Impact of polychlorinated dibenzo-p-dioxins, dibenzofurans, and biphenyls on human and environmental health, with special emphasis on application of the toxic equivalency factor concept.
The environmental and biological impacts of polychlorinated dibenzo- p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), and polychlorinated biphenyls (PCBs) were discussed with specific emphasis on the application of the toxic equivalency factor (TEF) concept. Primary sources of PCDDs, PCDFs, and PCBs included chemical reactions, combustion processes, photochemical reactions, source leakages, disposal of contaminated materials, and biochemical processes, while secondary sources included food and water intake, inhalation, and skin exposure. The analysis of PCDDs, PCDFs, and PCBs included high resolution chromatographic/spectrometric and/or sample extraction methods in addition to quality assurance and cell culture bioassays. PCDDs and PCDFs were found primarily in abiotic samples such as air, water, snow, soil, and sediments, and in biotic samples from aquatic organisms. Human tissue levels and dietary intake of PCDD/PCDFs and their congeners were mentioned with reference to values from the World Health Organization. The dermal effects, immunotoxicity and hepatotoxicity as well as biochemical, teratogenic, carcinogenic, and neurobehavioral effects due to PCDD, PCDF, and PCB exposure were attributed to the mediation by an aryl hydrocarbon (Ah) receptor mechanism of action. The criteria for dioxin like activity of a particular compound (Ah receptor binding, induction of dioxin specific biochemical/toxic responses, and persistence and accumulation in the food chain) were discussed in reference to risk management purposes and the applicability of the TEF concept in relation to risk management. The neurobehavioral, neurochemical, carcinogenic, and endocrine changes associated with nonAh receptor mediated effects were distinguished from Ah receptor responses. Short term experiments, bioassays, and interactive effects were mentioned as components in the role of kinetics in the TEF concept. Adverse effects resulting from occupational and accidental exposure in humans and environmental exposure among animals were discussed. The authors conclude that the applicability of the TEF concept is dependent on Ah receptor mediated toxic responses.