80 results on '"USE REGRESSION-MODELS"'
Search Results
2. Long-Term Exposure to Source-Specific Fine Particles and Mortality-A Pooled Analysis of 14 European Cohorts within the ELAPSE Project
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Chen, Jie, Hoek, Gerard, de Hoogh, Kees, Rodopoulou, Sophia, Andersen, Zorana J., Bellander, Tom, Brandt, Jorgen, Fecht, Daniela, Forastiere, Francesco, Gulliver, John, Hertel, Ole, Hoffmann, Barbara, Hvidtfeldt, Ulla Arthur, Verschuren, W. M. Monique, Joeckel, Karl-Heinz, Jorgensen, Jeanette T., Katsouyanni, Klea, Ketzel, Matthias, Mendez, Diego Yacaman, Leander, Karin, Liu, Shuo, Ljungman, Petter, Faure, Elodie, Magnusson, Patrik K. E., Nagel, Gabriele, Pershagen, Goran, Peters, Annette, Raaschou-Nielsen, Ole, Rizzuto, Debora, Samoli, Evangelia, van der Schouw, Yvonne T., Schramm, Sara, Severi, Gianluca, Stafoggia, Massimo, Strak, Maciej, Sørensen, Mette, Tjonneland, Anne, Weinmayr, Gudrun, Wolf, Kathrin, Zitt, Emanuel, Brunekreef, Bert, Thurston, George D., Chen, Jie, Hoek, Gerard, de Hoogh, Kees, Rodopoulou, Sophia, Andersen, Zorana J., Bellander, Tom, Brandt, Jorgen, Fecht, Daniela, Forastiere, Francesco, Gulliver, John, Hertel, Ole, Hoffmann, Barbara, Hvidtfeldt, Ulla Arthur, Verschuren, W. M. Monique, Joeckel, Karl-Heinz, Jorgensen, Jeanette T., Katsouyanni, Klea, Ketzel, Matthias, Mendez, Diego Yacaman, Leander, Karin, Liu, Shuo, Ljungman, Petter, Faure, Elodie, Magnusson, Patrik K. E., Nagel, Gabriele, Pershagen, Goran, Peters, Annette, Raaschou-Nielsen, Ole, Rizzuto, Debora, Samoli, Evangelia, van der Schouw, Yvonne T., Schramm, Sara, Severi, Gianluca, Stafoggia, Massimo, Strak, Maciej, Sørensen, Mette, Tjonneland, Anne, Weinmayr, Gudrun, Wolf, Kathrin, Zitt, Emanuel, Brunekreef, Bert, and Thurston, George D.
- Abstract
We assessed mortality risks associated with sourcespecific fine particles (PM2.5) in a pooled European cohort of 323,782 participants. Cox proportional hazard models were applied to estimate mortality hazard ratios (HRs) for source-specific PM2.5 identified through a source apportionment analysis. Exposure to 2010 annual average concentrations of source-specific PM2.5 components was assessed at baseline residential addresses. The source apportionment resulted in the identification of five sources: traffic, residual oil combustion, soil, biomass and agriculture, and industry. In single-source analysis, all identified sources were significantly positively associated with increased natural mortality risks. In multisource analysis, associations with all sources attenuated but remained statistically significant with traffic, oil, and biomass and agriculture. The highest association per interquartile increase was observed for the traffic component (HR: 1.06; 95% CI: 1.04 and 1.08 per 2.86 mu g/m(3) increase) across five identified sources. On a 1 mu g/m(3) basis, the residual oil-related PM2.5 had the strongest association (HR: 1.13; 95% CI: 1.05 and 1.22), which was substantially higher than that for generic PM2.5 mass, suggesting that past estimates using the generic PM2.5 exposure response function have underestimated the potential clean air health benefits of reducing fossil-fuel combustion. Source-specific associations with cause-specific mortality were in general consistent with findings of natural mortality.
