Submitted to: Handbook of Ecotoxicology
Publication Type: Book / Chapter
Publication Acceptance Date: 6/24/2002
Publication Date: N/A
Citation: N/A Interpretive Summary: Polychorinated biphenyls, furans, and dioxins are all members of a group of chlorinated pollutants with similar modes of toxicity and environmental occurrence. All these compounds are the result of manufacturing or commerce and they all bioaccumulate. This study summarizes these chemicals, including their sources, pathways, interactions, and effects with organisms sand the environment, updating the previous edition of this book. Removal mechanisms are described including photolysis and microbial degradation. Some of these compounds are more biologically active than others. The common effects of these compounds are extensively reviewed and species-specific factors such as uptake, disposition and metabolism, interspecies differences in concentration, tissue distribution, and ligand affinity to receptors are examined. All of the active compounds have a planar structure and their cumulative risks are much greater in many instances. Considered within a generally accepted model of additivity, individual toxicity equivalent concentrations are summed to derive a total value of exposure for an organism of interest and the foods it consumes.
Technical Abstract: The sources, pathways, and effects of PCBs, PCDDs, and PCDFs (polychorinated biphenyls, dioxins, and furans) are described. The releases of these chlorinated organics into the environment, water and air, and their terrestrial fate, bioaccumulation and abiotic dispersal are documented and updated from the previous edition of this book. Removal mechanisms are described including photolysis, and microbial degradation. Common effects of these compounds are extensively reviewed, especially their aryl hydrogenase receptor binding that best describes their common toxicity to dioxins. Species-specific factors such as uptake, disposition and metabolism of TCDD, as well as interspecies differences in concentration, tissue distribution and ligand affinity of the Ah receptor, all likely play a role in determining the relative sensitivity of organisms to TCDD. The mechanism of action of these planar halogenated hydrocarbons is of great importance because the cumulative risks are much greater in many instances. Considered within a generally accepted model of additivity, the individual toxicity equivalent concentrations of these congeners are summed to derive a total value of exposure in an organism of interest or in the foods it consumes.