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Scheers H.,Occupational and Environmental Medicine | Mwalili S.M.,Catholic University of Leuven | Faes C.,Hasselt University | Fierens F.,Belgian Interregional Environment Agency | And 3 more authors.
Environmental Health Perspectives | Year: 2011

Background: Numerous studies show associations between fine particulate air pollutants [particulate matter with an aerodynamic diameter ≤ 10 μm (PM10)] and mortality in adults. Objectives: We investigated short-term effects of elevated PM10 levels on infant mortality in Flanders, Belgium, and studied whether the European Union (EU) limit value protects infants from the air pollution trigger. Methods: In a case-crossover analysis, we estimated the risk of dying from nontraumatic causes before 1 year of age in relation to outdoor PM10 concentrations on the day of death. We matched control days on temperature to exclude confounding by variations in daily temperature. Results: During the study period (1998-2006), PM10 concentration averaged 31.9 ± 13.8 μg/m3. In the entire study population (n = 2,382), the risk of death increased by 4% [95% confidence interval (CI), 0-8%; p = 0.045] for a 10-μg/m3 increase in daily mean PM10. However, this association was significant only for late neonates (2-4 weeks of age; n = 372), in whom the risk of death increased by 11% (95% CI, 1-22%; p = 0.028) per 10-μg/m3 increase in PM10. In this age class, infants were 1.74 (95% CI, 1.18-2.58; p = 0.006) times more likely to die on days with a mean PM10 above the EU limit value of 50 μg/m3 than on days below this cutoff. Conclusions: Even in an affluent region in Western Europe, where infant mortality is low, days with higher PM air pollution are associated with an increased risk of infant mortality. Assuming causality, the current EU limit value for PM10, which may be exceeded on 35 days/year, does not prevent PM10 from triggering mortality in late neonates. Source

Janssen B.G.,Hasselt University | Munters E.,Hasselt University | Pieters N.,Hasselt University | Smeets K.,Hasselt University | And 8 more authors.
Environmental Health Perspectives | Year: 2012

Background: Studies emphasize the importance of particulate matter (PM) in the formation of reactive oxygen species and inflammation. We hypothesized that these processes can influence mitochondrial function of the placenta and fetus. Objective: We investigated the influence of PM10 exposure during pregnancy on the mitochondrial DNA content (mtDNA content) of the placenta and umbilical cord blood. Methods: DNA was extracted from placental tissue (n = 174) and umbilical cord leukocytes (n = 176). Relative mtDNA copy numbers (i.e., mtDNA content) were determined by real-time polymerase chain reaction. Multiple regression models were used to link mtDNA content and in utero exposure to PM10 over various time windows during pregnancy. Results: In multivariate-adjusted analysis, a 10-μg/m3 increase in PM10 exposure during the last month of pregnancy was associated with a 16.1% decrease [95% confidence interval (CI): -25.2, -6.0%, p = 0.003] in placental mtDNA content. The corresponding effect size for average PM10 exposure during the third trimester was 17.4% (95% CI: -31.8, -0.1%, p = 0.05). Furthermore, we found that each doubling in residential distance to major roads was associated with an increase in placental mtDNA content of 4.0% (95% CI: 0.4, 7.8%, p = 0.03). No association was found between cord blood mtDNA content and PM10 exposure. Conclusions: Prenatal PM10 exposure was associated with placental mitochondrial alterations, which may both reflect and intensify oxidative stress production. The potential health consequences of decreased placental mtDNA content in early life must be further elucidated. Source

Jacobs L.,Catholic University of Leuven | Emmerechts J.,Catholic University of Leuven | Mathieu C.,Catholic University of Leuven | Hoylaerts M.F.,Catholic University of Leuven | And 5 more authors.
Environmental Health Perspectives | Year: 2010

