Iiris Salonen

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.

Serum myeloperoxidase is independent of the risk factors of atherosclerosis

ObjectivesThe main hypothesis of the study was that as serum myeloperoxidase (MPO) concentration is known to indicate the progression of the atherosclerotic process, MPO may be associated with common risk factors of atherosclerosis. Therefore, the presence of these risk factors (especially elevated glucose and lipid concentrations) should predict an increased MPO level during the subsequent months. We also hypothesized an association of MPO with markers of other chronic diseases involving inflammation. MethodsFifty-three patients with ischemic heart disease were followed for 24 weeks by biweekly visits, during which the basic MPO level was measured (500 measurements in total, 2–12 per patient). The association of the patients’ typical MPO with the risk factors of atherosclerosis and other personal determinants was examined by trend analysis and analysis of variance. ResultsMPO was statistically significantly associated with blood leukocyte, neutrophil, and lymphocyte concentrations of the patients (P=0.001–0.003). MPO was also associated with high-sensitivity C-reactive protein (P=0.02). MPO was not associated with markers of lipid and glucose metabolism, of atherosclerosis, or of other chronic diseases. ConclusionContradictory to our hypotheses, the results indicate that the serum MPO level is independent of the commonly measured risk factors of atherosclerosis and markers of other chronic diseases. Consequently, the findings suggest that MPO-related acute pathologic events (such as plaque destabilization) are not associated with the preceding glucose or lipid values. However, the results support the third hypothesis and previously reported view that MPO is a marker of inflammation in patients of ischemic heart disease.

Exhaled nitric oxide and atherosclerosis

Eur J Clin Invest 2012

Determinants of interleukin-12 in stable ischaemic heart disease

ObjectiveThe aim of this study was to determine the relation of plasma interleukin-12 (IL-12) concentration to major risk factors of atherosclerosis and other personal characteristics in well-documented, stable ischaemic heart disease (IHD) patients. The hypothesis was that IL-12 is positively associated with inflammatory markers and risk factors of atherosclerosis. Materials and methodsClinical data were collected from 51 IHD patients by a questionnaire and from basic laboratory blood tests. The association of IL-12 with the biochemical, personal, health status and lifestyle determinants was investigated by regression analysis and analysis of variance. ResultsPlasma IL-12 concentration was associated inversely with the plasma concentration of triglycerides (P=0.001) and homocysteine (P=0.04). However, IL-12 was associated directly with the concentration of high-density lipoprotein cholesterol (P=0.03). IL-12 concentration was not strongly associated with other biochemical parameters nor with the health status, medication or lifestyle determinants. ConclusionThe results suggest that, contrary to the hypothesis, IL-12 was associated inversely with plasma levels of two known risk factors of coronary atherosclerosis (triglycerides, homocysteine) in stable, statin-medicated IHD patients. The lack of association of IL-12 with high-sensitivity C-reactive protein, erythrocyte sedimentation rate and the number of inflammatory cells in blood suggests that moderately elevated IL-12 did not imply ongoing systemic inflammation in these patients. Although increased IL-12 production is a sign of proinflammatory activity, it was associated directly with the plasma high-density lipoprotein cholesterol concentration. Overall, moderately elevated plasma IL-12 concentration may even be a good sign in stable IHD patients.