Sources of fine particulate air pollution and systemic inflammation

摘要

Background: Exposure to fine particles (PM2.5; diameter ＜2.5μm) is associated with cardiovascular health. Exposure to PM2.5 can accelerate systemic inflammation, which has been suggested to play an important role in the development of coronary heart diseases. The source of particulates affects their composition which may further modify cardiovascular effects. Aims: Our objective was to evaluate the association between source-specific PM2.5 and systemic inflammation among elderly subjects. Methods: We followed a panel of thirty-seven elderly subjects (＞59 years of age) monthly for 6 months with clinical visits (minimum of three) including a blood-withdrawal in Kuopio, Finland, between November 2008 and May 2009. We determined blood levels of interferon-gamma (IFN), interleukin(IL)-1, -6, -8, -10 and -12, as well as tumor necrosis factor (TNF) to be used as indicators of systemic inflammation. Across the whole study period, we measured daily levels of air pollution at a central outdoor measurement site. We conducted source-apportionment for fine particles using positive matrix factorization 3.0.2.2. by the U.S. Environmental Protection Agency. We analyzed immediate and delayed effects of source-specific PM2.5 on log-transformed levels of inflammation markers using mixed models with random patient effects adjusting for time-trend, temperature, relative humidity and barometric pressure. Results: Number of successful clinical visits was 206. We found relatively few associations between air pollution and markers of systemic inflammation. IFN had suggestive positive association with PM2.5 from wood burning (10.7% (5-day average, 95%-confidence interval (CI): -1.0 to 23.9 %)) and with traffic (7.8 % 11-day lag, CI: -0.88 to 17.3 %)). There was suggestive association also with traffic and TNF (2.7 % (1-day lag, CI: -0.36 to 5.9 %)). Conclusions: We found only limited evidence on the effects of source-specific PM2.5 on systemic inflammation.