Differential injurious effects of ambient and traffic‐derived particulate matter on airway epithelial cells

• DOI: 10.1111/resp.12381
• Publication Date: 2014-09-15T01:15:22Z
• Authors: Rakesh K. Kumar; Alexander M. Shadie; Martin P. Bucknall; Helen Rutlidge; Linda Garthwaite; Cristan Herbert; Brendan Halliburton; Kristy S. Parsons; Peter A.B. Wark
• Keywords: 0301 basic medicine; Chemokine CXCL1; Iron; Interleukin-1beta; 610; Respiratory Mucosa; Mice; 03 medical and health sciences; Soot; 11. Sustainability; Animals; Humans; RNA, Messenger; Particle Size; Polycyclic Aromatic Hydrocarbons; Cells, Cultured; mass spectrometry; Air Pollutants; Interleukin-6; Tumor Necrosis Factor-alpha; Interleukin-8; airway epithelium; Epithelial Cells; asthma; airborne pollutant; Trachea; 13. Climate action; pro-inflammatory cytokine; Cytokines; Particulate Matter

Abstract Background and objective Exposure to airborne particulate matter ( PM ) may promote development of childhood asthma trigger acute exacerbations existing via injury airway epithelial cells AEC ). Methods We compared the response ambient particulates with median aerodynamic diameters <10 μm or <2.5 from Sydney metropolitan region S ydney 10 2.5), traffic‐derived exhaust stack a motorway tunnel inert carbon black as control. Results strongly stimulated messenger RNA expression secretion pro‐inflammatory cytokines interleukin 6 IL ‐6) chemokine (C‐X‐C motif) ligand 1 CXCL 1) by mouse tracheal . In contrast, did not. Similarly, , 8 B human Mass spectrometric analysis showed that contained much higher levels elements associated dusts geological origin. soot various organic compounds, notably including long straight‐chain alkanes diesel‐derived polycyclic aromatic hydrocarbons. 2.5, well collected during period major dust storm, both which relatively lower iron but similar other crustal elements, not stimulate Conclusions Ambient is likely be more important than in causing leading production cytokines. The injurious effects related presence coarse fraction These findings are relevant pathogenesis asthma.