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- 2022
3. Long-term exposure to ambient air pollution and bladder cancer incidence in a pooled European cohort:the ELAPSE project
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Chen, Jie, Rodopoulou, Sophia, Strak, Maciej, de Hoogh, Kees, Taj, Tahir, Poulsen, Aslak Harbo, Andersen, Zorana J., Bellander, Tom, Brandt, Jorgen, Zitt, Emanuel, Fecht, Daniela, Forastiere, Francesco, Gulliver, John, Hertel, Ole, Hoffmann, Barbara, Hvidtfeldt, Ulla Arthur, Verschuren, W. M. Monique, Jorgensen, Jeanette T., Katsouyanni, Klea, Ketzel, Matthias, Lager, Anton, Leander, Karin, Liu, Shuo, Ljungman, Petter, Severi, Gianluca, Boutron-Ruault, Marie-Christine, Magnusson, Patrik K. E., Nagel, Gabriele, Pershagen, Goran, Peters, Annette, Rizzuto, Debora, van der Schouw, Yvonne T., Samoli, Evangelia, Sørensen, Mette, Stafoggia, Massimo, Tjønneland, Anne, Weinmayr, Gudrun, Wolf, Kathrin, Brunekreef, Bert, Raaschou-Nielsen, Ole, Hoek, Gerard, Chen, Jie, Rodopoulou, Sophia, Strak, Maciej, de Hoogh, Kees, Taj, Tahir, Poulsen, Aslak Harbo, Andersen, Zorana J., Bellander, Tom, Brandt, Jorgen, Zitt, Emanuel, Fecht, Daniela, Forastiere, Francesco, Gulliver, John, Hertel, Ole, Hoffmann, Barbara, Hvidtfeldt, Ulla Arthur, Verschuren, W. M. Monique, Jorgensen, Jeanette T., Katsouyanni, Klea, Ketzel, Matthias, Lager, Anton, Leander, Karin, Liu, Shuo, Ljungman, Petter, Severi, Gianluca, Boutron-Ruault, Marie-Christine, Magnusson, Patrik K. E., Nagel, Gabriele, Pershagen, Goran, Peters, Annette, Rizzuto, Debora, van der Schouw, Yvonne T., Samoli, Evangelia, Sørensen, Mette, Stafoggia, Massimo, Tjønneland, Anne, Weinmayr, Gudrun, Wolf, Kathrin, Brunekreef, Bert, Raaschou-Nielsen, Ole, and Hoek, Gerard
- Abstract
BACKGROUND: The evidence linking ambient air pollution to bladder cancer is limited and mixed.METHODS: We assessed the associations of bladder cancer incidence with residential exposure to fine particles (PM2.5), nitrogen dioxide (NO2), black carbon (BC), warm season ozone (O-3) and eight PM2.5 elemental components (copper, iron, potassium, nickel, sulfur, silicon, vanadium, and zinc) in a pooled cohort (N = 302,493). Exposures were primarily assessed based on 2010 measurements and back-extrapolated to the baseline years. We applied Cox proportional hazard models adjusting for individual- and area-level potential confounders.RESULTS: During an average of 18.2 years follow-up, 967 bladder cancer cases occurred. We observed a positive though statistically non-significant association between PM2.5 and bladder cancer incidence. Hazard Ratios (HR) were 1.09 (95% confidence interval (CI): 0.93-1.27) per 5 mu g/m(3) for 2010 exposure and 1.06 (95% CI: 0.99-1.14) for baseline exposure. Effect estimates for NO2, BC and O-3 were close to unity. A positive association was observed with PM2.5 zinc (HR 1.08; 95% CI: 1.00-1.16 per 10 ng/m(3)).CONCLUSIONS: We found suggestive evidence of an association between long-term PM2.5 mass exposure and bladder cancer, strengthening the evidence from the few previous studies. The association with zinc in PM2.5 suggests the importance of industrial emissions.
