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209. Elemental constituents of particulate matter and newborn's size in eight European cohorts

Author

Pedersen, Marie, Gehring, Ulrike, Beelen, Rob, Wang, Meng, Giorgis-Allemand, Lise, Andersen, Anne-Marie Nybo, Basagana, Xavier, Bernard, Claire, Cirach, Marta, Forastiere, Francesco, de Hoogh, Kees, Grazulevicviene, Regina, Gruzieva, Olena, Hoek, Gerard, Jedynska, Aleksandra, Klumper, Claudia, Kooter, Ingeborg M., Kramer, Ursula, Kukkonen, Jaakko, Porta, Daniela, Postma, Dirkje S., Raaschou-Nielsen, Ole, van Rossem, Lenie, Sunyer, Jordi, S0rensen, Mette, Tsai, Ming-Yi, Vrijkotte, Tanja G. M., Wilhelm, Michael, Nieuwenhuijsen, Mark J., Pershagen, Goran, Brunekreef, Bert, Kogevinas, Manolis, and Slama, Remy

Subjects
Infants (Newborn) -- Analysis -- Health aspects -- Growth -- Measurement, Air pollution -- Analysis -- Health aspects, Particles -- Health aspects -- Composition, Company growth, Environmental issues, Health
Abstract

BACKGROUND: The health effects of suspended particulate matter (PM) may depend on its chemical composition. Associations between maternal exposure to chemical constituents of PM and newborn's size have been little examined. OBJECTIVE: We aimed to investigate the associations of exposure to elemental constituents of PM with term low birth weight (LBW; weight < 2,500 g among births after 37 weeks of gestation), mean birth weight, and head circumference, relying on standardized fine-scale exposure assessment and with extensive control for potential confounders. METHODS: We pooled data from eight European cohorts comprising 34,923 singleton births in 1994-2008. Annual average concentrations of elemental constituents of PM ≤ 2.5 and [less than or equal to] 10 µm ([PM.sub.2.5] and [PM.sub.10]) at maternal home addresses during pregnancy were estimated using land-use regression models. Adjusted associations between each birth measurement and concentrations of eight elements (copper, iron, potassium, nickel, sulfur, silicon, vanadium, and zinc) were calculated using random-effects regression on pooled data. RESULTS: A 200-ng/[m.sup.3] increase in sulfur in [PM.sub.2.5] was associated with an increased risk of LBW (adjusted odds ratio = 1.36; 95% confidence interval: 1.17, 1.58). Increased nickel and zinc in [PM.sub.2.5] concentrations were also associated with an increased risk of LBW. Head circumference was reduced at higher exposure to all elements except potassium. All associations with sulfur were most robust to adjustment for [PM.sub.2.5] mass concentration. All results were similar for [PM.sub.10]. CONCLUSION: Sulfur, reflecting secondary combustion particles in this study, may adversely affect LBW and head circumference, independently of particle mass., Introduction Low birth weight (LBW; birth weight < 2,500 g) is a predictor of infant morbidity and mortality. The evidence for associations between exposure to airborne particulate matter (PM) and [...]

Published
2016
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211. Genetic landscape of chronic obstructive pulmonary disease identifies heterogeneous cell-type and phenotype associations

