Urch B, Speck M, Corey P, Wasserstein D, Manno M, Lukic KZ, Brook JR, Liu L, Coull B, Schwartz J, Gold DR, Silverman F.
Inhal Toxicol. 2010 Feb;22(3):210-8.
Epidemiological studies have established significant associations between ambient pollutants, including fine particulate matter (PM(2.5)) 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 PM(2.5) and O(3), no studies have previously examined their joint effects. The study objective was to examine the independent and combined associations between ambient PM(2.5) and O(3) and acute respiratory/inflammatory responses. Using their concentrated ambient particle (CAP) facility for PM(2.5), the authors studied 10 mild asthmatic and 13 nonasthmatic individuals. The 2-h exposures included CAP (range 48-199 microg/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 PM(2.5) 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 PM(2.5), providing evidence to support the epidemiological findings of associations between ambient levels of particles and cardiopulmonary morbidity and mortality.
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