Polybrominated dibenzo-p-dioxins and furans (PBDD/Fs): Contamination in food, humans and dietary exposure

Abstract

Polybrominated dibenzo-p-dioxins and dibenzofurans (PBDD/Fs) have been recognised as environmental pollutants for decades but their occurrence in food has only recently been reported. They elicit the same type of toxic response as analogous polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) with similar potencies and effects, and share similar origins - inadvertent production during combustion and occurrence as by-products in industrial chemicals. Surprisingly, PBDD/Fs have received considerably less attention than PCDD/Fs, perhaps because determination requires a higher degree of analytical competence, a result of the higher adsorptivity and lability associated with carbon-bromine bonding. For most populations, the principal exposure pathway is dietary intake. The PBDD/F toxicity arising from occurrence in foods has often been expressed as toxic equivalents (TEQs) using the same scheme developed for PCDD/Fs. This approach is convenient, but resulting TEQ estimates are more uncertain, given the known differences in response for some analogous congeners and also the different patterns of PBDD/F occurrence confirmed by the newer data. Further studies to consolidate potency factors would help to refine TEQ estimates. Characteristically, most foods and human tissues show more frequent and higher PBDF concentrations relative to PBDDs, reflecting major source patterns. Occurrence in food ranges from <0.01 to several thousand pg/g (or up to 0.3 pg TEQ/g whole weight) which is comparable to PCDD/F occurrence (ΣPBDD/F TEQs are underestimated as not all relevant congeners are included). Plant based foods show higher PBDD/F: PCDD/F TEQ ratios. Reported PBDD/F dietary intakes suggest that some population groups, particularly young children, may exceed the revised tolerable weekly intake for dioxin-like contaminants (2 pg TEQ/kg bw/week), even for mean consumption estimated with lower bound data. It is evident that the omission of PBDD/Fs from the TEQ scheme results in a significant underestimation of the cumulative toxicity and associated risk arising from this mode of action.

Keywords: AhR mediated toxicity; Dietary intake; Dioxin-like; PBDEs; Tissue burdens; Toxicology.