Author

Sakornsakolpat, Phuwanat, Prokopenko, Dmitry, Lamontagne, Maxime, Reeve, Nicola F., Guyatt, Anna L., Jackson, Victoria E., Shrine, Nick, Qiao, Dandi, Bartz, Traci M., Kim, Deog Kyeom, Lee, Mi Kyeong, Latourelle, Jeanne C., Li, Xingnan, Morrow, Jarrett D., Obeidat, Ma’en, Wyss, Annah B., Bakke, Per, Barr, R. Graham, Beaty, Terri H., Belinsky, Steven A., Brusselle, Guy G., Crapo, James D., de Jong, Kim, DeMeo, Dawn L., Fingerlin, Tasha E., Gharib, Sina A., Gulsvik, Amund, Hall, Ian P., Hokanson, John E., Kim, Woo Jin, Lomas, David A., London, Stephanie J., Meyers, Deborah A., O’Connor, George T., Rennard, Stephen I., Schwartz, David A., Sliwinski, Pawel, Sparrow, David, Strachan, David P., Tal-Singer, Ruth, Tesfaigzi, Yohannes, Vestbo, Jørgen, Vonk, Judith M., Yim, Jae-Joon, Zhou, Xiaobo, Bossé, Yohan, Manichaikul, Ani, Lahousse, Lies, Silverman, Edwin K., Boezen, H. Marike, Wain, Louise V., Tobin, Martin D., Hobbs, Brian D., Cho, Michael H., Batini, Chiara, Zhao, Jing Hua, Wielscher, Matthias, Weiss, Stefan, Kentistou, Katherine A., Cook, James P., Hui, Jennie, Karrasch, Stefan, Imboden, Medea, Harris, Sarah E., Marten, Jonathan, Enroth, Stefan, Kerr, Shona M., Surakka, Ida, Vitart, Veronique, Lehtimäki, Terho, Ewert, Ralf, Gieger, Christian, Homuth, Georg, Joshi, Peter K., Langenberg, Claudia, Lind, Lars, Luan, Jian’an, Mahajan, Anubha, Murray, Alison, Porteous, David J., Rawal, Rajesh, Smith, Blair H., Timmers, Paul R. H. J., Raitakari, Olli T., Kähönen, Mika, Polasek, Ozren, Gyllensten, Ulf, Rudan, Igor, Deary, Ian J., Probst-Hensch, Nicole M., Schulz, Holger, James, Alan L., Wilson, James F., Stubbe, Beate, Zeggini, Eleftheria, Jarvelin, Marjo-Riitta, Wareham, Nick, Hayward, Caroline, Morris, Andrew P., Agusti, Alvar, Anderson, Wayne, Bakerly, Nawar, Bals, Robert, Barnes, Kathleen C., Bleecker, Eugene R., Bowler, Russell, Brightling, Christopher, de Bruijne, Marleen, Castaldi, Peter J., Celli, Bartolome, Coxson, Harvey O., Crystal, Ron, de Jong, Pim, Dirksen, Asger, Dy, Jennifer, Foreman, Marilyn, Garcia-Aymerich, Judith, Gevenois, Pierre, Ghosh, Soumitra, Gietema, Hester, Hansel, Nadia, Hersh, Craig P., Hoffman, Eric, Kalsheker, Noor, Kauczor, Hans-Ulrich, Laitinen, Tarja, Lambrechts, Diether, Lee, Sang-Do, Litonjua, Augusto A., Loth, Daan W., Lutz, Sharon M., Lynch, David, MacNee, William, McDonald, Merry-Lynn, Newell, John D., Nordestgaard, Borge G., Oh, Yeon-Mok, Paré, Peter D., Pistolesi, Massimo, Postma, Dirkje S., Puhan, Milo, Regan, Elizabeth, Rich, Stephen S., Seo, Joon Beom, Short, Andrea, Stoel, Berend, Sverzellati, Nicola, ter Riet, Gerben, Van Beek, Edwin J. R., van Ginneken, Bram, Vogelmeier, Claus F., Wanner, Adam, Washko, George, Wauters, Els, Wouters, Emiel F. M., Young, Robert P., Zeigler-Heitbrock, Loems, SpiroMeta Consortium, Understanding Society Scientific Group, International COPD Genetics Consortium, Institute for Molecular Medicine Finland, Groningen Research Institute for Asthma and COPD (GRIAC), Life Course Epidemiology (LCE), Beeldvorming, MUMC+: DA BV Medisch Specialisten Radiologie (9), MUMC+: MA Longziekten (3), RS: NUTRIM - R3 - Respiratory & Age-related Health, Pulmonologie, General practice, APH - Aging & Later Life, APH - Personalized Medicine, ACS - Diabetes & metabolism, Epidemiology, Pulmonary Medicine, Medical Informatics, and Radiology & Nuclear Medicine

Subjects
Male, Lydia Becker Institute, Pulmonary Fibrosis, LD SCORE REGRESSION, Gene Expression, Genome-wide association study, Pulmonary Disease, Chronic Obstructive, 0302 clinical medicine, Pulmonary fibrosis, GWAS, Lung, GENOME-WIDE ASSOCIATION, ACIDIC-MAMMALIAN-CHITINASE, LUNG-FUNCTION, EXTRACELLULAR-MATRIX, PREDOMINANT EMPHYSEMA, CONNECTIVITY MAP, ATOPIC ASTHMA, RISK LOCI, 0303 health sciences, COPD, education.field_of_study, Smoking, 1184 Genetics, developmental biology, physiology, Middle Aged, 3. Good health, Phenotype, medicine.anatomical_structure, Medical genetics, Female, Rare cancers Radboud Institute for Health Sciences [Radboudumc 9], Adult, medicine.medical_specialty, Population, Biology, Polymorphism, Single Nucleotide, Article, 03 medical and health sciences, All institutes and research themes of the Radboud University Medical Center, ResearchInstitutes_Networks_Beacons/lydia_becker_institute_of_immunology_and_inflammation, Genetics, medicine, Genetic predisposition, Humans, Genetic Predisposition to Disease, education, Aged, 030304 developmental biology, Asthma, medicine.disease, respiratory tract diseases, Genetic Loci, Case-Control Studies, Immunology, 3111 Biomedicine, 030217 neurology & neurosurgery, Genome-Wide Association Study
Abstract

