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Endotoxin in concentrated coarse and fine ambient particles induces acute systemic inflammation in controlled human exposures
  1. Behrooz Behbod1,
  2. Bruce Urch2,5,
  3. Mary Speck2,
  4. James A Scott2,3,
  5. Ling Liu4,
  6. Raymond Poon4,
  7. Brent Coull1,
  8. Joel Schwartz1,
  9. Petros Koutrakis1,
  10. Frances Silverman2,3,5,6,8,
  11. Diane R Gold1,7
  1. 1Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA
  2. 2Gage Occupational & Environmental Health Unit, St. Michael's Hospital, University of Toronto, Toronto, Ontario, Canada
  3. 3Division of Occupational and Environmental Health, Dalla Lana School of Public Health, University of Toronto, Toronto, Ontario, Canada
  4. 4Health Canada, Ottawa, Ontario, Canada
  5. 5Southern Ontario Centre for Atmospheric Aerosol Research (SOCAAR), Toronto, Ontario, Canada
  6. 6Divisions of Occupational and Respiratory Medicine, Department of Medicine, University of Toronto, Toronto, Ontario, Canada
  7. 7The Channing Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA
  8. 8Keenan Research Centre, Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, Ontario, Canada
  1. Correspondence to Dr Behrooz Behbod, Environmental Health, Harvard School of Public Health, 401 Park Drive West, Boston, MA 02215, USA; bbehbod{at}post.harvard.edu

Abstract

Background Knowledge of the inhalable particulate matter components responsible for health effects is important for developing targeted regulation.

Objectives In a double-blind randomised cross-over trial of controlled human exposures to concentrated ambient particles (CAPs) and their endotoxin and (1→3)-β-D-glucan components, we evaluated acute inflammatory responses.

Methods 35 healthy adults were exposed to five 130-min exposures at rest: (1) fine CAPs (∼250 µg/m3); (2) coarse CAPs (∼200 µg/m3); (3) second coarse CAPs (∼200 µg/m3); (4) filtered air; and (5) medical air. Induced sputum cell counts were measured at screening and 24 h postexposure. Venous blood total leucocytes, neutrophils, interleukin-6 and high-sensitivity C reactive protein (CRP) were measured pre-exposure, 3 and 24 h postexposure.

Results Relative to filtered air, an increase in blood leucocytes 24 h (but not 3 h) postexposure was significantly associated with coarse (estimate=0.44×109 cells/L (95% CI 0.01 to 0.88); n=132) and fine CAPs (0.68×109 cells /L (95% CI 0.19 to 1.17); n=132), but not medical air. Similar associations were found with neutrophil responses. An interquartile increase in endotoxin (5.4 ng/m3) was significantly associated with increased blood leucocytes 3 h postexposure (0.27×109 cells/L (95% CI 0.03 to 0.51); n=98) and 24 h postexposure (0.37×109 cells/L (95% CI 0.12 to 0.63); n=98). This endotoxin effect did not differ by particle size. There were no associations with glucan concentrations or interleukin-6, CRP or sputum responses.

Conclusions In healthy adults, controlled coarse and fine ambient particle exposures independently induced acute systemic inflammatory responses. Endotoxin contributes to the inflammatory role of particle air pollution.

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