In vitro inflammatory and cytotoxic effects of size-segregated particulate samples collected during long-range transport of wildfire smoke to Helsinki.

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 (TNFalpha, 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.

Chemical and in vitro toxicologic characterization of wintertime and springtime urban-air particles with an aerodynamic diameter below 10 microm in Helsinki.

OBJECTIVES: The chemical composition and toxicity of wintertime urban-air particulate matter with an aerodynamic diameter of <10 microm (PM10), derived mostly from long-range transport and local combustion sources, were compared with those of springtime PM10 derived mostly from the resuspension of road dust. METHODS: Water-soluble ions and elements and polycyclic aromatic hydrocarbons (PAH) were analyzed from seasonally pooled PM10 samples collected at a busy traffic site in Helsinki in 1999. These PM10 samples were also tested for cytotoxicity [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide test] and the production of proinflammatory cytokines [tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6)] and nitric oxide (NO) in the mouse macrophage cell line RAW 264.7. Their oxidative capacity and the associated DNA (deoxyribonucleic acid) damage were investigated by electron paramagnetic resonance and the formation of 8-hydroxy-2'-deoxyguanosine (8-OH-DG) in isolated calf thymus DNA, respectively. RESULTS: The late wintertime and springtime PM10 had similar compositions of water-soluble ions and elements, but the winter PM10 had a higher content of PAH. The spring PM10 was a much more potent inducer of TNF-alpha and IL-6 production than the winter PM10 was, but there were no consistent differences in cytotoxic potency. In contrast, the winter PM10 was a significantly more potent inducer of NO production and 8-OH-DG formation. The large cytokine responses to the spring PM10 were caused by its insoluble fraction and largely inhibited by the endotoxin antagonist polymyxin B. The transition metal chelator deferoxamine did not modify the proinflammatory or cytotoxic responses to the PM10 samples. CONCLUSIONS: The toxicity profile of urban-air PM10 changed with season in a subarctic climate. Particulate-bound endotoxin from soil gram-negative bacteria is suggested as a highly proinflammatory constituent of springtime resuspended road dust.