Facts about Dioxins
The Minnesota Department of Health (MDH) considers "dioxins" to be a group
of related compounds that exhibit a similar spectrum of health effects.
Dioxins are extremely persistent and once released remain in the environment
a very long time. Since the 1980's regulatory and voluntary actions have
dramatically reduced the amount of dioxins released into the environment
and the amount of dioxins to which people are exposed. Based on recent
measures it appears that levels in our bodies are decreasing. However,
when current body burdens in the population are compared to the levels
of concern derived from animal and human studies it is clear that it is
desirable and necessary to further reduce human exposure.
Updated October 2006
We all have some amount of dioxins in our bodies. Dietary intake of animal fat is the major route of exposure for the general population. For most people, eating a varied, balanced, low-fat diet will result in reduced fat intake and will reduce exposure to dioxins. A low-fat diet, aside from reducing your exposure to dioxins, also will reduce your chances of developing heart disease, high blood pressure, certain cancers, and diabetes.
For additional information about dioxins, see the links below or contact the Health Risk Assessment Unit. For Minnesota Department of Health guidance about how to evaluate dioxin health risks, see Methods for Estimating the Carcinogenic Health Risks from Dioxin-like Compounds (PDF: 107KB/9 pages).
- What are dioxins?
- Why are we concerned about dioxins?
- Where do dioxins come from?
- What happens to dioxins once they enter the environment?
- How might you be exposed to dioxins?
- How can you minimize your exposure to dioxins?
- What are the Minnesota Department of Health (MDH), other state agencies and federal governmental agencies doing about dioxin?
- Where can you get more information on dioxin?
What are dioxins?
The term "dioxins" is used to refer to a family of complex but related chlorinated compounds with similar chemical structures and biological activity. This family is composed of specific compounds from three chemical groups: polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), and polychlorinated biphenyls (PCBs).
Only a subset of the compounds in these three groups exhibit "dioxin-like" toxicity: 7 of the 75 PCDD compounds (i.e., those with chlorine substitutions in the 2,3,7, and 8 positions), 10 of the 135 PCDF compounds (i.e., those with chlorine substitution in the 2,3,7, and 8 positions), and 12 of the 209 PCB compounds (those containing 4 or more chlorines with 1 or no substitutions at the 2, 2', 6, or 6' position). These 29 compounds are identified as having varying levels of "dioxin-like" toxicity.
Throughout this web page, the term "dioxins" refers to the group of 29 compounds identified in the table below.
List of Chemicals That Have Varying Dioxin-like Toxicity
|Polychlorinated Dibenzo-p-dioxins (PCDDs)||Polychlorinated Dibenzofurans (PCDFs)||Polychlorinated Biphenyls (PCBs)|
|2,3,7,8-TetraCDD (TCDD)||2,3,7,8-TetraCDF||3,3'4,4'-TetraCB (PCB 77)|
|1,2,3,7,8-PentaCDD||1,2,3,7,8-PentaCDF||3,4,4',5-TetraCB (PCB 81)|
|1,2,3,4,7,8-HexaCDD||2,3,4,7,8-PentaCDF||2,3,3',4,4'-PentaCB (PCB 105)|
|1,2,3,6,7,8-HexaCDD||1,2,3,4,7,8-HexaCDF||2,3,4,4',5-PentaCB (PCB 114)|
|1,2,3,7,8,9-HexaCDD||1,2,3,6,7,8-HexaCDF||2,3',4,4',5-PentaCB (PCB 118)|
|1,2,3,4,6,7,8-HeptaCDD||2,3,4,6,7,8-HexaCDF||2',3,4,4',5-PentaCB (PCB 123)|
|1,2,3,4,6,7,8,9-OctaCDD||1,2,3,7,8,9-HexaCDF||3,3',4,4',5-PentaCB (PCB 126)|
|1,2,3,4,6,7,8-HeptaCDF||2,3,3',4,4',5-HexaCB (PCB 156)|
|1,2,3,4,7,8,9-HeptapCDF||2,3,3',4,4',5'-HexaCB (PCB 157)|
|1,2,3,4,6,7,8,9-OctaCDF||2,3',4,4',5,5'-HexaCB (PCB 167)|
|3,3',4,4',5,5'-HexaCB (PCB 169)|
|2,3,3',4,4',5,5'-HeptaCB (PCB 189)|
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Dioxins are almost insoluble in water, but are quite soluble in organic solvents and fats. The generic molecular structures are shown below.
Why are we concerned about dioxins?
