Taina Siponen

Low-level exposure to ambient particulate matter is associated with systemic inflammation in ischemic heart disease patients

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.

Source-specific fine particulate air pollution and systemic inflammation in ischaemic heart disease patients.

Objective 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. Methods 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 Agencys 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. Results 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. Conclusions 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.

Impact of Wood Combustion for Secondary Heating and Recreational Purposes on Particulate Air Pollution in a Suburb in Finland

Little information is available on the concentrations of ambient fine particles (PM2.5) in residential areas where wood combustion is common for recreational purposes and secondary heating. Further, the validity of central site measurements of PM2.5 as a measure of exposure is unclear. Therefore, outdoor PM2.5 samples were repeatedly collected at a central site and home outdoor locations from a panel of 29 residents in a suburb in Kuopio, Finland. Source apportionment results from the central site were used to estimate the contributions from local sources, including wood combustion, to PM2.5 and absorption coefficient (ABS) at home outdoor locations. Correlations between the central and home outdoor concentrations of PM2.5, ABS, and their local components were analyzed for each home. At the central site, the average PM2.5 was 6.0 μg m(-)(3) during the heating season, and the contribution from wood combustion (16%) was higher than the contribution from exhaust emissions (12%). Central site measurements predicted poorly daily variation in PM2.5 from local sources. In conclusion, wood combustion significantly affects air quality also in areas where it is not the primary heating source. In epidemiological panel studies, central site measurements may not sufficiently capture daily variation in exposure to PM2.5 from local wood combustion.

Acute effects of visits to urban green environments on cardiovascular physiology in women: A field experiment

Background: Epidemiological studies have reported positive associations between the amount of green space in the living environment and mental and cardiovascular human health. In a search for effect mechanisms, field studies have found short‐term visits to green environments to be associated with psychological stress relief. Less evidence is available on the effect of visits on cardiovascular physiology. Objectives: To evaluate whether visits to urban green environments, in comparison to visits to a built‐up environment, lead to beneficial short‐term changes in indicators of cardiovascular health. Methods: Thirty‐six adult female volunteers visited three different types of urban environments: an urban forest, an urban park, and a built‐up city centre, in Helsinki, Finland. The visits consisted of 15 min of sedentary viewing, and 30 min of walking. During the visits, blood pressure and heart rate were measured, and electrocardiogram recorded for the determination of indicators of heart rate variability. In addition, levels of respirable ambient particles and environmental noise were monitored. Results: Visits to the green environments were associated with lower blood pressure (viewing period only), lower heart rate, and higher indices of heart rate variability [standard deviation of normal‐to‐normal intervals (SDNN), high frequency power] than visits to the city centre. In the green environments, heart rate decreased and SDNN increased during the visit. Associations between environment and indicators of cardiovascular health weakened slightly after inclusion of particulate air pollution and noise in the models. Conclusions: Visits to urban green environments are associated with beneficial short‐term changes in cardiovascular risk factors. This can be explained by psychological stress relief with contribution from reduced air pollution and noise exposure during the visits. Future research should evaluate the amount of exposure to green environments needed for longer‐term benefits for cardiovascular health. HighlightsVolunteers visited an urban forest, an urban park, and a built‐up city centre.Beneficial changes in cardiovascular physiology were observed in green environments.This may be explained by stress relief and lower air pollution and noise exposure.