Dioxins and Furans


Polychlorinated dibenzo-para-dioxins (dioxins) and polychlorinated dibenzofurans (furans) are two groups of planar tricyclic compounds that have very similar chemical structures and properties. They may contain between 1 and 8 chlorine atoms; dioxins have 75 possible positional isomers and furans have 135 positional isomers. They are generally very insoluble in water, are lipophilic and are very persistent.

The chemical properties of each of the isomers has not been elucidated, further complicating a discussion of their properties which vary with the number of chlorine atoms present.

Neither dioxins nor furans are produced commercially, and they have no known use. They are by-products resulting from the production of other chemicals.

Dioxins may be released into the environment through the production of pesticides and other chlorinated substances. Furans are a major contaminant of PCBs (Polychlorinated biphenyls). Both dioxins and furans are related to a variety of incineration reactions, and the synthesis and use of a variety of chemical products. Dioxins and furans have been detected in emissions from the incineration of hospital waste, municipal waste, hazardous waste, car emissions, and the incineration of coal, peat and wood. Of the 210 dioxins and furans, 17 contribute most significantly to the toxicity of complex mixtures. In order to facilitate a comparison of mixtures, International Toxicity Equivalency Factors (TEFs) have been assigned to individual dioxins and furans based on a comparison of toxicity to 2,3,7,8-tetrachlorodibenzodioxin (2,3,7,8-TCDD). For example, 2,3,7,8-TCDF has been shown to be approximately one-tenth as toxic as 2,3,7,8-TCDD in animal tests, and its toxic equivalent value is 0.1. TEFs are regarded as risk management tools and they do not necessarily represent actual toxicity with respect to all endpoints. Rather, they tend to overestimate the toxicity of mixtures.

Usage in South East Asia


Used or Found in Country?

Years of Usage



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Viet Nam


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Potential Effects on Humans

At the present time, the only persistent effect associated with Dioxin exposure in humans is Chloracne (an acne-like eruption of blackheads, cysts, and pustules).

Other health effects that have been reported include peripheral neuropathies, fatigue, depression, personality changes, hepatitis, enlarged liver, abnormal enzyme levels and porphyria cutanea tarda, though no causal relationships were established in every case.

Results of a study on 1,520 workers known to have been exposed to 2,3,7,8-TCDD for a period of at least one year, and with a latency of at least twenty years between exposure and diagnosis of disease, revealed a slightly, but significantly elevated mortality from soft tissue sarcoma and cancers of the respiratory system. As with other studies, interpretation of results was limited by the small number of deaths and by possible confounders including smoking and other occupational exposures.

Two more recent studies followed a young population from the area of the Seveso, Italy industrial accident. The first, a cancer study, examined a cohort of people aged 0-19 years living in the accident area at the time of the accident, for the period 1977-1986. While a consistent tendency toward increased risk was apparent, none of the relative risks were significantly elevated. Non-significant increases in thyroid cancer and myeloid leukemia were also observed. The study is limited, however, by the relatively short latency periods, the definition of exposure based on place of residence and the limited number of events.

The second study examined the mortality of the same cohort of people for the same time period. Among the exposed, mortality owing to all causes did not deviate from expectations, however, as noted above, this study provides only limited evidence.

Direct exposure of humans to furans has been reported in two incidents of rice oil contamination by PCBs contaminated with PCDFs, in Japan (Yusho) and Taiwan (Yucheng). While it is possible that the effects observed in these incidents may be due to the presence of furans, the similarity of structure, effects and mode of action of PCBs and PCDFs precludes a definite conclusion on the causative agent.

Studies in exposed human populations and in non-human primates have shown that halogenated aromatic hydrocarbons produce measurable alterations in both innate and acquired immunity, although significant deficits in immunocompetence have not been conclusively associated with these changes.

IARC has concluded that while there is inadequate evidence for the carcinogenicity of 2,3,7,8-TCDD in humans, there is sufficient evidence in experimental animals. IARC has classified 2,3,7,8-TCDD as a possible human carcinogen (Group 2B). Other chlorinated dibenzodioxins (other than 2,3,7,8-TCDD) are deemed not classifiable as to their carcinogenicity in humans.

Potential Effects on Plants and Animals

The acute oral toxicity in laboratory animals is highly variable, with LD50 values ranging from 0.6 µg/kg body weight in guinea pigs to 1,157 µg/kg in hamsters.

Effects of dioxin exposure that are common to most, and sometimes all species include wasting, lymphoid involution, hepatotoxicity, chloracne and epidermal changes, and gastric lesions.

Other characteristic responses include:

  • edema, ascites and hypopericardium in chickens;
  • fetal death and resorption in rats; and
  • fetal wastage, embryotoxicity and malformations in mice.

