Belgian Interregional Environment Agency

Brussels, Belgium

Belgian Interregional Environment Agency

Brussels, Belgium
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Mwalili S.M.,Catholic University of Leuven | Faes C.,Hasselt University | Fierens F.,Belgian Interregional Environment Agency | Nawrot T.S.,Hasselt University
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.

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.

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.

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.

Janssen B.G.,Hasselt University | Godderis L.,Catholic University of Leuven | Pieters N.,Hasselt University | Poels K.,Catholic University of Leuven | And 10 more authors.
Particle and Fibre Toxicology | Year: 2013

Background: There is evidence that altered DNA methylation is an important epigenetic mechanism in prenatal programming and that developmental periods are sensitive to environmental stressors. We hypothesized that exposure to fine particles (PM2.5) during pregnancy could influence DNA methylation patterns of the placenta.Methods: In the ENVIRONAGE birth cohort, levels of 5'-methyl-deoxycytidine (5-mdC) and deoxycytidine (dC) were quantified in placental DNA from 240 newborns. Multiple regression models were used to study placental global DNA methylation and in utero exposure to PM2.5 over various time windows during pregnancy.Results: PM2.5 exposure during pregnancy averaged (25th-75th percentile) 17.4 (15.4-19.3) μg/m3. Placental global DNA methylation was inversely associated with PM2.5 exposures during whole pregnancy and relatively decreased by 2.19% (95% confidence interval [CI]: -3.65, -0.73%, p = 0.004) for each 5 μg/m3 increase in exposure to PM2.5. In a multi-lag model in which all three trimester exposures were fitted as independent variables in the same regression model, only exposure to PM2.5 during trimester 1 was significantly associated with lower global DNA methylation (-2.13% per 5 μg/m3 increase, 95% CI: -3.71, -0.54%, p = 0.009). When we analyzed shorter time windows of exposure within trimester 1, we observed a lower placental DNA methylation at birth during all implantation stages but exposure during the implantation range (6-21d) was strongest associated (-1.08% per 5 μg/m3 increase, 95% CI: -1.80, -0.36%, p = 0.004).Conclusions: We observed a lower degree of placental global DNA methylation in association with exposure to particulate air pollution in early pregnancy, including the critical stages of implantation. Future studies should elucidate genome-wide and gene-specific methylation patterns in placental tissue that could link particulate exposure during in utero life and early epigenetic modulations. © 2013 Janssen et al.; licensee BioMed Central Ltd.

Adriaenssens S.,Ghent University | Adriaenssens S.,Belgian Interregional Environment Agency | Staelens J.,Ghent University | Staelens J.,Flemish Environment Agency | And 5 more authors.
Ecosystems | Year: 2012

Nitrogen (N) retention by tree canopies is believed to be an important process for tree nutrient uptake, and its quantification is a key issue in determining the impact of atmospheric N deposition on forest ecosystems. Due to dry deposition and retention by other canopy elements, the actual uptake and assimilation by the tree canopy is often obscured in throughfall studies. In this study, 15N-labeled solutions ( 15NH + 4 and 15NO - 3) were used to assess dissolved inorganic N retention by leaves/needles and twigs of European beech, pedunculate oak, silver birch, and Scots pine saplings. The effects of N form, tree species, leaf phenology, and applied NO - 3 to NH + 4 ratio on the N retention were assessed. Retention patterns were mainly determined by foliar uptake, except for Scots pine. In twigs, a small but significant 15N enrichment was detected for NH + 4, which was found to be mainly due to physicochemical adsorption to the woody plant surface. The mean 15NH + 4/ 15NO - 3retention ratio varied considerably among species and phenological stadia, which indicates that the use of a fixed ratio in the canopy budget model could lead to an over- or underestimation of the total N retention. In addition, throughfall water under each branch was collected and analyzed for 15NH + 4, 15NO - 3, and all major ions. Net throughfall of 15NH + 4 was, on average, 20 times higher than the actual retention of 15NH + 4 by the plant material. This difference in 15NH + 4 retention could not be attributed to pools and fluxes measured in this study. The retention of 15NH + 4 was correlated with the net throughfall of K +, Mg 2+, Ca 2+, and weak acids during leaf development and the fully leafed period, while no significant relationships were found for 15NO - 3 retention. This suggests that the main driving factors for NH + 4 retention might be ion exchange processes during the start and middle of the growing season and passive diffusion at leaf senescence. Actual assimilation or abiotic uptake of N through leaves and twigs was small in this study, for example, 1-5% of the applied dissolved 15N, indicating that the impact of canopy N retention from wet deposition on forest productivity and carbon sequestration is likely limited. © 2012 Springer Science+Business Media, LLC.

