Superfund Research Program
Development of a Demonstrable Model of Dioxin Formation
Project Leader: Barry Dellinger
Grant Number: R01ES015450
Funding Period: 2006-2009
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Project investigators developed demonstrable and practical models for the formation of polychlorinated dibenzo-pdioxins and dibenzofurans (PCDD/F), polybrominated dibenzo-p-dioxins and dibenzofurans (PBDD/F), and mixed bromo and chloro congeners (PCBDD/F) in combustion and thermal processes (cumulatively referred to as PXDD/F). It is well documented that PCDD/F will be formed in virtually any combustion/thermal process that contains a source of chlorine and carbon as well as a catalytically active transition metal such as copper, there is emerging data that PBDD/F and PCBDD/F will also form if there is a source of bromine. Since Superfund Sites contain a high concentration of both chlorinated and brominated hydrocarbons, PXDD/F represent a significant health hazard from thermal treatment or accidental fires of hazardous wastes. PCDD/F and PBDD/F may be formed by gas-phase or surface mediated pathways.
A reaction kinetic model for the surface-mediated formation of dioxins on 5% CuO / silica catalysts was developed. An expanded reaction kinetic model, including 16 surface reactions, was proposed to explain the yields of PCDD/F obtained in an experimental study of the reaction of 2-chlorophenol over a CuO/silica surface. One of the main conclusions from this work was the surface mechanism can be based on the gas phase mechanism for PCDD/F formation from multi-chlorinated phenols widely discussed in the literature. Consequently, to develop a surface model it is important to clarify the model details in the gas-phase.
The research team developed a core, reaction-kinetic model for surface mediated formation of PCDD and PCDF. They also developed extensive data indicating that persistent free radicals (PFRs) are formed and are key intermediates in the formation of PCDD/F on metal oxide surfaces.
The researchers defined the impact of ultrafine particulate matter (PM0.1) on pulmonary pathophysiology of neonatal rats. Acute inhalation exposure to combustion generated by-products resulted in increased airway resistance, decreased elastance, and macrophage and neutrophilic inflammation. Changes in pulmonary pathophysiology may have long-term consequences for the host either initiating/predisposing to airways disease. Results from the studies suggest that inhalation exposure to 2-monochlorophenol containing PFRs on fine particles of CuO on silica (2-MCP230) leads to an increase in oxidative stress in vivo , which correlates with increased pulmonary inflammation and dysfunction.
Researchers also defined the impact of PM0.1-induced increases in reactive oxygen species leading to pulmonary and/or immune dysfunction in adults. In an effort to determine if 2-MCP230 particle systems influenced the generation of intracellular ROS, the research team examined GSSG and GSH levels in lung homogenates as a preliminary measure of pulmonary oxidative stress and antioxidant capacity.