1,721,142 research outputs found
High temperatures trigger suicide mortality in Brussels, Belgium: A case-crossover study (2002-2011)
No full textBACKGROUND: Temperature may trigger the risk of suicide, however, the extent and shape of the associations show geographical variation. Here, we investigate the short-term effects of temperature on suicide deaths occurring in Brussels between January 1st, 2002 and December 31st, 2011. METHODS: We conducted a bidirectional time-stratified case-crossover study with cases being suicide deaths occurring among Brussels residents aged 5 years or older. Cases were matched by day of the week with control days from the same month and year. The exposure was the daily average temperature measured at the Uccle station (Brussels) and obtained from the Belgian Royal Meteorological Institute. We combined conditional logistic regression with distributed lag non-linear models (DLNM) to obtain one week (lag 0-6) cumulative risk ratios (RR) and their 95% confidence intervals (CI) for the effects of moderate and extreme cold (5th and 1st percentiles of temperature, respectively) and moderate and extreme heat (95th and 99th percentiles of temperature, respectively), relative to the median temperature. RESULTS: In total, 1891 suicide deaths were included. The median temperature was 11.6 °C, moderate and extreme cold temperatures were 0 and -3.1 °C, respectively, and moderate and extreme high temperatures were 20.9 and 24.4 °C, respectively. The cumulative risk of suicide mortality was almost twice higher among lags 0 to 6 for both moderate and extreme heat, relative to the period median temperature (e.g. moderate heat RR = 1.80 CI:1.27-2.54). No statistically significant associations were observed for cold temperatures. CONCLUSIONS: In Brussels, a western European city with temperate climate, high temperatures may trigger suicide deaths up to one week later. In the context of climate change, adaptation strategies must take into consideration the effects of temperature on mental health.sponsorship: Lidia Casas and Bianca Cox are recipients of post-doctoral fellow-ships of the Research Foundation Flanders (FWO) , grant numbers 12I1517N and 12Q0517N, respectively. (Research Foundation Flanders (FWO)|12I1517N, Research Foundation Flanders (FWO)|12Q0517N)status: Publishe
Pulmonale toxiciteit van nanopartikels, invloed op de barrière van het longepitheel
No full textmso-ansi-language:EN-US" lang="EN-US">Nanotechnology is already being used in severalindustries for a very diverse range of products: personal care products,cosmetics, sunscreens, clothing, sporting goods, electronics, food and beverages,paints and coatings. The production of nanoparticles and their marketing willincrease even more in the coming years.mso-ansi-language:EN-US" lang="EN-US">It is generally assumed that the physical and chemicalcharacteristics that define nanoparticles (NPs) unique properties are alsoresponsible for the possible adverse effects. Due to their small size, which isin the range of biological molecules (proteins, lipids, DNA
), NPs mightdistribute to the smallest biological structures, access and interact with finecellular and molecular structures. mso-ansi-language:EN-US" lang="EN-US">Inhalation is considered to be the most importantroute of exposure, but the deleterious effects induced by inhalation of NPs arenot limited to the lungs, since the cardiovascular system may also be affected.Moreover, some human subpopulations may be more susceptible to the deleteriouseffects induced by nanoparticle inhalation, e.g. people withpre-existingcardiovascular disease and the elderly.mso-ansi-language:EN-US" lang="EN-US">The objectives of this project were to:line-height:150%;mso-list:l0 level1 lfo1">font-family:Symbol;mso-fareast-font-family:Symbol;mso-bidi-font-family:Symbol;mso-ansi-language:EN-US" lang="EN-US">· mso-bidi-font-size:11.0pt;line-height:150%;mso-ansi-language:EN-US" lang="EN-US">Optimize acoculture model of the lung-blood barrier to study the adverse pulmonary andextra-pulmonary effects after NP administration (to the pulmonary / apical compartment) line-height:150%;mso-list:l0 level1 lfo1">font-family:Symbol;mso-fareast-font-family:Symbol;mso-bidi-font-family:Symbol;mso-ansi-language:EN-US" lang="EN-US">· mso-bidi-font-size:11.0pt;line-height:150%;mso-ansi-language:EN-US" lang="EN-US">Study