Antwerpen, Belgium
Antwerpen, Belgium

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Objectives: Rotavirus vaccination has been reimbursed in Belgium since November 2006 with a high uptake (>85%). Economic analyses of the vaccine have been reported, including estimates of indirect cost gain related to the reduction in work absenteeism. The objective of this study was to evaluate the latter parameter using real-life data. Design and setting: A simple model estimated the reduction in absent workdays per working mother with a firstborn baby after the introduction of the rotavirus vaccine. Next, data on work absences were retrospectively analysed (from 2003 to 2012) using a database of administrative employees (n=11 600 working women per year) in the City of Antwerp. Observed reductions in absenteeism after the introduction of the vaccine were compared with the results from the model. These reductions would most likely be observed during the epidemic periods of rotavirus (from January to the end of May) for short-duration absences of ≤5 days. We compared data from outside epidemic periods (from June to December), expecting no changes over time prevaccine and postvaccine introduction, as well as with a control group of women aged 30-35 years with no first child. Results: Model estimates were 0.73 working days gained per working mother. In the database of the City of Antwerp, we identified a gain of 0.88 working days during the epidemic period, and an accumulated gain of 2.24 days over a 3-year follow-up period. In the control group, no decrease in absenteeism was measured. Giving vaccine access to working mothers resulted in an estimated accumulated net cost gain of € 187 per mother. Conclusions: Reduction in absenteeism among working mothers was observed during periods of the epidemic after the introduction of the rotavirus vaccine in Belgium. This reduction is in line with estimates of indirect cost gains used in economic evaluations of the rotavirus vaccine.


Finne P.,University of Tampere | Fallah M.,University of Tampere | Hakama M.,University of Tampere | Ciatto S.,Instituto per Lo Studio e la Prevenzione Oncologica | And 5 more authors.
European Journal of Cancer | Year: 2010

Background: Lead-time is defined as the time by which screening advances the diagnosis compared with absence of screening. A sufficiently long lead-time needs to be achieved so that cancer can be detected while still curable. A very short lead-time may indicate poor sensitivity of the screening test, while a very long lead-time suggests overdiagnosis. Material and methods: In the first screening round, a total of 56,294 men aged 55-74 years were screened with serum prostate specific antigen (PSA) in five countries of the European Randomised Study of Screening for Prostate Cancer (ERSPC) with an overall detection rate (prevalence) of 2.8% (1972 prostate cancers). Prostate cancer incidence among 92,142 men randomly allocated to the control arm of the trial was also assessed. Lead-time was estimated as the time required to accumulate a similar cumulative risk of prostate cancer in the control arm to the detection rate in the intervention arm, i.e. from the ratio of detection rate (prevalence of screen-detected cases) and expected incidence (cumulative risk). Results: Using a serum PSA cut-off of 4 ng/ml, the mean lead-time in the whole study population was estimated as 6.8 years (95% confidence interval (95% CI) 7.9-8.4). It was 8 years in The Netherlands, 6 in Sweden and Finland, 5 in Italy and 4 in Belgium. The mean lead-time was similar, 6-7 years, at ages 50-64 years, but close to 8 years among men aged 65-74 years. A lower PSA cut-off level of 3 ng/ml used in Sweden and The Netherlands prolonged the mean lead-time by approximately 1 year. Lead-time based on advanced prostate cancer only was slightly shorter, mean 5.3 years (95% CI 4.6-6.0). The lead-time for the second screening round was slightly shorter than that for the first (5.9, 95% CI 5.4-6.4), reflecting a similar relation between detection rate and control group incidence. Conclusion: The lead-time for prostate cancer found in ERSPC substantially exceeded that found for breast, cervical and colorectal cancer screening. One round of prostate cancer screening can advance clinical diagnosis by 4-8 years. Overdiagnosis or detection of non-progressive tumours may contribute substantially to the lead-time. © 2010 Published by Elsevier Ltd.


