Comparative Toxicity of Fresh and Aged Anthropogenic Smoke Particles Emitted from Different Burning Conditions

YONG HO KIM, Aditya Sinha, Ingrid George, David DeMarini, Andrew Grieshop, Ian Gilmour, U.S. Environmental Protection Agency

     Abstract Number: 712
     Working Group: Health-Related Aerosols

Abstract
We demonstrated previously that, on a mass basis, mutagenicity associated with particulate matter (PM) from flaming smoke is greater than smoldering PM. This finding, however, is limited to fresh smoke emissions, which are different from the actual smoke (i.e., photochemically aged smoke) to which most people downwind of combustion events are exposed. Thus, we investigated how chemicals of combustion smoke change in the atmosphere and how such changes promote similar or distinct toxicity outcomes. We generated anthropogenic smoke (a mixture of plastic, plywood, and cardboard smoke) from two different burning conditions (smoldering vs. flaming) with and without photochemical aging and determined toxicity (i.e., mutagenicity and toxicity equivalent) of the smoke particles. Photochemical aging resulted in increased oxygenated volatile organic compound (VOC) emissions but largely degraded particle-bound polycyclic aromatic hydrocarbons (PAHs) in the smoke. Due to the PAH degradation, mutagenicity of the aged smoke from flaming combustion was up to 4 times lower than that of the fresh smoke on a per-particle mass basis. However, on the basis of particle emitted per fuel mass burned (emission factor basis), the aged and fresh smoke particles exhibited similar mutagenic activities, with higher (up to 3 times) in smoldering than flaming smoke. Similarly, the PAH toxicity equivalent of the aged smoldering smoke was 3 times higher than that of the aged flaming smoke particles, suggesting that smoke PAHs in the smoldering smoke were more photochemically stable during aging. These findings increase understanding of the evolution of smoke emitted at different burning conditions and the role of photochemical transformations on mutagenicity and PAH-induced toxicity. [This abstract does not represent EPA policy.]