Determinants of the Proinflammatory Action of Ambient Particulate Matter in Immortalized Murine Macrophages

Proinflammatory cytokine
DOI: 10.1289/ehp.1002105 Publication Date: 2010-07-27T15:46:15Z
ABSTRACT
Proximity to traffic-related pollution has been associated with poor respiratory health in adults and children.We wished test the hypothesis that particulate matter (PM) from high-traffic sites would display an enhanced capacity elicit inflammation.We examined inflammatory potential of coarse [2.5-10 µm aerodynamic diameter (PM(2.5-10))] fine [0.1-2.5 (PM(0.1-2.5))] PM collected nine throughout Europe contrasting traffic contributions. We incubated murine monocytic-macrophagic RAW264.7 cells samples these (20 or 60 µg/cm²) quantified their stimulate release arachidonic acid (AA) production interleukin-6 tumor necrosis factor-α (TNFα) as measures potential. Responses were then related composition: metals, hydrocarbons, anions/cations, endotoxin content.Inflammatory responses ambient varied markedly on equal mass basis, PM(2.5-10) displaying largest signals contrasts among sites. Notably, we found no evidence at observed some distant traffic. Correlation analyses indicated much sample-to-sample contrast proinflammatory response was content transition metals (especially iron copper) PM(2.5-10). Use metal chelator diethylene triamine pentaacetic inhibited AA release, whereas recombinant endotoxin-neutralizing protein partially TNFα production, demonstrating different components triggered through separate pathways.We close proximity sources displayed activity cells.
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