theadverse effects after pulmonary nanoparticle administration in two differentanimal models that reflect susceptible human subpopulations.mso-ansi-language:EN-US" lang="EN-US">The most important physical and chemicalcharacteristics of NPs were reviewed in detail (Chapter 1) and links betweenthese characteristics and the observed toxic effects were made where possible.It is generally assumed that the smaller a particle, the more toxic it is. Forother characteristics, a clear relation is less evident. Currently, we also lackclarity as to which characteristics are most important for determiningpotential hazards.mso-ansi-language:EN-US" lang="EN-US">A coculture model of the lung-blood barrier wasdeveloped where human bronchial epithelial cells (16HBE14o-) with monocytes(THP-1) and human microvascular endothelial cells (HLMVEC) were seeded onopposite sides of a permeable membrane, representing the lungs and pulmonarycirculation respectively. The roleof chemically-activated macrophage-likecells in the co-culture was investigated and it was observed that these cellsdisturbed the barrier integrity by disrupting the epithelial tight junctions(Chapter 2). Non-activated monocytes were shown to be activated by SiO2NPs and lipopolysaccharide (LPS), taken as a positive control, withoutdisturbing the barrier integrity. The toxicity of SiO2 and TiO2NPs at non-cytotoxic concentrations was assessed, with LPS and TBHP as positivecontrols for inflammation and oxidative stress (Chapter 3). Both NPs decreasedthe barrier integrity and total glutathione concentrations in the pulmonarycompartment. In a time-course experiment, oxLDL was decreased 24 hours afterexposure to the two types of nanoparticles. SiO2 NPs induced themost pronounced inflammatory response, which resembled that caused by LPS.mso-ansi-language:EN-US" lang="EN-US">Bmal1 (brain and muscle ARNT-like protein-1) knockout mice(Bmal1-/-) have a disturbed circadian rhythm, causing them toprematurely age, 13.0pt;line-height:150%;mso-ansi-language:EN-US" lang="EN-US">and have a mso-ansi-language:EN-US" lang="EN-US">procoagulant 12.0pt;mso-bidi-font-size:13.0pt;line-height:150%;mso-ansi-language:EN-US" lang="EN-US">phenotype(Chapter 4). These mice (Bmal1+/+and Bmal1-/-), togetherwith 18 month old mice (Chapter 5) were usedas animal models reflecting peoplewith pre-existing cardiovascular disease and the elderly, respectively and weresubacutely exposed to MWCNT or ZnO NPs and additionally TiO2 NPswere studied in the old mice. In the Bmal1 mice, tEN-US" lang="EN-US">he MWCNTs and ZnO NPs showed opposite pulmonary toxicity butsimilarprocoagulant effects. Moreover, the observed pulmonary effects correlated withthe hemostatic effects and these correlations were more apparent in the Bmal1-/-mice suggesting it is a sensitive model to study the pulmonary andextra-pulmonary toxicity after pulmonary administration ofNPs. In the oldmice, the MWCNTs and ZnO NPs induced pulmonary inflammation together with acuteprocoagulant effects. Moreover, histological analysis showed the presence ofMWCNTs in the heart and the induction of fibrosis induced by ZnO NPs.mso-ansi-language:EN-US" lang="EN-US"> mso-ansi-language:EN-US" lang="EN-US">In conclusion, we observed that inflammation andoxidative stress were the driving mechanisms in both normal">in vitro and in vivostudies causing the observed toxic effects. Moreover, we demonstrated thatpulmonary NP exposure evoked hemostatic toxicity, providing further evidencethat the lungs and the cardiovascular system are linked. 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Epidemiological research towards a better understanding of the relationship between air pollution and human health.
No full textBackground
In the past few decades, exposure to air pollution has been found to be associated with all-cause mortality, cardiovascular and respiratory morbidity, both in the short term (acute exposure) and the long term (chronic exposure). According to the most recent report by the World Health Organisation (WHO, 2014), 3.7 million deaths worldwide and per year are attributed to ambient air pollution, placing it in the top 10 of risk factors.