Chronic obstructive pulmonary disease (COPD) is the leading cause of respiratory mortality worldwide. Genetic risk loci provide novel insights into disease pathogenesis. We performed a genome-wide association study in 35,735 cases and 222,076 controls from the UK Biobank and additional studies from the International COPD Genetics Consortium. We identified 82 loci with P-value < 5 × 10−8; 47 were previously described in association with either COPD or population-based lung function. Of the remaining 35 novel loci, 13 were associated with lung function in 79,055 individuals from the SpiroMeta consortium. Using gene expression and regulation data, we identified enrichment for loci in lung tissue, smooth muscle and several lung cell types. We found 14 COPD loci shared with either asthma or pulmonary fibrosis. COPD genetic risk loci clustered into groups of quantitative imaging features and comorbidity associations. Our analyses provide further support to the genetic susceptibility and heterogeneity of COPD., Editorial summary Genome-wide analysis of chronic obstructive pulmonary disease identifies 82 loci, 35 of which are new. Integration of gene expression and genomic annotation data shows enrichment of signals in lung tissue, smooth muscle and several lung cell types.

Published
2019
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212. Exploring the relevance and extent of small airways dysfunction in asthma: baseline data from the AssessmenT of smalL Airways involvemeNT In aSthma (ATLANTIS) prospective cohort study

Author

Postma, Dirkje S., Brightling, C, Baldi, S, Van den Berge, M, Fabbri, LM, Gagnatelli, A, Papi, A, Van der Molen, T, Rabe, KF, Siddiqui, S, Singh, Dave, Nicolini, G, and Kraft, M

Subjects
mental disorders, behavioral disciplines and activities, respiratory tract diseases
Abstract

Background Small airways dysfunction (SAD) is well-recognized in asthma, yet its role in asthma severity and asthma control is unclear. Our study aimed to assess which (combination of) biomarkers, physiological testing and imaging markers best measures the presence and extent of SAD in asthma. Methods This multinational observational study investigated participants without and with asthma (GINA severity stage 1-5). Asthma inclusion criteria were: 1) age 18-65 years; 2) clinical asthma diagnosis > 6 months, confirmed by a chest physician 2, supported by objective evidence of any of the following at the baseline visit or in the previous 5 years: a) positive airway hyperresponsiveness to methacholine, or b) positive reversibility (ΔFEV1≥ 12% and ≥ 200 mL within 30 minutes after 400 μg of salbutamol pMDI with or without a spacer or c) PEF variability >20%, measured during 7 days or d) documented reversibility after a cycle (e.g. 4 weeks) of maintenance anti-asthma treatment; 3) stable asthma on any previous regular asthma treatment (“rescue” β2-agonists alone included) at a stable dose for > 8 weeks before baseline; 4) lifetime smoking ≤ 10 pack-years. They underwent spirometry, body plethysmography, impulse oscillometry (IOS), Multiple Breath Nitrogen Washout (MBNW), computed tomography (CT) and questionnaires. Structural equation modeling (SEM) was applied in asthma to assess the contribution of all physiological and CT parameters to SAD. With SEM, we defined a clinical-SAD and CT-SAD score. Asthma subjects were classified in SAD groups using model-based clustering. Asthma severity, control and health care utilization in the past year were compared with the SAD scores and SAD groups. Findings We investigated 773 asthma and 99 control participants (median [interquartiles] age 46 [34, 54] and 41 [29, 52] years, 58% and 57% females, respectively). All physiologic measures contributed to the clinical SAD model with SEM analysis. The prevalence of SAD in asthma was dependent on the measure used and lowest with MBNW Sacin that reflects ventilation heterogeneity in the most peripheral, pre-acinar/acinar airways. IOS and spirometry, reflecting dysfunction of small-to-midsized airways, contributed most to the Clinical-SAD score and differentiated the two SAD Groups. Clinical-SAD Group1 (n=452) had “milder“ SAD, i.e. comparable MBNW Sacin with controls. Group2 (n=312) had more abnormal physiologic SAD measures than Group1, particularly IOS and spirometry, and more severe asthma (asthma control, treatments, exacerbations, quality of life). Clinical-SAD scores were higher in Group2 (“more severe” SAD) and related to asthma control, severity, and exacerbations. Clinical-SAD and CT-SAD scores did not significantly correlate. Interpretation SAD is a complex and silent signature of asthma, which is likely to be directly or indirectly captured by combinations of physiologic tests: spirometry, body plethysmography, IOS, and MBNW. SAD is present across all asthma severity and particularly in severe disease. The clinical classification of SAD in two groups, i.e. a “milder” and “more severe” SAD group, by the easy-to conduct measures IOS and spirometry, is meaningful given its association with GINA asthma severity stages, asthma control, quality of life, and exacerbations. The longitudinal part of ATLANTIS will show the relevance of the SAD score for future risks in asthma, and additionally which parameter best associates with future asthma control. Moreover, we will report on development of a Small Airways Dysfunction Tool (SADT), a questionnaire as an easy measure to suggest SAD, and on the measures of inflammation that best discriminate between the large and small airways’ compartments, with bronchial and transbronchial biopsies, in a smaller subset of participants.