Dioxins interfere with the basic and common Ah (aryl hydrocarbon) receptor involved in cellular regulatory processes. The Ah receptor is a member of a family of gene regulatory proteins. When dioxins interact with this receptor a chain of events begins that, to a certain extent, the body is able to interrupt and correct. However, studies in animals show that dioxins given in large enough quantities or at important stages of development, can alter normal growth and function of almost every system in the body.
There are many difficulties in evaluating dioxins' health effects in humans. The available data are limited to studies involving occupational or accidental exposures to complex mixtures of potentially toxic compounds that included dioxins. Therefore, it is not certain that all observed effects are attributable only to dioxins. Also, the mixtures in these studies were often contained in an unusual matrix (e.g., pesticide mixtures, contaminated rice cooking oil) that may not resemble the environmental matrices or mixtures to which most people are exposed.
Adult occupational or accidental exposure to chemical mixtures that include dioxins has been associated with an increased prevalence of chloracne, hyperpigmentation of the skin, mild liver toxicity (e.g., transient elevations in liver enzymes), and changes in male reproductive hormones. Some of the studies have reported additional health effects such as changes in thyroid hormone levels, endometriosis, diabetes, and alterations in immune function, however, these health effects have not been consistently reported (i.e., some studies have found the effects and some have not).
A great deal of attention has been paid to developmental effects of dioxins. Studies in humans have focused on exposures to the fetus during pregnancy and exposures to infants as a result of breastfeeding. Exposures to chemical mixtures that include dioxins during pregnancy have been associated with subtle developmental changes. The health effects include changes in liver function, thyroid hormone levels, immune cell levels, and decreased performance in tests of learning and intelligence. While breast milk may contain dioxins, the nutrients and nurturing of breastfeeding appear to offer unique protection from dioxins' adverse effects on the nervous system such that breast-fed babies outperform bottle-fed babies on tests of learning. Higher exposures during pregnancy (e.g., accidental exposure to cooking oil contaminated with electrical oil containing PCBs and PCDFs) are linked to decreases in infant size and weight, delayed physical development, and changes in population sex ratios at birth.
Due to the limitations in the studies of humans (e.g., presence of multiple chemicals, unusual matrices, uncertain exposure amounts, etc.) there are significant uncertainties in our current understanding of the relationship between exposure to dioxins and risk of health effects in humans. Studies in laboratory animals, which have the advantage of administering known amounts of dioxins under controlled laboratory conditions, provide most of the current information on the health effects that are known to be associated with exposure to dioxins.
Animal studies have shown that exposure to dioxins cause a broad range of health effects, with the severity of the effect depending on dose, age, gender, and species. The observed health effects include changes in the level or activity of enzymes and hormones, organs weight changes, altered reproduction and normal development of offspring, and immune dysfunction. High doses cause a failure of animals to grow, called wasting disease, which is fatal. Low doses cause small changes in cell function-such as changes in levels of thyroid hormones or enzyme activity. Doses to the fetus or young animal may also delay or harm development of tissues and the nervous system. These harmful effects include prenatal mortality; mineralization defects of teeth; cleft palate; changes in genitalia, sex organs, and glands; delayed sexual maturation; growth retardation; and functional changes in learning and sexual behavior (demasculization). Effects on reproduction include decreased fertility, endometriosis, decreased litter size, shortened gestation, changes in male sex organ weights and morphology, and decreased spermatogenesis.
Cancer is also a health effect of concern for dioxins. Several studies suggest that workers exposed to high levels of 2,3,7,8-TCDD over many years have an increased risk of developing cancer. The relationship of apparent increases in cancer in these occupationally exposed populations to calculations of general population risk remains uncertain. Animal studies have conclusively shown that 2,3,7,8-TCDD is a carcinogen capable of increasing the incidence of tumors at multiple sites.
The Minnesota Department of Health (MDH), United States Environmental Protection Agency (U.S. EPA) , National Toxicology Program (NTP) and the International Agency for Cancer Research (IARC) have characterized 2,3,7,8-TCDD as a "human carcinogen". The MDH and the U.S. EPA have classified dioxins as "likely" human carcinogens.
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Where do dioxins come from?
Current ambient levels of dioxins are largely the result of human activities. Polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) are inadvertently produced through a number of human activities as well as by natural processes. Although no longer produced in the United States, PCBs were once manufactured and widely used as coolants and lubricants in electrical equipment.
Dioxins are released into the air from combustion processes such as commercial, municipal or medical waste incineration, from burning fuels (e.g., wood, coal, oil), and burning of household trash. Chlorine bleaching of pulp and paper, certain types of chemical manufacturing and industrial processing can create low quantities of dioxin. Dioxins have also been detected at low concentrations in cigarette smoke, home-heating systems, and exhaust from cars. Burning of materials that contain chlorine, such as plastics, wood treated with pentachlorophenol (PCP), and pesticide-treated waste produce dioxins. Dioxins can also be formed during forest fires and volcanic eruptions.