Background: Population studies suggest that persons with diabetes are more sensitive to the effects of particulate matter (PM) air pollution. However, the biological mechanisms of a possible prothrombotic effect underlying this enhanced susceptibility remain largely unknown. Objective: We hypothesized that exposure to PM causes prothrombotic changes in persons with diabetes, possibly via systemic inflammation. Methods: Our study included 137 nonsmoking adults with diabetes who were outpatients at the University Hospital Leuven. Recent exposure (2 hr before examination) to ambient PM was measured at the entrance of the hospital. Individual chronic exposure to PM was assessed by measuring the area occupied by carbon in airway macrophages obtained by sputum induction. Platelet function was measured ex vivo with the PFA-100 platelet function analyzer, which simulates a damaged blood vessel; we analyzed the function of platelets in primary hemostasis under high shear conditions. Total and differential blood leukocytes were counted. Results: Independent of antiplatelet medication, an interquartile range (IQR) increase of 39.2 μg/m3 in PM10 (PM with aerodynamic diameter ≤ 10 μm) concentration measured 2 hr before the clinical examination (recent exposure) was associated with a decrease of 21.1 sec [95% confidence interval (CI), -35.3 to -6.8] in the PFA-100 closure time (i.e., increased platelet activation) and an increase in blood leukocytes of 512 per microliter of blood (95% CI, 45.2-979). Each area increase of 0.25 μm2 (IQR) in carbon load of airway macrophages (chronic exposure) was associated with an increase of 687 leukocytes per microliter of blood (95% CI, 224-1,150). Conclusions: A relevant increase in recent PM exposure was associated with a change in platelet function toward a greater prothrombotic tendency. The magnitude of the change was about two-thirds (in the opposite direction) of the average effect of antiplatelet medication. Diabetic patients showed evidence of proinflammatory response to both recent and chronic exposure to PM air pollution. Source

Emmerechts J.,Catholic University of Leuven | Jacobs L.,Catholic University of Leuven | van Kerckhoven S.,Catholic University of Leuven | Loyen S.,Catholic University of Leuven | And 6 more authors.
Journal of Thrombosis and Haemostasis | Year: 2012

Summary. Background:Epidemiological studies suggest an association between exposure to particulate matter (PM) in air pollution and the risk of venous thromboembolism (VTE). Objectives:To investigate the underlying pathophysiological pathways linking PM exposure and VTE. Patients and methods:We assessed potential associations between PM exposure and coagulation and inflammation parameters, including circulating microvesicles, in a group of 233 patients with diabetes. Results:The numbers of circulating blood platelet-derived and annexin V-binding microvesicles were inversely associated with the current levels of PM2.5 or PM10, measured on the day of sampling. Recent past exposure to PM10, up to 1week prior to blood sampling, estimated at the patients' residential addresses, was associated with elevated high-sensitivity C-reactive protein (CRP), leukocytes and fibrinogen, as well as with tissue factor (TF)-dependent procoagulant changes in thrombin generation assays. When longer windows of past exposure were considered, up to 1year preceding blood sampling, procoagulant changes were evident from the strongly increased numbers of red blood cell-derived circulating microvesicles and annexin V-binding microvesicles, but they no longer associated with TF. Past PM exposure was never associated with activated partial thromboplastin time (aPTT), prothrombin time (PT), or factor (F) VII, FVIII, FXII or D-dimers. Residential distance to a major road was only marginally correlated with procoagulant changes in FVIII and thrombin generation. Conclusions:Increases in the number of microvesicles and in their procoagulant properties, rather than increases in coagulation factors per se, seem to contribute to the risk of VTE, developing during prolonged exposure to air pollutants. © 2011 International Society on Thrombosis and Haemostasis. Source

Verleden S.E.,Catholic University of Leuven | Scheers H.,Catholic University of Leuven | Nawrot T.S.,Catholic University of Leuven | Nawrot T.S.,Hasselt University | And 11 more authors.
American Journal of Transplantation | Year: 2012

Acute rejection represents amajor problem after organ transplantation, being a recognized risk for chronic rejection and mortality. Recently, it became clear that lymphocytic bronchiolitis (LB, B-grade acute rejection) is more important than previously thought, as it predisposes to chronic rejection. We aimed to verify whether daily fluctuations of air pollution, measured as particulate matter (PM) are related to histologically proven A-grade rejection and/or LB and bronchoalveolar lavage (BAL) fluid cellularity after lung transplantation. We fitted a mixedmodel to examine the association between daily variations in PM10 and A-grade rejection/LB on 1276 bronchoscopic biopsies (397 patients, 416 transplantations) taken between 2001 and 2011. A difference of 10 μg/m3 in PM10 3 days before diagnosis of LB was associated with an OR of 1.15 (95% CI 1.04-1.27; p = 0.0044) but not with A-grade rejection (OR = 1.05; 95% CI 0.95-1.15; p = 0.32). Variations in PM 10 at lag day 3 correlated with neutrophils (p = 0.013), lymphocytes (p = 0.0031) and total cell count (p = 0.024) in BAL. Importantly, we only found an effect of PM10 on LB in patients not taking azithromycin. LB predisposed to chronic rejection (p < 0.0001). The risk for LB after lung transplantation increased with temporal changes in particulate air pollution, and this was associated with BAL neutrophilia and lymphocytosis. Azithromycin was protective against this PM effect. © Copyright 2012 The American Society of Transplantation and the American Society of Transplant Surgeons. Source

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