Goeminne P.C.,University Hospital Gasthuisberg | Kicinski M.,CSIC - Center for Environmental Sciences | Vermeulen F.,UZ Leuven | Fierens F.,Belgian Interregional Environment Agency | And 5 more authors.
Chest | Year: 2013

Background: Pulmonary exacerbations in cystic fibrosis (CF) contribute to the burden of disease, with a negative impact on quality of life, costs, and lung function. Our aim was to evaluate whether exacerbations, defined by antibiotic use, were triggered by daily fluctuations in air pollution. Methods: In a case-crossover analysis, we evaluated 215 patients with CF and pollution data from January 1, 1998, to December 31, 2010. Exacerbation was defined as the start of IV or oral antibiotic use in a home or hospital setting. We calculated regional background levels of particulate matter with a diameter < 10 μm (PM10), ozone, and nitrogen dioxide (NO2) on the day of the event and on the 2 days prior to the event at each patient's home address. We matched for day of the week and controlled for temperature on the day of the event and the 2 preceding days. In the month where antibiotic treatment was started, all days with the same temperature (± 2°C) as the event day served as control days, excluding 3 days before and after the start of treatment. Results: A total of 215 patients (male sex, 49%, mean age, 21 ± 13 years) had 2,204 antibiotic treatments (1,107 IV and 1,097 oral). Over a period of 12 years, an increase in risk of antibiotic use was associated with increasing concentrations of PM10, NO2, and ozone on the event day and for NO2 on the day before. A tendency toward significance was seen the day before antibiotic use for PM10 and ozone. Overall, a rise in OR was seen from 2 days before until the day of the start of antibiotics. Conclusions: In patients with CF and exacerbations, ambient concentrations of ozone, PM10, and NO2 play a role in triggering an exacerbation. © 2013 American College of Chest Physicians.

PubMed | Belgian Interregional Environment Agency, Flemish Institute for Technological Research, Hasselt University and University of Milan
Type: | Journal: Environmental health : a global access science source | Year: 2016

Studies emphasize the importance of particulate matter (PM) in the formation of reactive oxygen species and inflammation. We hypothesized that PM exposure during different time windows in pregnancy influences mitochondrial 8-hydroxy-2-deoxyguanosine (8-OHdG) levels, which is an established biomarker for oxidative stress, in both maternal and foetal blood.We investigated maternal (n=224) and cord blood (n=293) from mother-newborn pairs that were enrolled in the ENVIRONAGE birth cohort. We determined mitochondrial 8-OHdG by quantitative polymerase chain reaction (qPCR). Multivariable regression models were used to assess the association between mitochondrial 8-OHdG with PM10 and PM2.5 exposure over various time windows during pregnancy.In multivariable analysis, PM10 exposure during the entire pregnancy was positively associated with levels of mitochondrial 8-OHdG in maternal blood. For an IQR increment in PM10 exposure an increase of 18.3 % (95 % confidence interval (CI): 5.6 to 33.4 %, p=0.004) in 8-OHdG was observed. PM10 exposure during the last trimester of pregnancy was positively associated with levels of 8-OHdG (28.1, 95 % CI: 8.6 to 51.2 %, p=0.004, for an IQR increment in PM10). In a similar way, PM2.5 exposure was significantly associated with an increase of mitochondrial 8-OHdG levels in maternal blood during the entire pregnancy (13.9, 95 % CI: 0.4 to 29.4 %, p=0.04 for an IQR increment in PM2.5 exposure) and third trimester of pregnancy (28.1, 95 % CI: 3.6 to 58.4 %, p=0.02 for an IQR increment in PM2.5 exposure). In umbilical cord blood, 8-OHdG levels were significantly associated with PM10 exposure during first and second trimester of pregnancy with respectively an increase of 23.0 % (95 % CI: 5.9 to 42.8 %, p=0.007) and 16.6 % (95 % CI: 1.8 to 33.5 %, p=0.03) for an IQR increment in PM10 exposure.We found PM-associated increased mitochondrial oxidative DNA damage during pregnancy in both mothers and their newborns. Accordingly, our study showed that particulate air pollution exposure in early life plays a role in increasing systemic oxidative stress, at the level of the mitochondria, both in mother and foetus.

