewailly, E., et al. Exposure of Remote Maritime Populations to Coplanar PCBs, Environmental Health Perspectives Journal 1994; 102(Suppl 1): p. 205-209.

5. Brouwer, A., et al. Report of the WHO Working Group on the Assessment of Health Risks for Human Infants from Exposure to PCDDs, PCDFs and PCBs, Chemosphere 1998; 37(9-12): p. 1627-1643.

6. WHO. Levels of PCBs, PCDDs and PCDFs in Human Milk, 1996, WHO European Centre for Environment and Health: Bilthoven.

7. Schecter, A., et al. Dioxins, Dibenzofurans and Selected Chlorinated Organic Compounds in Human Milk and Blood from Cambodia, Germany, Thailand, the U.S.A., the U.S.S.R., and Vietnam, Chemosphere 1991; 23: p. 1903-1912.

8. Alawi, M.A., et al. Dioxins and Furans in the Jordanian Environment, Part 2: Levels of PCDD and PCDF in Human Milk Samples from Jordan,Chemosphere 1996; 33(12): p. 2469-74.

9. Rogan, W.J., et al. Should the Presence of Carcinogens in Breast Milk Discourage Breast Feeding?, Regulatory Toxicology and Pharmacology 1991; 13: p. 228-240.

10. Schecter, A., et al. Congener-specific Levels of Dioxins and Dibenzofurans in U.S. Food and Estimated Daily ToxicEequivalent Intake, Environmental Health Perspectives Journal 1994; 102(11): p. 962-966.

11. Schecter, A., et al. Chlorinated Dioxins and Dibenzofurans in Human Tissue from General Populations: A Selective Review, Environmental Health Perspectives Supplements 1994; 102(Supple 1): p. 159-171.

12. Peterson, A. Compilation of European Union Dioxin Exposure and Health Data Task 5 - Human Tissue and Milk Levels, 1999, European Commission Environment and UK Department of the Environment, Transport and the Regions: Oxfordshire.

13. Yrjanheikki, E.J. Levels of PCBs, PCDDs and PCDFs in Breast Milk: Results of WHO Coordinated Interlaboratory Quality Control Studies and Analytical Field Studies, 1989: Copenhagen.

14. Clench-Aas, J., et al. PCDD and PCDF in Human Milk from Scandinavia, with Special Emphasis on Norway, Journal of Toxicology and Environmental Health 1992; 37: p. 73-83.

15. Startin, J.R., M. Rose, and C. Offen. Analysis of PCDDs and PCDFs in Human Milk from the UK, Chemosphere 1989; 19: p. 985-88.

16. Wearne, S.J., et al. Time Trends in Human Dietary Exposure to PCDDs, PCDFs and PCBs in the UK, Organohalogen Compounds 1996; 31: p. 1-6.

17. Lunden, A. and K. Noren. Polychlorinated Naphthalenes and Other Organochlorine Contaminants in Swedish Human Milk, 1972-1992. Archives of Environmental Contamination and Toxicology 1998; 34: p. 414-23.

18. Noren, K. and D. Meironyte. Certain Organochlorine and Organobromine Contaminants in Swedish Human Milk in Perspective of Past 20-30 Years, Chemosphere 2000; 40: p. 1111-1123.

19. Deml, E., I. Mangelsdorf, and H. Greim. Chlorinated Dibenzodioxins and Dibenzofurans (PCDD/F) in Blood and Human Milk of Non-occupationally Exposed Persons Living in the Vicinity of a Municipal Waste Incinerator, Chemosphere 1996; 33: p. 1941-1950.

20. Beck, H., A. Dross, and W. Mathar. Dependence of PCDD and PCDF Levels in Human Milk on Various Parameters in Germany. II. Chemosphere 1992; 25: p. 1015-20.

21. Beck, H., et al. Dependence of PCDD and PCDF Levels in Human Milk on Various Parameters in the Federal Republic of Germany, Chemosphere 1989; 18: p. 1063-66.

22. Beck, H., A. Dross, and W. Mathar. PCDD and PCDF Exposure and Levels in Humans in Germany, Environmental Health Perspectives Journal 1994; 102(Suppl 1): p. 173-185.

23. Frommberger, R. Polychlorinated Dibenzo-p-dioxins and Polychlorinated Dibenzofurans in Cumulative Samples of Human Milk from Baden-Wurttemberg, FRG, Chemosphere 1990; 20: p. 333-42.

24. Papke, O. PCDD/PCDF: Human Background Data for Germany, a 10-Year Experience, Environmental Health Perspectives Journal 1998; 106(Suppl 2): p. 723-731.

25. Furst, P., et al. PCDD and PCDF Levels in Human Milk - Dependence on Period of Lactation, Chemosphere 1989; 18: p. 439-44.

26. Hooper, K., et al. Analysis of Breast Milk to Assess Exposure to Chlorinated Contaminants in Kazakhstan: Levels of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in Agricultural Villages of Southern Kazakhstan, Environmental Health Perspectives Journal 1998; 106(12): p. 797-806.

27. Hooper, K., et al. Analysis of Breast Milk to Assess Exposures to Chlorinated Contaminants in Kazakhstan: Sources of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) Exposure in an Agricultural Region of Southern Kazakhstan, Environmental Health Perspectives Journal 1999; 107(6): p. 447-456.

28. Petreas, M., et al. Analysis of Human Breast Milk to Assess Exposure to Chlorinated Contaminants in Kazakhstan, Organohalogen Compounds 1996; 30: p. 20-23.

29. Somogyi, A. Nuturing and Breast-feeding: Exposure to Chemicals in Breast Milk. Environmental Health Perspectives Journal 1993; 101(Suppl 2): p. 45-52.

30. Vartiainen, T., et al. PCDD, PCDF, and PCB Concentrations in Human Milk from Two Areas in Finland, Chemosphere 1997; 34(12): p. 2571-2583.

31. Lutter, C., et al. Breast Milk Contamination in Kazakhstan: Implications for Infant Feeding, Chemosphere 1998; 37(9-12): p. 1761-72.

last revised 5.22.01