A three-generation study was conducted in which rats were fed diets containing 2,3,7,8-TCDD. Significant decreases in fertility and neonatal survival were observed in the group receiving 0.1 µg TCDD/kg/day. At 0.01 µg TCDD/kg/day, fertility was significantly reduced in the f1 and f2 generations. Decreases in litter size, gestation survival and neonatal survival and growth were also observed at this dose level. No effect on fertility, litter size at birth or post natal body weight was observed in any generation of the 0.001 µg TCDD/kg/day group.

Some teratogenic effects have been observed in mice in association with dioxin and furan exposure, including hydronephrosis and cleft palate. The most teratogenic isomer was 2,3,4,7,8-pentachlorodibenzofuran, with an ED50 values of 36 µg/kg for cleft palate and 7 µg/kg for hydronephrosis. Teratogenic responses observed are similar to those seen with TCDD, but these compounds are only 1/10 to 1/100 as potent.

Dioxins, specifically 2,3,7,8-TCDD, are associated with a variety of adverse effects on the reproductive systems of both male and female rats. Male reproductive toxicity has included altered regulation of luteinizing hormone secretion, reduced testicular steroidogenesis, reduced plasma androgen concentrations, reduced testis and accessory sex organ weights, abnormal testis morphology, decreased spermatogenesis, and reduced fertility. Signs of female reproductive toxicity included hormonal irregularities in the oestrous cycle, reduced litter size and reduced fertility.

A review of recent literature concerning 2,3,7,8-TCDD effects on immunocompetence suggests that 2,3,7,8-TCDD either indirectly (in the case of T-cells) or directly (in the case of B-cells) affects the maturational or differentiative processes of immunocompetent cells.

Exposure of fish to dioxins and furans results in a delayed mortality that can continue many days post-exposure. Rainbow trout exposed to 2,3,7,8-TCDD and to 2,3,7,8-TCDF for 28 days, followed by a 28 day depuration period, had a 56-day LC50 of 46 pg/L for TCDD and a NOEC for TCDD based on growth and mortality, below the lowest exposure concentration of 38 pg/L. The 56-day NOEC for TCDF was calculated to be 1.79 ng/L for mortality and 0.41 ng/L for growth. Mortality and behavioural changes such as lethargic swimming, feeding inhibition and lack of response to external stimuli continued after the 28-day exposure period ended.

Early life stages of fish are very sensitive to the effects of dioxins, furans, and PCBs. Parts per trillion concentrations of these structurally related chemicals in lake trout and rainbow trout eggs exhibit toxicity through sac fry mortality associated with yolk sac edema and hemorrhages.

Great blue heron eggs collected from sites of low, intermediate and high contamination had levels of 2,3,7,8-TCDD in eggs of 10 ng/kg (wet weight), 135 ng/kg and 211 ng/kg, respectively. Although there was no effect on mortality of chicks, effects of contamination included decreased growth with increased TCDD level, depression of skeletal growth with increased TCDD levels and subcutaneous edema which increased with increasing PCDD and PCDF contamination. Also observed were shortened beaks and a scarcity of down follicles in the chicks from the more contaminated sites.

Mink administered TCDD experienced the wasting syndrome associated with TCDD intoxication and gastric lesions at higher dosages. A 28-day oral LD50 value was calculated to be 4.2 µg TCDD/kg body weight.

Accumulation Studies

Dioxins and furans are considered to be very stable and persistent, as illustrated by the half life of TCDD in soil of 10-12 years. This persistence, combined with high partition coefficients (up to 8.20 for OCDD) provides the necessary conditions for these compounds to bioconcentrate in organisms.

As with most other organochlorines, food is a major source of dioxins and furans in the general population, with food of animal origin contributing the most to human body burdens.

In a survey of dioxins in US food, total PCDD/Fs ranged from 0.42 ppt to 61.8 ppt (wet weight) (total TEq range: 0.02 to 1.5 ppt). The estimated daily intake for adults ranged from 0.3 to 3.0 pg TEqs/kg body weight, and for breast fed infants the range was 35.3 to 52.6 pg TEqs/kg body weight.

Recent estimates of adult average daily intake for Canada, Germany and the Netherlands are 1.52, 2, and 1 pg TEQ/kg bodyweight, respectively. These are below the TDI of 10 pg/kg body weight for lifetime exposure estimated by WHO.

Bioconcentration factors of 26,707 has been reported in rainbow trout (Salmo gairdneri) exposed to 2,3,7,8-TCDD.

The chemical properties of dioxins and furans (low water solubility, high stability and semi-volatility) favour their long range transport and these compounds have been detected in Arctic organisms.


For more information:

Adapted from Persistent Organic Pollutants: Information on POPs, their alternatives and alternative approaches (United Nations Environmental Programme (UNEP) 1995).

Soil Sampling For Dioxins In Da Nang, Viet Nam
Source: Hatfield Consultants
Hatfield Consultants The World Bank funded by the Canadian POPs Trust Fund through the      
Canadian International Development Agency
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