Ambient air pollution consists of particulate matter (PM) and gases, such as NO2, SO2, and ozone. Of all pollutants, PM is most reliably associated with human disease. It is usually classified according to particle size, with PM10 (particles smaller than 10 µm) as the most commonly studied fraction. The European Union (EU) has set two limit values for PM10 concentrations: annual mean levels of PM10 must not exceed 40 μg/m³ (25 µg/m³ for PM2.5), and daily averages must not exceed 50 μg/m³ on more than 35 days/year, for any monitoring station in the EU member states. In contrast, the WHO advises that annual averages of PM10 levels should not exceed 20 μg/m³ (10 µg/m³ for PM2.5) and that daily averages should not exceed 50 μg/m³ on more than 3 day/year.
Objectives
The general objective of this PhD project was to gain more insight in the relationship between PM and human health in susceptible subgroups, such as infants, lung-transplanted patients and elderly. Also, in two of the four studies conducted within the scope of this thesis, I investigated the possible biological mechanisms involved in the pathway from PM inhalation to disease. Finally, I aimed to evaluate EU limit values and WHO guidelines for ambient PM concentrations, based on our study results.
Main study results
In a first study (Chapter 1), I investigated effects of daily variation in environmental PM10 on risk of infant mortality (<1y of age) in Flanders. 2382 infants died during the study period (1998-2006). The PM10 concentration averaged 31.9 µg/m³, and there were 321 days (an average of 35.7 days per year) with a mean daily concentration exceeding 50 µg/m³. This means that the EU air quality standards were met for the yearly average, but barely for the daily average. It is clear, however, that the more stringent WHO guideline values were not met at all in Flanders.
Using a bidirectional time-stratified case-crossover (CCO) design, I found that PM10 was associated with infant mortality, especially in the late neonatal stage (i.e. between one week and one month of age, N=372). For each 10 µg/m³ increment of PM10, the risk of late neonatal mortality increased with 11% (95% CI 1-22%). On days with average PM10 levels exceeding the EU limit value of 50 µg/m³, the risk of mortality was 74% higher (95% CI 18-158%) than on days below that value. The current EU limit value for PM10 is not protective to prevent triggering infant mortality. Moreover, the linear shape of the association between exposure and mortality gives no evidence for a threshold or a save level.
In a second study (Chapter 2), we investigated whether graft rejection after lung transplantation (LTx) could be linked to recent exposure to PM air pollution, and which underlying mechanisms are involved. In the period 2001-2011, transbronchial biopsies were repeatedly executed in 397 LTx recipients at the UZ Leuven. I linked estimated PM10 levels for each patient’s home address with symptoms of graft rejection and related physiological parameters.
We found that a 10 µg/m³ increase in PM10 concentration 3 days before biopsy increased the risk of lymphocytic airway disease (LAD) with 12% (95% CI 1-25%). LAD is the pathological correlate of acute graft rejection after LTx. Additionally, PM10 exposure was positively associated with BAL counts of neutrophils and lymphocytes, indicating that inflammation plays a part in the physiological pathway. Preventive treatment with the antibiotic azithromycin appeared to block the effect of PM10 on acute graft rejection.
In chapter 3, I investigated whether a decrease or increase of exposure to air pollution during several days (compared to a person’s ‘normal’ level) can already result in changes in biomarkers of cardiovascular health. During the course of one year, we measured air pollution exposure, carotid arterial stiffness (a well-established marker of cardiovascular disease), and other biomarkers in a panel of 20 retired and healthy men and women in different locations: during a 10-day stay in Milan (Italy, PM10 > 50 µg/m³), during a similar 10-day stay in Vindeln (rural area in northern Sweden, PM10 < 10 µg/m³) and at regular time points in Leuven (reference location, PM10 ≈ 30 µg/m³).
Compared with Leuven, exposure to pollutants was higher in Milan and lower in Vindeln, with the highest contrast found for NO2 (averages: Milan 63.7 µg/m³; Vindeln 4.4 µg/m³).We found strong associations between 7-days exposure to air pollution and arterial stiffness, e.g. a 4.4% decrease in compliance (i.e. an increase in stiffness) for a 10 µg/m³ increment in PM10. However, no direct inflammatory effects, measured as concentration of plasma CRP and leukocytes, were detected.
Stroke, or cerebrovascular accident, is a prominent cause of mortality and it has been linked with exposure to air pollution. I performed a meta-analysis of the current literature to quantify the pooled association between stroke and long-term exposure to PM10 or PM2.5 (Chapter 4).
