Polybrominated dibenzo-p-dioxins and dibenzofurans: literature review and health assessment.

Abstract

Polybrominated dibenzo-p-dioxins (PBDDs) and dibenzofurans (PBDFs) occur as trace (ppb) contaminants in brominated flame retardants and are produced during combustion of these chemicals. They are also formed when organics are incinerated in the presence of bromine, e.g., in municipal and industrial incinerators and in internal-combustion engines. Combustion of organics in the presence of both bromine and chlorine results in the formation of mixed (i.e., bromo, bromo/chloro and chloro) halogenated dibenzo-p-dioxins and dibenzofurans (HDDs and HDFs). There are 4600 potential mixed congeners. The biological effects of PBDDs and PBDFs are similar, if not identical, to those of PCDDs and PCDFs. Both groups of compounds induce hepatic aryl hydrocarbon hydroxylase (AHH) and ethoxyresorufin-o-deethylase (EROD) in rats and cause wasting and thymic atrophy in rats and guinea pigs. Tetrabrominated dinenzo-p-dioxin (TBDD) and dibenzofuran (TBDF) are reproductive toxins in mice and produce skin lesions in the rabbit-ear acnegenic test. The brominated compounds appear to bind to the same cytosolic receptors believed to mediate the toxicities of the chlorinated analogs. When compared on a molar-concentration basis, the brominated compounds are equipotent to the chlorinated analogs. TBDD is absorbed after oral, dermal, or intratracheal administration in rats, stored in the liver and adipose tissue, and eliminated in the feces through biliary excretion. The biological half-lives of the brominated compounds appear to be somewhat shorter than those of the corresponding chlorinated species. The brominated compounds, like their chlorinated congeners, have the potential to cause dermal, hepatic, and gastrointestinal toxicities in humans.(ABSTRACT TRUNCATED AT 250 WORDS)