Numerous epidemiological studies have recognized the health effect of atmospheric fine particulate matters (PM2.5). In some studies, correlation was observed between hospitalization of cardiovascular and respiratory patients and the contents of V, Ni, and elementary carbon in PM2.5. Oxidative stress has emerged as a unifying mechanism for PM2.5 toxicities. However, due to the use of complex atmospheric particle samples, the molecular mechanisms, and in particular the chemical components responsible for the oxidative stress remain to be resolved. In our study, selected organic chemicals and metal ions were adsorbed onto synthetic carbon black nanoparticles, and employed as PM2.5 model to investigate the mechanisms of PM2.5 oxidative stress at molecular and cellular levels. The advantage of this approach is ease of manipulation on the chemical composition and quantity of the particle model. Generation of reactive oxygen species (ROS) in cell-free systems was quantified to evaluate the potential of the particle model to induce oxidative stress via chemical routes. After exposure of A549 alveolar epithelial cells or RAW264.7 macrophage cells, cellular distribution and particle uptake and excretion kineticls were investigated, and the cellular dose of the particle was determined. Cellular ROS concentrations were measured at various exposure doses. By manipulating the chemical composition and quantity of the particle model, it is hoped that the chemical component(s) responsible for PM2.5 oxidative stress will be revealed in our studies.

Investigation of chemical constituents responsible for PM2.5 induced oxidative stress using synthesized carbon black nanoparticles

256th National Meeting (2018)

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