De Coster S.,Ghent University | De Coster S.,Vrije Universiteit Brussel | van Leeuwen D.M.,Maastricht University | Jennen D.G.J.,Maastricht University | And 9 more authors.
Environmental and Molecular Mutagenesis | Year: 2013

Flanders, Belgium, is one of the most densely populated areas in Europe. The Flemish Environment and Health Survey (2002-2006) aimed at determining exposure to pollutants of neonates, adolescents, and older adults and to assess associated biological and health effects. This study investigated genome wide gene expression changes associated with a range of environmental pollutants, including cadmium, lead, PCBs, dioxin, hexachlorobenzene, p,p'-DDE, benzene, and PAHs. Gene expression levels were measured in peripheral blood cells of 20 adults with relatively high and 20 adults with relatively low combined internal exposure levels, all non-smokers aged 50-65. Pearson correlation was used to analyze associations between pollutants and gene expression levels, separately for both genders. Pollutant- and gender-specific correlation analysis results were obtained. For organochlorine pollutants, analysis within genders revealed that genes were predominantly regulated in opposite directions in males and females. Significantly modulated pathways were found to be associated with each of the exposure biomarkers measured. Pathways and/or genes related to estrogen and STAT5 signaling were correlated to organochlorine exposures in both genders. Our work demonstrates that gene expression in peripheral blood is influenced by environmental pollutants. In particular, gender-specific changes are associated with organochlorine pollutants, including gender-specific modulation of endocrine related pathways and genes. These pathways and genes have previously been linked to endocrine disruption related disorders, which in turn have been associated with organochlorine exposure. Based on our results, we recommend that males and females be considered separately when analyzing gene expression changes associated with exposures that may include chemicals with endocrine disrupting properties. Environ. Mol. Mutagen. 54:574-588, 2013. © 2013 Wiley Periodicals, Inc.


Morrens B.,University of Antwerp | Bruckers L.,Hasselt University | Hond E.D.,Flemish Institute for Technological Research | Nelen V.,Provincial Institute of Hygiene | And 7 more authors.
International Journal of Hygiene and Environmental Health | Year: 2012

Background: Environmental justice research suggests that inequalities in the distribution of environmental exposure to chemical pollution systematically disadvantage the lower social strata of society. The effects of these inequalities on the human exposure to pollution are however to a large extend unknown. The purpose of this study is to assess social gradients in human biomonitoring results of a representative sample of Flemish adolescents. Methods: We investigate the associations between individual socioeconomic status (SES), measured by parental educational attainments, and internal body concentration of seven chemical compounds in biological samples of 1642 adolescents aged 14-15 in Flanders (Belgium): PCBs, HCB, DDE, lead, cadmium, benzene and PAHs. Social gradients in average and high exposure to these biomarkers were examined with geometric means and odds ratios (with 95% confidence intervals), using multiple regression models, controlling for covariates and confounders. Results: Depending on the (type of) pollutant, adolescents with a lower SES either have higher or lower internal concentrations. Chlorinated compounds (PCBs and pesticides HCB and DDE) are positively associated with SES (higher exposures for higher SES), while heavy metals (lead and cadmium) are negatively associated (higher exposures for lower SES). For metabolites of organic compounds (benzene and PAHs) we find no association with SES. Socially constructed factors, such as dietary and lifestyle habits, play an important role in these relations. Conclusions: Our study suggests that the association between individual SES and the internal body concentration of exposure to environmental pollutants in Flemish adolescents is more complex than can be assumed on the basis of the environmental justice hypothesis. © 2011 Elsevier GmbH.


Den Hond E.,Flemish Institute for Technological Research | Dhooge W.,Ghent University | Bruckers L.,Hasselt University | Schoeters G.,Flemish Institute for Technological Research | And 9 more authors.
Journal of Exposure Science and Environmental Epidemiology | Year: 2011

Flanders is densely populated with much industry and intensive farming. Sexual maturation of adolescents (aged 14-15 years) was studied in relation to internal exposure to pollutants. Serum levels of pollutants and sex hormones were measured in 1679 participants selected as a random sample of the adolescents residing in the study areas. Data on sexual development were obtained from the medical school examination files. Self-assessment questionnaires provided information on health, use of medication and lifestyle factors. In boys, serum levels of hexachlorobenzene (HCB), p,p′-DDE and polychlorinated biphenyls (sum of marker PCB138, 153 and 180) were significantly and positively associated with pubertal staging (pubic hair and genital development). Higher levels of serum HCB and blood lead were associated with, respectively, a lower and a higher risk of gynecomastia. In girls, significant and negative associations were detected between blood lead and pubic hair development; higher exposure to PCBs was significantly associated with a delay in timing of menarche. Environmental exposures to pollutants at levels actually present in the Flemish population are associated with measurable effects on pubertal development. However, further understanding of toxic mode of action and sensitive windows of exposure is needed to explain the current findings. © 2011 Nature America, Inc. All rights reserved.


