An air filter intervention study of endothelial function among healthy adults in a woodsmoke-impacted community.
BACKGROUND
Particulate air pollution is associated with cardiovascular morbidity. One hypothesized mechanism involves oxidative stress, systemic inflammation, and endothelial dysfunction.


OBJECTIVE
To assess an intervention's impact on particle exposures and endothelial function among healthy adults in a woodsmoke-impacted community. We also investigated the underlying role of oxidative stress and inflammation in relation to exposure reductions.


METHODS
Portable air filters were used in a randomized crossover intervention study of 45 healthy adults exposed to consecutive 7-day periods of filtered and nonfiltered air.


RESULTS
Reactive hyperemia index was measured as an indicator of endothelial function via peripheral artery tonometry, and markers of inflammation (C-reactive protein, interleukin-6, and band cells) and lipid peroxidation (malondialdehyde and 8-iso-prostaglandin F(2α)) were quantified. Air filters reduced indoor fine particle concentrations by 60%. Filtration was associated with a 9.4% (95% confidence interval, 0.9-18%) increase in reactive hyperemia index and a 32.6% (4.4-60.9%) decrease in C-reactive protein. Decreases in particulate matter and the woodsmoke tracer levoglucosan were associated with reduced band cell counts. There was limited evidence of more pronounced effects on endothelial function and level of systemic inflammation among males, overweight participants, younger participants, and residents of wood-burning homes. No associations were noted for oxidative stress markers.


CONCLUSIONS
Air filtration was associated with improved endothelial function and decreased concentrations of inflammatory biomarkers but not markers of oxidative stress. Our results support the hypothesis that systemic inflammation and impaired endothelial function, both predictors of cardiovascular morbidity, can be favorably influenced by reducing indoor particle concentrations.
Simon Fraser University, Faculty of Health Sciences, 8888 University Drive, Burnaby, British Columbia V5A 1S6, Canada. allenr@sfu.ca
Ryan W
RW
Allen
Chris
C
Carlsten
Barbara
B
Karlen
Sara
S
Leckie
Stephan
S
van Eeden
Sverre
S
Vedal
Imelda
I
Wong
Michael
M
Brauer
D000328:Adult; D000393:Air Pollutants / Q000097:blood* / Q000652:urine*; D015415:Biomarkers / Q000097:blood / Q000652:urine; D001955:British Columbia; D002097:C-Reactive Protein; D018592:Cross-Over Studies; D015237:Dinoprost / Q000652:urine; D042783:Endothelial Cells; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005374:Filtration / Q000379:methods*; D006801:Humans; D006940:Hyperemia; D007249:Inflammation / Q000097:blood; D019570:Inhalation Exposure; D015227:Lipid Peroxidation; D008297:Male; D008315:Malondialdehyde / Q000652:urine; D008875:Middle Aged; D018384:Oxidative Stress; D012016:Reference Values; D012906:Smoke; D055815:Young Adult
D000393:Air Pollutants; D015415:Biomarkers; D012906:Smoke; D008315:Malondialdehyde; D002097:C-Reactive Protein; D015237:Dinoprost