Abstract
The impact of long-range transport (LRT) episodes of wildfire smoke on the inflammogenic and cytotoxic activity of urban air particles was investigated in the mouse RAW 264.7 macrophages. The particles were sampled in four size ranges using a modified Harvard high-volume cascade impactor, and the samples were chemically characterized for identification of different emission sources. The particulate mass concentration in the accumulation size range (PM
1–0.2) was highly increased during two LRT episodes, but the contents of total and genotoxic polycyclic aromatic hydrocarbons (PAH) in collected particulate samples were only 10–25% of those in the seasonal average sample. The ability of coarse (PM
10–2.5), intermodal size range (PM
2.5–1), PM
1–0.2 and ultrafine (PM
0.2) particles to cause cytokine production (TNFα, IL-6, MIP-2) reduced along with smaller particle size, but the size range had a much smaller impact on induced nitric oxide (NO) production and cytotoxicity or apoptosis. The aerosol particles collected during LRT episodes had a substantially lower activity in cytokine production than the corresponding particles of the seasonal average period, which is suggested to be due to chemical transformation of the organic fraction during aging. However, the episode events were associated with enhanced inflammogenic and cytotoxic activities per inhaled cubic meter of air due to the greatly increased particulate mass concentration in the accumulation size range, which may have public health implications.