The amount of dioxins that have been released from various sources has changed significantly over time. Historically, the majority of dioxins released were from commercial, municipal, and medical waste incineration, the manufacture and use of certain herbicides, and chlorine bleaching of pulp and paper. Regulatory and voluntary actions have dramatically reduced these sources of dioxins such that they are no longer the major contributors of release of dioxins to the environment in the United States. These sources of dioxin emissions, however, still occur elsewhere in the world. Currently uncontrolled burning of household trash and accidental fires at landfills are thought to be among the largest sources of dioxins in the United States. For more information on backyard burning of household trash, see the Minnesota Pollution Control Agency.
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What happens to dioxins once they enter the environment?
When released into the air, dioxins disperse and travel long distances and eventually deposit from the atmosphere onto land, surface water and vegetation. Dioxins are extremely persistent compounds. Environmental levels from both human-made and natural sources will take years to decline.
Dioxins do not easily dissolve in water and therefore most of the dioxins that enter surface water become strongly attached to particles and eventually settle in the sediment. Dioxins that deposit on land bind strongly to soil particles. However, the presence of other chemical pollutants in contaminated soil, such as those found at Superfund sites, may dissolve dioxins, making it easier for dioxins to move through the soil. Particles and oils contaminated with dioxins can occasionally result in contamination of groundwater. Soil erosion and surface runoff can also transport dioxins into surface water.
Terrestrial and aquatic animals consume dioxins on plants and in the air, water, sediment, and soil. Dioxins are difficult for the body to breakdown and are slowly excreted. Concentrations usually increase at each step in the food chain, e.g., dioxins in plants are concentrated in the bodies of plant eating animals and are then further concentrated when meat eating animals eat plant eating animals. This process, known as biomagnification, is the reason low levels of dioxins in water, sediment, soil and vegetation can result in elevated concentrations in terrestrial and aquatic animals. Since dioxins do not easily dissolve in water they tend to move into the fat of animals and plants. The U.S. EPA draft dioxin reassessment proposes that most dioxins enter the food chain by being deposited from the atmosphere.
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How might you be exposed to dioxins?
Because dioxins have been in our environment for a long time and are so widespread, we all have some amount of dioxins in our bodies. Current exposures to dioxins are largely due to past releases. Regulatory and voluntary actions have dramatically reduced several of the major historic sources of dioxins. Based on recent measurements by the Center for Disease Control it appears that the levels of dioxins in our bodies are also decreasing. For more information about dioxin exposures, see the CDC National Report on Human Exposure to Environmental Chemicals.
For the general population most exposure to dioxins occurs through the diet, with over 95% of dioxin intake for a typical adult coming through intake of animal fats in fish, meat and dairy products. Small amounts of exposure occur from breathing contaminated air, from inadvertent ingestion of contaminated soil, and from absorption through the skin from contact with contaminated media (e.g., soil, water). The actual intake of dioxins for any one person will depend on a number of factors, including the amount and duration of exposure (e.g., dietary habits) and the concentration of dioxin in the contacted media (e.g., food, soil, water, air).
People whose diet consists of locally harvested foods may have higher or lower exposure to dioxins than people who eat food from the global commercial market. Local sources that introduce dioxins into environmental media or the food chain (e.g., hazardous waste sites, backyard burn barrels) may significantly increase one's exposure to dioxins.
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How can you minimize your exposure to dioxins?
Eating a varied, balanced, low-fat diet will result in reduced fat consumption and reduced exposure to dioxins for most people. The Dietary Guidelines for Americans recommends eating a variety of foods; maintaining a healthy weight; choosing a diet low in fat by eating fish, lean meat and low or fat free dairy products; and increasing consumption of fruit, vegetables and grain products. Fish, meat and dairy products are important sources of nutrients and an important part of a balanced diet. You can reduce fat by trimming visible fat from meat and removing skin from fish and poultry. Attempting to eliminate all fat from your diet is not recommended. For more information, see Fish Consumption Advice.
Benefits of a balanced low fat diet, aside from reduced exposure to dioxins, also include reducing your chances of developing heart disease, high blood pressure, certain cancers and the most common type of diabetes.
Breast milk can be a source of exposure to dioxins. Studies have shown that the benefits of breastfeeding outweigh the potential risks associated with dioxin intake. Breast milk is known to be the best form of nutrition for infants. Breast fed infants show gains over bottle-fed infants in growth, immunity and development. Due to its benefits to both the mother and child breastfeeding is strongly encouraged. For more information, see the American Academy of Pediatrics and The National Women's Health Information Center.