Dhooge W.,Ghent University | Den Hond E.,Flemish Institute for Technological Research | Koppen G.,Flemish Institute for Technological Research | Bruckers L.,Hasselt University | And 8 more authors.
Journal of Exposure Science and Environmental Epidemiology | Year: 2011

Flanders is densely populated with much industry and intensive farming. Hormonal status of 14- to 15-year-old male adolescents was studied in relation to internal exposure to pollutants. A total of 887 participants were selected as a random sample of the adolescents residing in the study areas. Confounding factors and significant covariates were taken into account. Serum levels of testosterone, free testosterone and estradiol, and the aromatase index showed significant positive associations with serum levels of marker polychlorobiphenyls (sum of PCBs 138, 153, and 180) and of hexachlorobenzene (HCB) and a negative association with urinary cadmium concentration. Serum levels of estradiol also showed a positive association with serum levels of dichlorodiphenyldichloroethylene (DDE). A doubling of serum concentrations of marker PCBs and HCB and of urinary concentration of cadmium were, respectively, associated with an increase of 16.4% (P < 0.00001) and 16.6% (P < 0.001) and a decrease of 9.6% (P < 0.001) in serum testosterone concentration. Similar findings were made after additional adjustment for concurrent exposures. Associations between biological effects and internal exposures were, in terms of the regression coefficient, often stronger at exposures below the median. Environmental exposures to pollutants resulting in normal levels of internal exposure were associated with quite substantial differences in hormone concentrations. © 2011 Nature America, Inc. All rights reserved.


PubMed | Flemish Institute for Technological Research, Hasselt University, Vrije Universiteit Brussel, University of Milan and 4 more.
Type: | Journal: Chemosphere | Year: 2016

Polycyclic aromatic hydrocarbons (PAHs) are of interest to human biomonitoring studies due to their carcinogenic potential. Traditionally metabolites of these compounds, like 1-hydroxypyrene, are monitored in urine, but recent methods allow the determination of the parent compounds in urine, which give additional information regarding sources and toxicity of PAHs. In order to assess the feasibility of incorporating these methods in a human biomonitoring study, the 16 USEPA parent PAHs were determined in 20 urine samples. These samples were obtained from 10 boys and 10 girls aged 14-16 years, participating in the third Flemish Environment and Health Study (Flanders, Belgium). Of these 16 parent PAHs, nine could be determined in more than 95% of the samples and three (including benzo(a)pyrene) in more than 50%. Several correlations were found between different PAHs, but not between pyrene and its metabolite 1-hydroxypyrene. Diagnostic PAH ratios in urine and air samples pointed towards combustion sources and are in line with the ratios in environmental samples. Benzo(a)pyrene, naphthalene and fluorene have the highest carcinogenic potential in our cohort, when using toxic equivalency factors. Some associations between PAH congeners and determinants of exposure were found, while fluorene and acenaphthylene were positively associated with thyroid hormone levels and benzo(a)pyrene showed a positive correlation with DNA damage by comet assay. These results confirm that parent PAHs in urine are useful as biomarkers of exposure in biomonitoring studies.


Pieters N.,Hasselt University | Koppen G.,Flemish Institute for Technological Research | Smeets K.,Hasselt University | Napierska D.,Catholic University of Leuven | And 12 more authors.
PLoS ONE | Year: 2013

