Concentrated ambient fine particles and not ozone induce a systemic interleukin-6 response in humans

Epidemiological studies have established significant associations between ambient pollutants, including fine particulate matter (PM2.5) and ozone (O-3), and cardiopulmonary morbidity and mortality. One mechanism that has been proposed is a pulmonary/systemic inflammatory response. Although controlled human exposure studies have examined the independent inflammatory responses of PM2.5 and O-3, no studies have previously examined their joint effects. The study objective was to examine the independent and combined associations between ambient PM2.5 and O-3 and acute respiratory/inflammatory responses. Using their concentrated ambient particle (CAP) facility for PM2.5, the authors studied 10 mild asthmatic and 13 nonasthmatic individuals. The 2-h exposures included CAP (range 48-199 mu g/m(3)) and filtered air (FA), with/without O-3 (120 ppb), in a randomized block design. Response measures included pulmonary function and inflammatory indices in induced sputum (interleukin [IL]-6, cytology) and blood (IL-6, tumor necrosis factor [TNF]-alpha) measured before and after exposures. Three hours post exposure, there was an increase in blood levels of IL-6, but only after CAP alone exposures; the IL-6 increase was associated with increasing PM2.5 mass concentration (p = .005). Some individuals switched to shallow breathing during CAP+O-3, possibly accounting for an attenuation of the resultant blood IL-6 response. Asthmatic and nonasthmatic responses were similar. There were no adverse changes in pulmonary function or other inflammatory measures. The study demonstrated an acute IL-6 response to PM2.5, providing evidence to support the epidemiological findings of associations between ambient levels of particles and cardiopulmonary morbidity and mortality.