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• W1663120187 abstract "Abstract Background and objective Exposure to airborne particulate matter ( PM ) may promote development of childhood asthma and trigger acute exacerbations of existing asthma via injury to airway epithelial cells ( AEC ). Methods We compared the response of AEC to ambient particulates with median aerodynamic diameters of <10 μm or <2.5 μm from the Sydney metropolitan region ( S ydney PM 10 or PM 2.5), to traffic‐derived particulates from the exhaust stack of a motorway tunnel or to inert carbon black as a control. Results S ydney PM 10 strongly stimulated messenger RNA expression and secretion of the pro‐inflammatory cytokines interleukin 6 ( IL ‐6) and chemokine (C‐X‐C motif) ligand 1 ( CXCL 1) by mouse tracheal AEC . In contrast, traffic‐derived particulates did not. Similarly, PM 10 stimulated expression of IL 6 , IL 8 and IL 1 B by human AEC . Mass spectrometric analysis showed that PM 10 contained much higher levels of elements associated with dusts of geological origin. In contrast, tunnel soot contained much higher levels of various organic compounds, notably including long straight‐chain alkanes and diesel‐derived polycyclic aromatic hydrocarbons. S ydney PM 2.5, as well as PM 10 collected during a period including a major dust storm, both of which contained relatively lower levels of iron but similar levels of other crustal elements, did not stimulate expression or secretion of CXCL 1 by mouse AEC . Conclusions Ambient PM 10 is likely to be more important than traffic‐derived PM in causing injury to AEC leading to production of pro‐inflammatory cytokines. The injurious effects may be related to the presence of iron in the coarse fraction of airborne PM . These findings are likely to be relevant to the pathogenesis of asthma." @default.
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• W1663120187 date "2014-09-14" @default.
• W1663120187 modified "2023-10-16" @default.
• W1663120187 title "Differential injurious effects of ambient and traffic-derived particulate matter on airway epithelial cells" @default.
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• W1663120187 doi "https://doi.org/10.1111/resp.12381" @default.
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