I identified 20 studies on long-term PM exposure and stroke. The association between PM and stroke was positive in North America (N=7 studies), Europe (N=8), and China (N=3, with extremely high exposures), and negative in Japan (N=2). The estimated effect of PM2.5 [6% increase (95% CI 2-11%) in stroke risk for a 5 µg/m³ increment in PM2.5] was higher than the corresponding result using PM10 [2% increase (95% CI -2 to 7%) in stroke risk for a 10 µg/m³ increment in PM10). This indicates the importance of measuring PM2.5 directly and confirms the hypothesis that PM2.5 is more hazardous than the coarse fraction (PM2.5-10).
Conclusions
In this thesis, I found detrimental health effects of air pollution in different susceptible populations and for different time windows of exposure. Both short-term exposure (1 to 3 days) and long-term exposure (several months to years) can trigger acute events, such as stroke, lung graft rejection or infant mortality, but long-term exposure can also accelerate the development of chronic cardiovascular or respiratory diseases, such as atherosclerosis or lung cancer. The two panel studies (LTx and health elderly) provided mixed results concerning the role of inflammation in the process, as measured by levels of leukocytes and plasma CRP.
Compared to other environmental factors, such as smoking, diet and physical activity, individual risk estimates are rather small, but exposure to air pollution is involuntary and ubiquitous. Given the fact that the whole population is exposed, our studies demonstrated that air pollution is an important public health issue. In Belgium (and in Western Europe in general), yearly ambient concentrations of PM10 have decreased over the past 10 years to levels well below the EU limit value of 40 µg/m³, but still above the WHO guideline value of 20 µg/m³, especially in urban areas, where most people live. In accordance with other studies, we found no indications for a threshold or ‘save’ level of air pollution, so public health will benefit from every single µg/m³ decrease in concentration. This is a shared responsibility of policymakers, industry, and the general population (since road traffic and household combustion of wood are important and even increasing sources of air pollution) alike.status: Publishe
Toxiciteit van nanopartikels. Cytotoxiciteit - Ontwikkeling van een in vitro translocatie model van het pulmonaal epitheel - In vivo toxiciteit en lichaamsverdeling
No full textEngineered nanopartikels worden gemaakt door de mens op het nano-nivea u (< 100 nm). In vergelijking met de overeenkomstige grove materialen, b ezitten nanomaterialen andere fysische en chemische eigenschappen, die l eiden tot vele commerciële en medische toepassingen. Echter, er is een g roeiend besef van de mogelijke nadelige gevolgen van nanomaterialen voor de gezondheid. In grootte zijn engineered nanopartikels gelijkaardig aan ultrafijne partikels, welke in milieutoxicologie worden bestudeerd e n geassocieerd zijn met een toename in longziekten en cardiovasculaire a andoeningen. Bovendien zijn er aanwijzingen dat ingeademde ultrafijne pa rtikels kunnen transloceren naar de bloedsomloop. Een nieuwe discipline nanotoxicologie is geïntroduceerd om specifieke problemen van nanopart ikels te onderzoeken. In deze doctoraatsthesis hebben we ons gericht op: 1) de cytotoxiciteit van nanopartikels 2) de extrapulmonale translocatie van partikels naar de bloedsomloop 3) de in vivo toxiciteit en lichaamsverdeling van bepaalde nanopartik els na intraveneuze toediening Om de extrapulmonale translocatie van nanopartikels te onderzoeken, hebb en we een in vitro model van het pulmonaal epitheel ontwikkeld. Drie types longcellen werden onderzocht voor mogelijk gebruik in het in vitro model. De A549 cellen waren niet in staat om tight junctions te vo rmen, dit in tegenstelling tot Calu-3 cellen en primaire rat type II pne umocyten. Vervolgens werden de cultuurcondities geoptimaliseerd om de ho ogst mogelijke TEER te verkrijgen. Dit model werd nadien gebruikt om de translocatie van nanopartikels doorheen het longepitheel te bestuderen. In een eerste studie werd ongeveer 6% translocatie gevonden van 46 nm po lystyreen partikels; in een tweede studie met 25 nm quantum dots werd ge en translocatie aangetoond. Een conditie van beperkte oxidatieve stress beïnvloedde dit niet, echter, in condities van grote oxidatieve stress met aantasting van de tight junctions werd 30% translocatie van de qu antum dots aangetoond. De literatuur over in vitro studies met nanopartikels neemt exponenti eel toe. Echter, verschillende en vaak niet gevalideerde methoden word en gebruikt, en soms is het protocol beperkt of onduidelijk. Dit gaf aan