As stated above, local sources such as backyard burning of household trash and cigarettes can introduce dioxins into the environment. Individuals who burn their trash or smoke can decrease their own exposure as well as exposure to family members and neighbors by discontinuing these activities.
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What are the Minnesota Department of Health, other state agencies and federal governmental agencies doing about dioxin?
Minnesota Department of Health:
The Minnesota Department of Health (MDH) Environmental Health Division develops educational materials, such as this web page, to provide information to the general public as well as provides risk assessment consultation to other state and local agencies. The MDH role is primarily advisory and typically consists of providing toxicity or risk evaluation guidance. The MDH issued guidance for estimating the carcinogenic health risks from dioxins in 2003, based in part on information contained in the EPA 2003 draft dioxin reassessment. The National Research Council (NRC) of the National Academies has recently completed a comprehensive review of the EPA 2003 draft assessment. The NRC report contained conclusions and recommendations on how the EPA 2003 draft reassessment could be improved. The MDH is reviewing the NRC report as well as other relevant scientific data generated since the draft reassessment (e.g., the chronic toxicological study conducted by the National Toxicology Program. MDH does not recommend any changes to its 2003 guidance at this time.
The MDH also conducts public health evaluations at hazardous waste sites where dioxin has been found. MDH staff review available information and request additional information, if necessary, about conditions at the site. If there is evidence that people are being exposed or could be exposed, MDH staff will seek to determine if there is potential for health impacts. In situations where potential exposure to harmful levels of dioxin is identified, the MDH works with local units of government, community groups, regulatory agencies and companies to prevent or reduce human exposure.
Pollution Control Agency (MPCA):
651-296-6300 or 1-800-657-3864
The Minnesota Pollution Control Agency (MPCA) provides state coordination for several U.S. EPA program areas (See Section on U.S. EPA activities below). Examples of these include the Lake Superior Binational Program, ambient surface water quality standards, water and air permitting requirements, and remediation of contaminated land and ground water.
The MPCA uses a dioxin standard applicable to waters in the Lake Superior basin, and site-specific dioxin criteria elsewhere, to control the discharge of dioxin to surface waters. The standards or criteria can be the basis for permit effluent limits that must be met by dischargers in cases where dioxin is a concern, such as at a few ground water remediation sites. If the dioxin standard is exceeded in a water body, the MPCA may conduct a Total Maximum Daily Load (TMDL) study to determine the source(s), both point and nonpoint, of the dioxin. In a later phase of the TMDL a plan is developed to bring the water body back into compliance with the standard. The lower part of the St. Louis River has been identified as exceeding the dioxin standard. For more information about TMDL's and which parts of the St. Louis River are affected, see TMDL's and Minnesota Waterways.
In addition, the MPCA continues to work on reducing the amount of on-site residential garbage disposal that occurs in the state with a focus on burn barrels in particular. Proper waste management, health, and environmental impacts are the primary focus used in reduction and educational efforts. Programs are primarily focused at the county and city level and aimed at targeted citizen groups and rural residents. Health impacts from burn barrel emissions, including dioxin, are part of the educational message used to change behavior. The MOEA also continues to partner with other agencies and organizations such as the MPCA, Minnesota Department of Natural Resources (DNR), MDH, and Bi-National Toxics Strategy Dioxin Burn Barrel Group on burn barrel reduction strategies. For more information on burn barrel reduction and education efforts in Minnesota, see the MOEA's burn barrel page.
Department of Agriculture:
651-201-6000 or 1-800-967-2474 or TTY: 1-800-627-3529
The U.S. EPA pursues control and management of dioxins through its major program areas (e.g., air, surface water, land, chemical production). Under the authority of the Clean Air Act (CAA) and the Resource Conservation and Recovery Act (RCRA) U.S. EPA has promulgated stringent emission requirements from municipal, medial and hazardous waste incinerators.
The U.S. EPA has published ambient water quality criteria and promulgated a maximum contaminant level (MCL) for public drinking water systems. These criteria serve as guidance for states in establishing state ambient water quality standards. The state standards are then utilized to set discharge limits in permits.
Under the Superfund and RCRA Corrective Action programs U.S. EPA investigates and cleans up contaminated land. Regulatory authority under the RCRA Hazardous Waste Identification and Disposal Rules has permitted U.S. EPA to develop rules to identify and limit disposal options for dioxin containing wastes. The Toxic Substance Control Act (TSCA) New Chemicals Program allows the U.S. EPA to prevent the manufacture of new chemicals that are significantly contaminated with dioxins.
