THE TOXICITY OF BROMINATED AND MIXED-HALOGENATED DIBENZO-P-DIOXINS AND DIBENZOFURANS - AN OVERVIEW

Brominated dibenzo-p-dioxins and dibenzofurans can be formed under lab oratory conditions by pyrolysis of flame retardants based on polybromi nated biphenyls and biphenyl ethers. Their occurrence in the environme nt, however, is due to combustion processes such as municipal waste in cineration and internal combustion engines. As these processes general ly take place in the presence of an excess of chlorine, predominantly mixed brominated and chlorinated compounds have been identified so far in environmental samples. Brominated dibenzo-p-dioxins or dibenzofura ns bind to the cytosolic Ah receptor about as avidly as their chlorina ted congeners and induce hepatic microsomal enzymes with comparable po tency. The same holds true for mixed brominated-chlorinated compounds. Cross pathologic symptoms-hypothyroidism, thymic atrophy, wasting of body mass, lethality-also occur at doses that on a molar concentration basis, are virtually identical to those seen with the chlorinated com pounds. Their potency to induce malformations in mice following prenat al exposure is equivalent to that of chlorinated dibenzo-p-dioxins and dibenzofurans. Possible activities as (co)carcinogens and endocrine d isrupters have not been evaluated, but are likely to exist Considering the overall similarity in action of chlorinated and brominated dibenz o-p-dioxins and dibenzofurans, environmental and health assessments sh ould be based on molar body burdens without discrimination for the nat ure of the halogen.