Low-level exposure to ambient particulate matter is associated with systemic inflammation in ischemic heart disease patients
ABSTRACT Short-term exposure to ambient air pollution is associated with increased cardiovascular mortality and morbidity. This adverse health effect is suggested to be mediated by inflammatory processes. The purpose of this study was to determine if low levels of particulate matter, typical for smaller cities, are associated with acute systemic inflammation. Fifty-two elderly individuals with ischemic heart disease were followed for six months with biweekly clinical visits in the city of Kotka, Finland. Blood samples were collected for the determination of inflammatory markers interleukin (IL)-1β, IL-6, IL-8, IL-12, interferon (IFN)γ, C-reactive protein (CRP), fibrinogen, myeloperoxidase and white blood cell count. Particle number concentration and fine particle (particles with aerodynamic diameters <2.5 μm (PM(2.5))) as well as thoracic particle (particles with aerodynamic diameters <10 μm (PM(10))) mass concentration were measured daily at a fixed outdoor measurement site. Light-absorbance of PM(2.5) filter samples, an indicator of combustion derived particles, was measured with a smoke-stain reflectometer. In addition, personal exposure to PM(2.5) was measured with portable photometers. During the study period, wildfires in Eastern Europe led to a 12-day air pollution episode, which was excluded from the main analyses. Average ambient PM(2.5) concentration was 8.7 μg/m(3). Of the studied pollutants, PM(2.5) and absorbance were most strongly associated with increased levels of inflammatory markers; most notably with C-reactive protein and IL-12 within a few days of exposure. There was also some evidence of an effect of particulate air pollution on fibrinogen and myeloperoxidase. The concentration of IL-12 was considerably (227%) higher during than before the forest fire episode. These findings show that even low levels of particulate air pollution from urban sources are associated with acute systemic inflammation. Also particles from wildfires may exhibit pro-inflammatory effects.
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ABSTRACT: Wildfire smoke dramatically increased ambient air pollutant levels.•Wildfire smoke consistently associated with increased risk of respiratory disease.•Suggestive evidence wildfire smoke linked with cardiovascular diseases and mortality.•Key challenge of exposure assessment: estimating fire-specific pollutants.Environmental Research 01/2015; 136. DOI:10.1016/j.envres.2014.10.015 · 3.95 Impact Factor
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ABSTRACT: Emissions from the fuel combustion in the energy production are causes of concern due to associated health risks, but little information is available on the impact of residential fuel burning on indoor air quality, where most of the human exposure occurs. In this complex study, concentrations of size-segregated particulate matter (PM), monocyclic and polycyclic aromatic compounds (MAHs and PAHs) at indoor and outdoor sites in six urban homes in the city of Kaunas, Lithuania, were determined over winter and summer sampling campaigns, specifically targeting the impact of the local fuel burning to the indoor air quality. PM levels observed in Kaunas during winter measurement campaign were higher compared to those in many other European settlements utilizing biomass for energy production. The particle size distribution analysis revealed that the major part of the PM mass in winter period consisted of fine particles (PM2.5). Both MAH and PAH levels were higher in winter. The indoor to outdoor ratios (I/O) of MAHs and PAHs revealed specific patterns depending on the presence of emissions sources indoors. Irrespectively of the season, I/O values were <1, suggesting that in case of the absence of an indoor pollution, the dominant source of organic compounds was from the outdoor environment. In homes with no PAH source inside, the I/O ratio equalled ranged from 0.05 to 0.36, suggesting the penetrated portion of outdoor combustion particles to the indoor air.Atmospheric Environment 11/2014; 97:83–93. DOI:10.1016/j.atmosenv.2014.08.010 · 3.06 Impact Factor
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ABSTRACT: To compare short-term effects of fine particles (PM2.5; aerodynamic diameter <2.5 µm) from different sources on the blood levels of markers of systemic inflammation. We followed a panel of 52 ischaemic heart disease patients from 15 November 2005 to 21 April 2006 with clinic visits in every second week in the city of Kotka, Finland, and determined nine inflammatory markers from blood samples. In addition, we monitored outdoor air pollution at a fixed site during the study period and conducted a source apportionment of PM2.5 using the Environmental Protection Agency's model EPA PMF 3.0. We then analysed associations between levels of source-specific PM2.5 and markers of systemic inflammation using linear mixed models. We identified five source categories: regional and long-range transport (LRT), traffic, biomass combustion, sea salt, and pulp industry. We found most evidence for the relation of air pollution and inflammation in LRT, traffic and biomass combustion; the most relevant inflammation markers were C-reactive protein, interleukin-12 and myeloperoxidase. Sea salt was not positively associated with any of the inflammatory markers. Results suggest that PM2.5 from several sources, such as biomass combustion and traffic, are promoters of systemic inflammation, a risk factor for cardiovascular diseases. 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.Occupational and Environmental Medicine 12/2014; 72(4). DOI:10.1136/oemed-2014-102240 · 3.23 Impact Factor