Polycyclic aromatic hydrocarbons (PAHs) are widespread environmental pollutants that are formed in combustion processes. At the cellular level, exposure to PAHs causes oxidative stress and/or some of it congeners bind to DNA, which may interact with mitochondrial function. However, the influence of these pollutants on mitochondrial DNA (mtDNA) content remains largely unknown. We determined whether indoor exposure to PAHs is associated with mitochondrial damage as represented by blood mtDNA content. Blood mtDNA content (ratio mitochondrial/nuclear DNA copy number) was determined by real-time qPCR in 46 persons, both in winter and summer. Indoor PAH exposure was estimated by measuring PAHs in sedimented house dust, including 6 volatile PAHs and 8 non-volatile PAHs. Biomarkers of oxidative stress at the level of DNA and lipid peroxidation were measured. In addition to the epidemiologic enquiry, we exposed human TK6 cells during 24 h at various concentrations (range: 0 to 500 μM) of benzo(a)pyrene and determined mtDNA content. Mean blood mtDNA content averaged (±SD) 0.95±0.185. The median PAH content amounted 554.1 ng/g dust (25th-75th percentile: 390.7-767.3) and 1385 ng/g dust (25th-75th percentile: 1000-1980) in winter for volatile and non-volatile PAHs respectively. Independent for gender, age, BMI and the consumption of grilled meat or fish, blood mtDNA content decreased by 9.85% (95% CI: -15.16 to -4.2; p = 0.002) for each doubling of non-volatile PAH content in the house dust in winter. The corresponding estimate for volatile PAHs was -7.3% (95% CI: -13.71 to -0.42; p = 0.04). Measurements of oxidative stress were not correlated with PAH exposure. During summer months no association was found between mtDNA content and PAH concentration. The ability of benzo(a)pyrene (range 0 μM to 500 μM) to lower mtDNA content was confirmed in vitro in human TK6 cells. Based on these findings, mtDNA content can be a target of PAH toxicity in humans. © 2013 Pieters et al.


Koppen G.,Flemish Institute for Technological Research | Bloemen K.,Flemish Institute for Technological Research | Colles A.,Flemish Institute for Technological Research | Nelen V.,Provincial Institute of Hygiene | And 3 more authors.
Critical Reviews in Environmental Science and Technology | Year: 2011

The role of air pollution exposure on the development of asthma remains unclear. This can only be answered by prospective cohort studies. The authors give an overview of cohort studies focusing mainly on the role of early exposure, investigating the association between outdoor exposure early in life and respiratory or allergy symptoms in the growing children. Based on those studies, there is a suggestive evidence for a causal association between childhood asthma symptoms and exposure to traffic-related air pollutants. © 2011 Taylor & Francis Group, LLC.


PubMed | Environment & Health, Provincial Institute of Hygiene, Flemish Institute for Technological Research and Hasselt University
Type: | Journal: Environment international | Year: 2014

The current study aimed at assessing the associations between black carbon (BC) exposure and markers for airway inflammation and oxidative stress in primary school children in a Western European urban area.In 130 children aged 6-12 years old, the fraction of exhaled nitric oxide (FeNO), exhaled breath condensate (EBC) pH, 8-isoprostane and interleukin (IL)-1 were measured in two seasons. BC concentrations on the sampling day (2-h average, 8:00-10:00 AM) and on the day before (24-h average) were assessed using measurements at a central monitoring site. Land use regression (LUR) models were applied to estimate weekly average BC exposure integrated for the time spent at home and at school, and seasonal average BC exposure at the home address. Associations between exposure and biomarkers were tested using linear mixed effect regression models. Next to single exposure models, models combining different BC exposure metrics were used.In single exposure models, an interquartile range (IQR) increase in 2-h BC (3.10 g/m(3)) was linked with a 5.9% (95% CI: 0.1 to 12.0%) increase in 8-isoprostane. FeNO increased by 16.7% (95% CI: 2.2 to 33.2%) per IQR increase in 24-h average BC (4.50 g/m(3)) and by 12.1% (95% CI: 2.5 to 22.8%) per IQR increase in weekly BC (1.73 g/m(3)). IL-1 was associated with weekly and seasonal (IQR=1.70 g/m(3)) BC with respective changes of 38.4% (95% CI: 9.0 to 75.4%) and 61.8% (95% CI: 3.5 to 153.9%) per IQR increase in BC. An IQR increase in weekly BC was linked with a lowering in EBC pH of 0.05 (95% CI: -0.10 to -0.01). All associations were observed independent of sex, age, allergy status, parental education level and meteorological conditions on the sampling day. Most of the associations remained when different BC exposure metrics were combined in multiple exposure models, after additional correction for sampling period or after exclusion of children with airway allergies. In additional analyses, FeNO was linked with 24-h PM10 levels, but the effect size was smaller than for BC. 8-Isoprostane was not linked with either 2-h or 24-h concentrations of PM2.5 or PM10.BC exposure on the morning of sampling was associated with airway oxidative stress while 24-h and weekly exposures were linked with airway inflammation.

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