PubMed | University Hospitals Leuven, Ghent University, Maastricht University, Hasselt University and Belgian Interregional Environment Agency
Type: | Journal: Environmental research | Year: 2016

Several studies in singletons have shown that maternal exposure to ambient air pollutants is associated with restricted fetal growth. About half of twins have low birth weight compared with six percent in singletons. So far, no studies have investigated maternal air pollution exposure in association with birth weight and small for gestational age in twins. We examined 4760 twins of the East Flanders Prospective Twins Survey (2002-2013), to study the association between in utero exposure to air pollution with birth weight and small for gestational age. Maternal particulate air pollution (PM10) and nitric dioxide (NO2) exposure was estimated using a spatial temporal interpolation method over various time windows during pregnancy. In the total group of twins, we observed that higher PM10 and NO2 exposure during the third trimester was significantly associated with a lower birth weight and higher risk of small for gestational age. However, the association was driven by moderate to late preterm twins (32-36 weeks of gestation). In these twins born between 32 and 36 weeks of gestation, birth weight decreased by 40.2g (95% CI: -69.0 to -11.3; p=0.006) and by 27.3g (95% CI: -52.9 to -1.7; p=0.04) in association for each 10g/m increment in PM10 and NO2 concentration during the third trimester. The corresponding odds ratio for small for gestational age were 1.68 (95% CI: 1.27-2.33; p=0.0003) and 1.51 (95% CI: 1.18-1.95; p=0.001) for PM10 or NO2, respectively. No associations between air pollution and birth weight or small for gestational age were observed among term born twins. Finally, in all twins, we found that for each 10g/m increase in PM10 during the last month of pregnancy the within-pair birth weight difference increased by 19.6g (95% CI: 3.7-35.4; p=0.02). Assuming causality, an achievement of a 10g/m decrease of particulate air pollution may account for a reduction by 40% in small for gestational age, in twins born moderate to late preterm.

PubMed | Catholic University of Leuven, Belgian Interregional Environment Agency, Ghent University, Roosevelt University and University of Antwerp
Type: | Journal: Journal of environmental management | Year: 2016

For a sustainable future, we must sustainably manage not only the human/industrial system but also ecosystems. To achieve the latter goal, we need to predict the responses of ecosystems and their provided services to management practices under changing environmental conditions via ecosystem models and use tools to compare the estimated provided services between the different scenarios. However, scientific articles have covered a limited amount of estimated ecosystem services and have used tools to aggregate services that contain a significant amount of subjective aspects and that represent the final result in a non-tangible unit such as points. To resolve these matters, this study quantifies the environmental impact (on human health, natural systems and natural resources) in physical units and uses an ecosystem service valuation based on monetary values (including ecosystem disservices with associated negative monetary values). More specifically, the paper also focuses on the assessment of ecosystem services related to pollutant removal/generation flows, accounting for the inflow of eutrophying nitrogen (N) when assessing the effect of N leached to groundwater. Regarding water use/provisioning, evapotranspiration is alternatively considered a disservice because it implies a loss of (potential) groundwater. These approaches and improvements, relevant to all ecosystems, are demonstrated using a Scots pine stand from 2010 to 2089 for a combination of three environmental change and three management scenarios. The environmental change scenarios considered interannual climate variability trends and included alterations in temperature, precipitation, nitrogen deposition, wind speed, Particulate matter (PM) concentration and CO2 concentration. The addressed flows/ecosystem services, including disservices, are as follows: particulate matter removal, freshwater loss, CO2 sequestration, wood production, NOx emissions, NH3 uptake and nitrogen pollution/removal. The monetary ecosystem service valuation yields a total average estimate of 361-1242 euro ha(-1)yr(-1). PM2.5 (<2.5m) removal is the key service, with a projected value of 622-1172 euro ha(-1)yr(-1). Concerning environmental impact assessment, with net CO2 uptake being the most relevant contributing flow, a loss prevention of 0.014-0.029 healthy life years ha(-1)yr(-1) is calculated for the respective flows. Both assessment methods favor the use of the least intensive management scenario due to its resulting higher CO2 sequestration and PM removal, which are the most important services of the considered ones.

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