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: Abstract Studies have linked air pollution exposure to cardiovascular health effects, but it is not clear which components drive these effects. We examined the associations between air pollution exposure and circulating white blood cell (WBC) counts in humans. To investigate independent contributions of particulate matter (PM) characteristics, we exposed 31 healthy volunteers at five locations with high contrast and reduced correlations amongst pollutant components: two traffic sites, an underground train station, a farm and an urban background site. Each volunteer visited at least three sites and was exposed for 5 h with intermittent exercise. Exposure measurements on-site included PM mass and number concentration, oxidative potential (OP), elemental- and organic carbon, metals, O3 and NO2. Total and differential WBC counts were performed on blood collected before and 2 and 18 h post-exposure (PE). Changes in total WBC counts (2 and 18 h PE), number of neutrophils (2 h PE) and monocytes (18 h PE) were positively associated with PM characteristics that were high at the underground site. These time-dependent changes reflect an inflammatory response, but the characteristic driving this effect could not be isolated. Negative associations were observed for NO2 with lymphocytes and eosinophils. These associations were robust and did not change after adjustment for a large suite of PM characteristics, suggesting an independent effect of NO2. We conclude that short-term air pollution exposure at real-world locations can induce changes in WBC counts in healthy subjects. Future studies should indicate if air pollution exposure-induced changes in blood cell counts results in adverse cardiovascular effects in susceptible individuals.Inhalation Toxicology 02/2014; 26(3):141-65. · 1.89 Impact Factor
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ABSTRACT: Abstract Context: Urban particulate air pollution is associated with cardiovascular diseases and mortality, possibly mediated through systemic inflammation and increased blood viscosity. Objectives: To examine short-term effects of exposure to urban air pollution on blood biomarkers for systemic inflammation and coagulation in a panel of healthy adults living in Gothenburg, Sweden. Materials and methods: The 16 volunteers, all non-smokers, median age 35 years, were called for blood sampling the morning after a day with high levels of urban particulate matter (PM10 > 30 µg/m(3)) or a day with low levels (PM10 < 15 µg/m(3) and NO2 < 35 µg/m(3)). Associations between exposure to air pollution and each biomarker (C-reactive protein, fibrinogen, serum amyloid A, coagulation factor VIII, plasminogen activator inhibitor-1, p-selectin, soluble intercellular adhesion molecule-1, soluble vascular adhesion molecule-1, Clara cell protein 16 and surfactant protein D) were examined using a linear mixed-effects model. Results: In total, 12 sampling sessions were performed, six after high-pollution and six after low-pollution days, over 21 months. The ratio of air pollution levels between high- and low-pollution days was five for PM10 (median: 49 and 10 µg/m(3)) and two for NO2 (median: 47 and 24 µg/m(3)). No significant increase in blood levels of any of the biomarkers were seen after days with high air pollution levels compared with low levels. Conclusion: Biomarkers of inflammation and coagulation were not found to be significantly increased in the mornings after days with elevated levels of urban air pollution compared with low levels when performing repeated blood samplings in healthy volunteers.Inhalation Toxicology 02/2014; 26(2):84-94. · 1.89 Impact Factor
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ABSTRACT: Inhalation of ambient and workplace particulate air pollution is associated with increased risk of cardiovascular disease. One proposed mechanism for this association is that pulmonary inflammation induces a hepatic acute phase response, which increases risk of cardiovascular disease. Induction of the acute phase response is intimately linked to risk of cardiovascular disease as shown in both epidemiological and animal studies. Indeed, blood levels of acute phase proteins, such as C-reactive protein and serum amyloid A, are independent predictors of risk of cardiovascular disease in prospective epidemiological studies. In this review, we present and review emerging evidence that inhalation of particles (e.g., air diesel exhaust particles and nanoparticles) induces a pulmonary acute phase response, and propose that this induction constitutes the causal link between particle inhalation and risk of cardiovascular disease. Increased levels of acute phase mRNA and proteins in lung tissues, bronchoalveolar lavage fluid and plasma clearly indicate pulmonary acute phase response following pulmonary deposition of different kinds of particles including diesel exhaust particles, nanoparticles, and carbon nanotubes. The pulmonary acute phase response is dose-dependent and long lasting. Conversely, the hepatic acute phase response is reduced relative to lung or entirely absent. We also provide evidence that pulmonary inflammation, as measured by neutrophil influx, is a predictor of the acute phase response and that the total surface area of deposited particles correlates with the pulmonary acute phase response. We discuss the implications of these findings in relation to occupational exposure to nanoparticles. For further resources related to this article, please visit the WIREs website. Conflict of interest: The authors have declared no conflicts of interest for this article.Wiley Interdisciplinary Reviews Nanomedicine and Nanobiotechnology 06/2014; · 5.68 Impact Factor