Published
2019
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213. Additional file 1: of Limited overlap in significant hits between genome-wide association studies on two airflow obstruction definitions in the same population

Author

Plaat, Diana, Vonk, Judith, Lahousse, Lies, Jong, Kim, Faiz, Alen, Nedeljkovic, Ivana, Najaf Amin, Diemen, Cleo, Brusselle, Guy, Yohan BossĂŠ, Corry-Anke Brandsma, Hao, Ke, ParĂŠ, Peter, Duijn, Cornelia, Postma, Dirkje, and H. Boezen

Abstract

Supplementary methods, tables and figures. (DOCX 1790 kb)

Published
2019
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222. Genetics

Author

Gerritsen, Jorrit, primary, Feijen, Marlies, additional, and Postma, Dirkje S., additional

Published
2002
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228. A pooled analysis of FEV(sub 1) decline in COPD patients randomized to inhaled corticosteroids or placebo

Author

Soriano, Joan B., Sin, Don D., Zhang, Xuekui, Camp, Pat G., Anderson, Julie A., Anthonisen, Nick R., Buist, A. Sonia, Burge, P. Sherwood, Calverley, Peter M., Connett, John E., Petersson, Stefan, Postma, Dirkje S., Szafranski, Wojciech, and Vestbo, Jorgen

Subjects
Forced expiratory volume -- Analysis, Lung diseases, Obstructive -- Care and treatment, Lung diseases, Obstructive -- Patient outcomes, Lung diseases, Obstructive -- Research, Corticosteroids -- Research, Health
Published
2007

230. Effect of inhaled formoterol and budesonide on exacerbations of asthma

Author

Pauwells, Romain A., Lofdahl, Claes-Goran, Postma, Dirkje S., Tattersfield, Anne E., O'Byrne, Paul, Barnes, Peter J., and Ullman, Anders

Subjects
Asthma -- Drug therapy, Formoterol -- Evaluation, Budesonide -- Evaluation
Abstract

The addition of a long-acting beta 2-agonist, formoterol, to inhaled glucocorticoid therapy could result in the improvement of symptoms and lung function in patients with persistent asthma. A total of 852 patients with recurrent asthma were placed in one of four treatment groups. The addition of formoterol to a group receiving low doses of the glucocorticoid budesonide, as well as a group inhaling a higher dose of the steroid, decreased the frequency of both severe and mild symptoms. The higher dose of budesonide alone also lessened the number of exacerbations, especially of severe asthmatic incidents.

Published
1997

247. Childhood allergic rhinitis, traffic-related air pollution, and variability in the GSTP1, TNF, TLR2, and TLR4 genes: Results from the TAG Study

Author

Fuertes, Elaine, Brauer, Michael, MacIntyre, Elaina, Bauer, Mario, Bellander, Tom, von Berg, Andrea, Berdel, Dietrich, Brunekreef, Bert, Chan-Yeung, Moira, Gehring, Ulrike, Herbarth, Olf, Hoffmann, Barbara, Kerkhof, Marjan, Klümper, Claudia, Koletzko, Sibylle, Kozyrskyj, Anita, Kull, Inger, Heinrich, Joachim, Melén, Erik, Pershagen, Göran, Postma, Dirkje, Tiesler, Carla M.T., and Carlsten, Chris

Published
2013
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