Dioxin TEFs

Dioxins occur in widely varying mixtures in the environment. This is because each source of dioxin generates the individual congeners in different proportions, which may change over time and with transport from one environmental compartment to another through differential degradation, metabolism, uptake, or elimination rates.

It is generally understood that different dioxin congeners are not equally toxic to biota, as defined by their ability to cause specific toxic effects in animals, and despite sharing a common mechanism of action. Therefore, to assess the likely toxicological effect of a particular mixture of dioxin congeners, scientists from the World Health Organization (WHO) and the US Environmental Protection Agency (US EPA) developed TEFs for individual 2,3,7,8-substituted dioxin congeners and dioxin-like compounds. The TEF represents the toxicity of a specific congener relative to 2,3,7,8-TCDD, recognized as the most potent dioxin from the earliest toxicological studies. Until recently, WHO and US EPA recognized different TEF values for some dioxin congeners due to different interpretations of the available toxicological studies. Further, WHO developed separate sets of TEFs for mammals, birds, and fish in response to recognition of differences in sensitivities and toxicity of certain congeners among different taxa. Dioxin TEFs are summarized in Table 3.

When interpreting the significance of environmental levels of dioxins, it is common practice to multiply the environmental concentration of individual congeners and their TEFs to derive a toxicity equivalent concentration (TEQ). The effective concentration of a mixture of dioxins is estimated by summing the TEQs of the individual congeners to derive a TEQfor the mixture (TEQ„). That is,

where ci is the concentration of an individual compound and TEF,- is the corresponding factor.

The underlying premise for using a TEF scheme to evaluate dioxins is twofold: first, the mode of action of all 2,3,7,8-substituted dioxins and dioxin-like congeners is the same (i.e., AhR mediated); and, second, the combined effects of the individual dioxin congeners are dose additive. Additivity is an important prerequisite of the TEF concept. There is strong evidence supporting both of these assumptions for dioxins and dioxin-like compounds.

Table 3 World Health Organization (WHO) TEFs for mammalsa, birdsb, and fishb


Mammals WHO (2005)

Birds WHO (1998)

Fish WHO (1998)



1,2,3,7,8-PentaCDD 1,2,3,4,6,7,8-HeptaCDD OctaCDD


2,3,7,8-TetraCDF 1,2,3,7,8-PentaCDF 2,3,4,7,8-PentaCDF 1,2,3,4,7,8-HexaCDF OctaCDF

PCB congeners IUPAC # Non-ortho-PCBs CB#77 PCB#81 PCB#126 PCB#169

Mono-ortho-PCBs PCB#105 PCB#114 PCB#118 PCB#123 PCB#156 PCB#157 PCB#167 PCB#189





0.00003 0.00003 0.00003 0.00003 0.00003 0.00003 0.00003 0.00003











0.0001 0.0005 0.005 0.00005

<0.000005 <0.000005 <0.000005 <0.000005 <0.000005 <0.000005 <0.000005 <0.000005

aVan den Berg M, Birnbaum L, Denison M, etal. (2006) The 2005 World Health Organization re-evaluation of human and mammalian toxic equivalency factors for dioxins and dioxin-like compounds. Toxicological Sciences 93(2): 223-241.

bVan Den Berg M, Birnbaum L, Bosveld A, et al. (1998) Toxic equivalency factors (TEFs) for PCBs, PCDDs, PCDFs for humans and wildlife. Environmental Health Perspectives 106: 550-557.

Some uncertainties in the TEF scheme are worth noting. The WHO concluded, for example, that there is considerable evidence that the relative toxicity of different congeners varies significantly among different taxonomic groups (e.g., birds, fish, and mammals). These differences may be even broader as more information becomes known regarding ecotoxicity to invertebrates, reptiles, and amphibians. In addition, the underlying toxicology studies used to derive TEF values rely on single large doses that are not typically encountered by animals; repeated exposure to lower doses is more likely, which may result in significant differences in tissue retention and biological response. It has been suggested, therefore, that additional studies are needed to define whether TEFs should be based on intake or tissue levels.

Finally, the assumption that the combined effects of the congeners are additive may not be true in all cases. There are studies providing evidence that non-dioxin-like AhR agonists and antagonists are able to increase or decrease the toxicity of 2,3,7,8-substituted compounds. In addition, there are natural nonchlorinated AhR agonists in the diets of many animals, and some studies have suggested that the potential effects of these may be significant. Several groups of compounds have been identified for possible future inclusion in the dioxin TEF scheme concept based on mechanistic considerations, including 3,4,4'-TCB (PCB 37) and certain polybrominated dibenzo-/>-dioxins (PBDDs) and diben-zofurans (PBDFs), mixed halogenated dibenzo-/>-dioxins (PXCDDs) and dibenzofurans (PXCDFs), polychlori-nated and brominated naphthalenes (PCNs and PBNs), and polybrominated biphenyls (PBBs). However, for most if not all of these compounds, there is a distinct lack of human and wildlife exposure data.

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