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Diesel exhaust particles and airway inflammation
Citation:
GHIO, A. J., C. BAILEY, AND M. C. MADDEN. Diesel exhaust particles and airway inflammation. CURRENT OPINION IN BIOTECHNOLOGY. Current Biology Limited, London, Uk, 18(2):144-50, (2012).
Impact/Purpose:
Inflammation after DE and DEP exposure is evident at higher concentrations only; there appears to a threshold dose for DEP approximating 300 ug/m3. The
Description:
Purpose of review. Epidemiologic investigation has associated traffic-related air pollution with adverse human health outcomes. The capacity ofdiesel exhaust particles (DEP), a major emission source air pollution particle, to initiate an airway inflammation has subsequently been investigated. We review recent controlled human exposures to diesel exhaust (DE) and DEP and summarize the investigations into the associations between this emission source air pollution particle and airway inflammation. Recent findings. Using bronchoalveolar lavage, bronchial biopsies, and sputum collection, studies have demonstrated inflammation in the airways ofhealthy subjects after exposure to DE and DEP. This inflammation has included neutrophils, eosinophils, mast cells, and lymphocytes. Elevated expression and concentrations of inflammatory mediators have similarly been observed in the respiratory tract after DE and DEP. An increased sensitivity ofasthmatics to the proinflammatory effects of DEP has not been confirmed. Summary. Inflammation after DE and DEP exposure is evident at higher concentrations only; there appears to a threshold dose for DEP approximating 300 ug/m3. The lack ofa biological response to DEP at lower concentrations may reflect a contribution of gaseous constituents or interactions between DEP and gaseous air pollutants to the human inflammatory response and function loss. Key words: Vehicle emissions; air pollution; particulate matter; asthma; oxidants