leiding om enkele basis aspecten van cytotoxiciteitstesten met nanoparti kels te onderzoeken voor hun mogelijke interferentie of invloed op het r esultaat van de test. Op verschillende plaatsen van het protocol, zoals de celdensiteit en de nanopartikelsuspensie werden beperkingen gevonden. De celdensiteit beïnvloedde de uitkomst van Min-U-Sil cytotoxiciteit: v oor eenzelfde concentratie aan partikels varieerde de relatieve viabilit eit van 10% to 55%. Voor meerlagige koolstof nanobuizen werd interactie met het surfactant Tween80 gevonden, voor Min-U-Sil werd een verminderin g in cytotoxiciteit aangetoond in aanwezigheid van 10% foetaal kalf serum. In vivo werden de acute toxiciteit, pro-trombotische effecten en lich aamsverdeling onderzocht voor intraveneus geïnjecteerde quantum dots. In een eerste reeks van experimenten werden relatief hoge dosissen van 360 0, 20 of 144 pmol/muis toegediend en werden de analysen 1 uur na t oediening uitgevoerd. In een tweede reeks van experimenten werden lagere dosissen van 144, 14.4 of 1.44 pmol/muis geïnjecteerd en werden de effe cten bestudeerd in tijd (1, 4 of 24 uur). De hoogste dosissen QDs van 36 00 en 720 pmol/muis veroorzaakten pulmonale vasculaire trombose, waarbij de carboxyl-QDs meer potent waren dan de amine-QDs. Eén uur na injectie van 720 pmol/muis werd een vermindering in bloedplaatjes aantal vastges teld voor carboxyl-QDs maar niet voor amine-QDs. Een effect van de opper vlaktelading werd gevonden in al de geteste parameters. De lichaamsverde ling duidde op long, lever en bloed als voornaamste doelorganen. Verdere studies van de trombotische effecten, aan de hand van heparine behandel ing van de muizen en in vitro bloedplaatjesaggregatietesten, suggeree rden dat bloedstolling werd geïnitieerd door de negatieve oppervlaktelad ing van carboxyl-QDs. Door verder mechanistisch onderzoek naar de samenstelling- en physico-ch emisch gerelateerde toxiciteit van nanopartikels kunnen manieren gevonde n worden om de toxiciteit te voorspellen, wat kan leiden tot de producti e van veilige nanopartikels.status: Publishe
Telomere length and outcome of treatment for pulmonary tuberculosis in a gold mining community
No full textTelomere length (TL) is a marker of ageing and mitochondrial DNA (mtDNA) is an early marker of inflammation caused by oxidative stress. We determined TL and mtDNA content among active pulmonary tuberculosis (PTB) patients to assess if these cellular biomarkers differed between artisanal miners and non-miners, and to assess if they were predictive of treatment outcome. We conducted a prospective cohort study from August 2018 to May 2019 involving newly diagnosed PTB patients at three outpatient TB clinics in a rural Democratic Republic of Congo. We measured relative TL and mtDNA content in peripheral blood leukocytes (at inclusion) via qPCR and assessed their association with PTB treatment outcome. We included 129 patients (85 miners and 44 non-miners) with PTB (median age 40 years; range 5–71 years, 22% HIV-coinfected). For each increase in year and HIV-coinfection, TL shortened by − 0.85% (− 0.19 to − 0.52) (p ≤ 0.0001) and − 14% (− 28.22 to − 1.79) (p = 0.02) respectively. Independent of these covariates, patients with longer TL were more likely to have successful TB treatment [adjusted hazard ratio; 95% CI 1.27 for a doubling of leucocyte telomere length at baseline; 1.05–1.44] than patients with a shorter TL. Blood mtDNA content was not predictive for PTB outcome. For a given chronological age, PTB patients with longer telomeres at time of diagnosis were more likely to have successful PTB treatment outcome.sponsorship: P.D.M.C. K was fellow of the Fonds Marc Vervenne of the KU Leuven (Belgium) and he is supported by the US National Institutes of Health (NIH)-Fogarty Postdoctoral Fellowship: Grant no. 1D43TW010937-01A1. D.S.M is a FWO postdoc, with funding number: FWO Grant 12X9620N. Fieldwork has been supported by the KU Leuven Alumni Association and the University of Antwerp-USOS via the CEGEMI of the Catholic University of Bukavu. The costs of measuring Telomere length and mtDNA were covered by a grant of the European Research Council (ENVIRONAGE). The funders had no role in the study design, data collection, analysis, interpretation, or writing of the report. The corresponding author had full access to all the study data and had final responsibility for the decision to submit for publication. (US National Institutes of Health (NIH)-Fogarty Postdoctoral Fellowship|1D43TW010937-01A1, FWO|12X9620N, European Research Council (ENVIRONAGE), John E. Fogarty International Center for Advanced Study in the Health Sciences|D43TW010937, John E. Fogarty International Center for Advanced Study in the Health Sciences|R25TW011217, National Center for Advancing Translational Sciences|UL1TR001863)status: Publishe
