Andrew J Ghio1, Candice B Smith, Michael C Madden. 1. Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, US Environmental Protection Agency, Chapel Hill, North Carolina, USA. ghio.andy@epa.gov
Abstract
PURPOSE OF REVIEW: Epidemiologic investigation has associated traffic-related air pollution with adverse human health outcomes. The capacity of diesel exhaust particles (DEPs), a major emission source air pollution particle, to initiate an airway inflammation has subsequently been investigated. We review the recent controlled human exposures to diesel exhaust and DEPs, 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 of healthy individuals after exposure to diesel exhaust and DEPs. 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 diesel exhaust and DEP exposure. An increased sensitivity of asthmatic individuals to the proinflammatory effects of DEPs has not been confirmed. SUMMARY: Inflammation after diesel exhaust and DEP exposure is evident at higher concentrations only; there appears to be a threshold dose for DEPs approximating 300 μg/m. The lack of a biological response to DEPs at lower concentrations may reflect a contribution of gaseous constituents or interactions between DEPs and gaseous air pollutants to the human inflammatory response and function loss.
PURPOSE OF REVIEW: Epidemiologic investigation has associated traffic-related air pollution with adverse human health outcomes. The capacity of diesel exhaust particles (DEPs), a major emission source air pollution particle, to initiate an airway inflammation has subsequently been investigated. We review the recent controlled human exposures to diesel exhaust and DEPs, 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 of healthy individuals after exposure to diesel exhaust and DEPs. 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 diesel exhaust and DEP exposure. An increased sensitivity of asthmatic individuals to the proinflammatory effects of DEPs has not been confirmed. SUMMARY:Inflammation after diesel exhaust and DEP exposure is evident at higher concentrations only; there appears to be a threshold dose for DEPs approximating 300 μg/m. The lack of a biological response to DEPs at lower concentrations may reflect a contribution of gaseous constituents or interactions between DEPs and gaseous air pollutants to the human inflammatory response and function loss.
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