Majid Kajbafzadeh1, Michael Brauer1, Barbara Karlen2, Chris Carlsten3, Stephan van Eeden4, Ryan W Allen5. 1. School of Population and Public Health, The University of British Columbia, Vancouver, British Columbia, Canada. 2. School of Population and Public Health, The University of British Columbia, Vancouver, British Columbia, Canada Faculty of Health Sciences, Simon Fraser University, Burnaby, British Columbia, Canada. 3. School of Population and Public Health, The University of British Columbia, Vancouver, British Columbia, Canada Department of Medicine, The University of British Columbia, Vancouver, British Columbia, Canada. 4. Department of Medicine, The University of British Columbia, Vancouver, British Columbia, Canada. 5. Faculty of Health Sciences, Simon Fraser University, Burnaby, British Columbia, Canada.
Abstract
BACKGROUND:Combustion-generated fine particulate matter (PM2.5) is associated with cardiovascular morbidity. Both traffic-related air pollution and residential wood combustion may be important, but few studies have compared their impacts. OBJECTIVES: To assess and compare effects of traffic-related and woodsmoke PM2.5 on endothelial function and systemic inflammation (C reactive protein, interleukin-6 and band cells) among healthy adults in Vancouver, British Columbia, Canada, using high efficiency particulate air (HEPA) filtration to introduce indoor PM2.5 exposure gradients. METHODS: We recruited 83 healthy adults from 44 homes in traffic-impacted or woodsmoke-impacted areas to participate in this randomised, single-blind cross-over intervention study. PM2.5 concentrations were measured during two consecutive 7-day periods, one with filtration and the other with 'placebo filtration'. Endothelial function and biomarkers of systematic inflammation were measured at the end of each 7-day period. RESULTS:HEPA filtration was associated with a 40% decrease in indoor PM2.5 concentrations. There was no relationship between PM2.5 exposure and endothelial function. There was evidence of an association between indoor PM2.5 and C reactive protein among those in traffic-impacted locations (42.1% increase in C reactive protein per IQR increase in indoor PM2.5, 95% CI 1.2% to 99.5%), but not among those in woodsmoke-impacted locations. There were no associations with interleukin-6 or band cells. CONCLUSIONS: Evidence of an association between C reactive protein and indoor PM2.5 among healthy adults in traffic-impacted areas is consistent with the hypothesis that traffic-related particles, even at relatively low concentrations, play an important role in the cardiovascular effects of the urban PM mixture. TRIAL REGISTRATION NUMBER: http://www.clinicaltrials.gov (NCT01570062). Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
RCT Entities:
BACKGROUND: Combustion-generated fine particulate matter (PM2.5) is associated with cardiovascular morbidity. Both traffic-related air pollution and residential wood combustion may be important, but few studies have compared their impacts. OBJECTIVES: To assess and compare effects of traffic-related and woodsmoke PM2.5 on endothelial function and systemic inflammation (C reactive protein, interleukin-6 and band cells) among healthy adults in Vancouver, British Columbia, Canada, using high efficiency particulate air (HEPA) filtration to introduce indoor PM2.5 exposure gradients. METHODS: We recruited 83 healthy adults from 44 homes in traffic-impacted or woodsmoke-impacted areas to participate in this randomised, single-blind cross-over intervention study. PM2.5 concentrations were measured during two consecutive 7-day periods, one with filtration and the other with 'placebo filtration'. Endothelial function and biomarkers of systematic inflammation were measured at the end of each 7-day period. RESULTS: HEPA filtration was associated with a 40% decrease in indoor PM2.5 concentrations. There was no relationship between PM2.5 exposure and endothelial function. There was evidence of an association between indoor PM2.5 and C reactive protein among those in traffic-impacted locations (42.1% increase in C reactive protein per IQR increase in indoor PM2.5, 95% CI 1.2% to 99.5%), but not among those in woodsmoke-impacted locations. There were no associations with interleukin-6 or band cells. CONCLUSIONS: Evidence of an association between C reactive protein and indoor PM2.5 among healthy adults in traffic-impacted areas is consistent with the hypothesis that traffic-related particles, even at relatively low concentrations, play an important role in the cardiovascular effects of the urban PM mixture. TRIAL REGISTRATION NUMBER: http://www.clinicaltrials.gov (NCT01570062). Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
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