Bone resorption and environmental exposure to cadmium in children: a cross - sectional study
Full text linkAbstract Background Exposure to cadmium has been associated with osteoporosis and fracture risk in women and elderly, but studies in children are lacking. In the present study we investigate the association between markers of bone demineralization [urinary calcium (Ca) and deoxypyridinoline (DPD) excretion] and urinary cadmium (Cd) excretion (as an index of lifetime body burden). Methods 155 schoolchildren from 2 elementary schools in Lahore, Pakistan were included. Urinary Cd was measured as an index of lifetime exposure. We assessed the multivariate-adjusted association of exposure with markers of bone resorption, urinary DPD as well as with Ca excretion. Results Urinary Cd averaged 0.50 nmol/mmol creatinine and was not influenced by age, height, weight and socio-economic status (SES). Independent of gender, age, height, weight and SES a doubling of urinary Cd was associated with a 1.72 times (p Conclusions Even in young children, low-level environmental exposure to cadmium is associated with evidence of bone resorption, suggesting a direct osteotoxic effect with increased calciuria. These findings might have clinical relevance at older age.</p
Gezondheidseffecten van milieuverontreiniging en kinderarbeid in Lahore, Pakistan
No full textThe increasing trend of immigration from villages and small cities to larger cities resulted in increased social and commercial activities in the metropolitan cities of developing countries, for example, Pakistan. The urbanization resulted in increased vehicular traffic which contributes to outdoor environmental air pollution, in addition to other pollutants including trace elements entering the environment from other sources. Particulate air pollution (PM) has various health effects. The impact can be either short term or long term. The effect on human health depends on the type of pollutant, concentration, duration of exposure, and personal susceptibility. A large body of published scientific evidence shows increased hospital visits, cardiopulmonary morbidity and mortality on days with higher PM. Physiological systems of children being in the growing stage, place them among the most vulnerable populations affected by PM. According to the guidelines of WHO the annual permitted value of PM below 2.5 and 10 µm aerodynamic diameter (PM2.5 and PM10) is 10 and 20 µg/m3, respectively. Unlike the developed world where the legislation has already been made and implemented to regulate PM, developing countries stand behind. In Pakistan, though the legislation is present in its preliminary form, the authorities are not able to implement it fully. As a result, the environmental pollution is high in mega-cities like Lahore, where PM10 has been reported >300 µg/m3. Child labour is prevailingextensively in Asia and the Pacific (with an estimated 127.3 million children at work). In Pakistan, the National Child Labor survey conducted in 1996 by the Federal Bureau of Statistics, reported 3.3 million of the40 million children (in the 5-14 years age group) to be economically active on a full-time basis. Epidemiologic studies and research on young workers suggest that children have higher health risks than adults when exposed to hazardous working environments. Moreover, several potential adverse health impacts of occupational exposures need to be studied in children. Few studies have investigated health consequences of child labour. The aim of the present research was a) to study the health effects of outdoor PM among apparently healthy schoolchildren, b) to estimate the urinary concentrations of metals in schoolchildren and working children, and c) to study the health effects of occupational exposures among children employed in selected industries, that is, brick kiln, carpetweaving and surgical instruments manufacturing.In chapter 2, we report the exposure to PM2.5 and PM10 among schoolchildren from a low and ahigh pollution area in Lahore, Pakistan. Exposure assessment was done by measuring PM with a portable laser operated mass analyzer. Blood pressure (BP) was measured with an automated instrument. We found that children living and attending school in an area of very high traffic-related air pollution had a substantially higher systolic (7.6 mmHg) and diastolic (4.5 mmHg) BP compared with children living in an area with lower PM. In chapter 3, we report the relation between exposure to low level environmental cadmium (Cd) exposure and urinary excretion of calcium (Ca)and deoxypyridinoline (DPD), a marker of bone resorption. Exposure assessment was carried out by estimation of urinary Cd by inductively-coupled plasma mass spectrometry (ICP-MS) and DPD by enzyme linked immunosorbent assay (ELISA). We found a consistent association between biomarkers of bone resorption and bone demineralization and Cd exposure in 10-year old children. For each doubling in urinary Cd excretion, bone resorption estimated by DPD increased by 1.72 nmol/mmol creatinine.In chapter 4, we report the work-related exposure to metals among children working in surgical instruments manufacturing units. Estimation of 20 metals was done in spot urine samples by ICP-MS. 8-Hydroxydeoxyguanosine (8-OHdG), a marker of DNA damage was measured by ELISA. Among child workers, this biomonitoring study revealed a substantial exposure to several metals, especially chromium (Cr) and nickel (Ni), which are established carcinogens. Concentrations of Ni were associated with evidence of increased oxidative DNA damage.In chapter 5, we report the respiratory health and metal exposure among schoolchildren and working children from brick kilnand carpet weaving industries. Exposure assessment was done by estimating metals in spot urine by ICP-MS. Respiratory health was assessed by performing spirometry and measuring fractional exhaled nitric oxide (FeNO). We found a high prevalence of respiratory symptoms in children exposedto urban air pollution and in working children, as well as evidence of a high exposure to several toxic metals. The concentrations of urinary As are in the order of those found in other Asian regions with high environmental exposure to As. The sources and pathways of exposure and the health significance of these findings need to be further investigated.Among the selected populations of schoolchildren and children working ineither brick kiln, carpet weaving or surgical industry, we estimated the environmental and occupational exposures. We found a) significantly increased systolic and diastolic blood pressure among schoolchildren from high pollution urban area, b) association of markers of bone resorption (DPD) and bone demineralization (Ca) and Cd exposure, c) high exposures to Cr and Ni among children working in surgical industry and the association of Ni with 8-OHdG, and d) high prevalence of respiratory symptoms in schoolchildren and working children as well as high levels of urinary As.Although our cross-sectional findings have limitations, they haveidentified and confirmed significant health threats among children in Pakistan. Hence, general and specific preventive and control measures should be implemented.status: Publishe
On the impact of residential history in the spatial analysis of diseases with a long latency period: A study of mesothelioma in Belgium
No full textMesothelioma is a rare cancer caused by exposure to asbestos. Belgium has a known long history of asbestos production, resulting in one of the highest mesothelioma mortality rates worldwide. While the production of asbestos has stopped completely, the long latency period of mesothelioma, which can fluctuate between 20 and 40 years after exposure, causes incidences still to be frequent. Mesothelioma's long incubation time affects our assessment of its geographical distribution as well. Since patients' residential locations are likely to change a number of times throughout their lives, the location where the patients develop the disease is often far from the location where they were exposed to asbestos. Using the residential history of patients, we propose the use of a convolution multiple membership model (MMM), which includes both a spatial conditional autoregressive and an unstructured random effect. Pancreatic cancer patients are used as a control population, reflecting the population at risk for mesothelioma. Results show the impact of the residential mobility on the geographical risk estimation, as well as the importance of acknowledging the latency period of a disease. A simulation study was conducted to investigate the properties of the convolution MMM. The robustness of the results for the convolution MMM is assessed via a sensitivity analysis.sponsorship: During the largest part of this study, Thomas Neyens was funded as a postdoctoral researcher by the Research Foundation Flanders (12S7217N). The datasets used for this article were provided by the Belgian Cancer Registry in the framework of a research project funded by the Foundation against Cancer, Belgium (project 2012-222). (Research Foundation Flanders|12S7217N, Foundation against Cancer, Belgium|2012-222)status: Publishe
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
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