The U.S. EPA is also involved in international effort's to control, remediate, and prevent releases of persistent, bioaccumulative and toxic pollutants (PBTs), including dioxins. Among U.S. EPA's dioxin related activities is the 1997 Canada-U.S. Great Lakes Binational Toxics Strategy (BNS). (See, U.S. EPA's PBT strategy).
The Great Lakes Binational Toxics Strategy provides a framework for actions to reduce or eliminate persistent toxic substances, especially those which bioaccumulate, from the Great Lakes Basin. The United States dioxin goal calls for a 75 percent reduction of total releases of anthropogenic sources of dioxins and furans by the year 2006.
U.S. EPA, Environment Canada, the Lake Superior states (including Minnesota), and Ontario have entered into an additional agreement that includes a goal of zero discharge and zero emission of nine designated pollutants, including dioxin, into Lake Superior. This Lake Superior Binational Program has established a reduction schedule for dioxin, an inventory of sources, a dioxin "use tree" and identified dioxin reduction activities within the various jurisdictions. See Great Lakes Binational Toxics Strategy and the Lake Superior Binational Program.
For more information, see U.S. EPA's nationwide efforts to reduce dioxin emissions.
The FDA and USDA's Food Safety Inspection Service (FSIS) currently monitor for dioxins in the United States food and feed supply. Typically the levels found are consistent with U.S. EPA's estimates for background occurrence. If atypical levels are observed an investigation is launched by the FDA, FSIS and U.S. EPA to determine the source of dioxins. If the investigation determines a specific source of the increased dioxins the FDA and FSIS take action to reduce or remove the source.
In addition to exploring ways to expand the existing monitoring program the FDA and FSIS have requested a National Academy of Sciences' study in 2003 to examine potential opportunities for reducing dioxin input into the food supply.
For more information about dioxin in food, see the FDA Web site.
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Where can you get more information on dioxin?
The U.S. EPA is in the final stages of completing a comprehensive report entitled: Exposure and Human Health Reassessment of 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) and Related Compounds. This report is commonly referred to as the U.S. EPA dioxin reassessment. For the draft reassessment and other related U.S. EPA documents, see the National Center for Environmental Assessment dioxin web page.
The draft dioxin reassessment consists of three parts. Part I: Estimating Exposure to Dioxin-Like Compounds includes three volumes that focus on sources, levels of dioxin-like compounds in environmental media, and human exposures. Part II: Health Assessment for 2,3,7,8-Tetrachlorodibenzo-p-Dixoin (TCDD) and Related Compounds consists of two volumes that include information on health effects, mode of action, pharmacokinetics, dose-response, and the Toxic Equivalency Factors (TEFs). Part III: Integrated Summary and Risk Characterization for 2,3,7,8--Tetrachlorodibenzo-p-Dioxin (TCDD) and Related Compounds summarizes the overall conclusions of the reassessment including, key findings related to potential hazards, risks, and uncertainties.
The Interagency Working Group on Dioxin (IWG), composed of federal agencies that address health, food and the environment, has also prepared the fact sheet, Questions and Answers about Dioxins.
The U.S. EPA's draft reassessment and the IWG's "Questions and Answers" document were key sources of information utilized in preparation of this web page.
The Agency for Toxic Substances and Disease Registry (ATSDR) Toxicological Profile for Chlorinated Dibenzo-p-dioxins (CDDs) (December 1998) provides a concise characterization of toxicological and adverse health effects information.
The Center for Disease Control (CDC) Fourth National Report on Human Exposure to Environmental Chemicals (2009) provides an assessment of the exposure of the United States population to environmental chemicals by utilizing biomonitoring. Biomonitoring is the assessment of exposure to chemicals by measuring the chemical or its metabolites in human specimens such as blood or urine.
The World Health Organization (WHO) has prepared a fact sheet, Dioxins and their Effects on Human Health.
The National Research Council (NRC) of the National Academies has reviewed the EPA 2003 draft reassessment. The NRC report was issued in July 2006 and contains the committee's conclusions and recommendations on how EPA could improve the scientific robustness and clarity of the reassessment.
The National Toxicology Program (NTP) recently released the results of their long-term toxicology and carcinogenesis studies of TCDD. This study is one in a series of studies carried out as part of a multistudy NTP initiative examining the relative chronic toxicity and carcinogenicity of dioxin-like compounds (DLCs) and structurally-related polychlorinated biphenyls (PCBs).
The Office of Environmental Health Hazard Assessment of the California Environmental Protection Agency released a draft Public Health Goal for TCDD in Drinking Water in 2005.
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