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- 2022
4. Long-term exposure to ambient air pollution and bladder cancer incidence in a pooled European cohort: the ELAPSE project
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Jie Chen, Sophia Rodopoulou, Maciej Strak, Kees de Hoogh, Tahir Taj, Aslak Harbo Poulsen, Zorana J. Andersen, Tom Bellander, Jørgen Brandt, Emanuel Zitt, Daniela Fecht, Francesco Forastiere, John Gulliver, Ole Hertel, Barbara Hoffmann, Ulla Arthur Hvidtfeldt, W. M. Monique Verschuren, Jeanette T. Jørgensen, Klea Katsouyanni, Matthias Ketzel, Anton Lager, Karin Leander, Shuo Liu, Petter Ljungman, Gianluca Severi, Marie-Christine Boutron-Ruault, Patrik K. E. Magnusson, Gabriele Nagel, Göran Pershagen, Annette Peters, Debora Rizzuto, Yvonne T. van der Schouw, Evangelia Samoli, Mette Sørensen, Massimo Stafoggia, Anne Tjønneland, Gudrun Weinmayr, Kathrin Wolf, Bert Brunekreef, Ole Raaschou-Nielsen, Gerard Hoek, and Health effects Institute
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Male ,Cancer Research ,Nitrogen Dioxide ,PROFILE ,NO2 ,complex mixtures ,Article ,1117 Public Health and Health Services ,Rare Diseases ,USE REGRESSION-MODELS ,Air Pollution ,Humans ,1112 Oncology and Carcinogenesis ,Oncology & Carcinogenesis ,POPULATION ,RISK ,Air Pollutants ,Science & Technology ,MORTALITY ,DIESEL ,Incidence ,COMPONENTS ,MEN ,Environmental Exposure ,CARCINOGENICITY ,Zinc ,Oncology ,Urinary Bladder Neoplasms ,Female ,Particulate Matter ,Life Sciences & Biomedicine - Abstract
Background: The evidence linking ambient air pollution to bladder cancer is limited and mixed. Methods: We assessed the associations of bladder cancer incidence with residential exposure to fine particles (PM2.5), nitrogen dioxide (NO2), black carbon (BC), warm season ozone (O3) and eight PM2.5 elemental components (copper, iron, potassium, nickel, sulfur, silicon, vanadium, and zinc) in a pooled cohort (N = 302,493). Exposures were primarily assessed based on 2010 measurements and back-extrapolated to the baseline years. We applied Cox proportional hazard models adjusting for individual- and area-level potential confounders. Results: During an average of 18.2 years follow-up, 967 bladder cancer cases occurred. We observed a positive though statistically non-significant association between PM2.5 and bladder cancer incidence. Hazard Ratios (HR) were 1.09 (95% confidence interval (CI): 0.93–1.27) per 5 µg/m3 for 2010 exposure and 1.06 (95% CI: 0.99–1.14) for baseline exposure. Effect estimates for NO2, BC and O3 were close to unity. A positive association was observed with PM2.5 zinc (HR 1.08; 95% CI: 1.00–1.16 per 10 ng/m3). Conclusions: We found suggestive evidence of an association between long-term PM2.5 mass exposure and bladder cancer, strengthening the evidence from the few previous studies. The association with zinc in PM2.5 suggests the importance of industrial emissions.
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- 2022
5. Environmental factors shaping the gut microbiome in a Dutch population
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Gacesa, Ranko, Kurilshikov, Alexander, Vich Vila, Arnau, Sinha, Trishla, Klaassen, M, Bolte, L.A., Andreu-Sánchez, S., Chen, L., Collij, V., Hu, S., Dekens-Konter, J.A.M., Lenters, Virissa, Björk, J.R., Swarte, J.C., Swertz, Morris A., Jansen, B.H.R., Gelderloos-Arends, J., Jankipersadsing, Soesma A, Hofker, M., Vermeulen, Roel, Sanna, S., Harmsen, H J M, Wijmenga, Cisca, Fu, J., Zhernakova, A., Weersma, Rinse K., IRAS OH Epidemiology Chemical Agents, Groningen Institute for Gastro Intestinal Genetics and Immunology (3GI), Microbes in Health and Disease (MHD), Center for Liver, Digestive and Metabolic Diseases (CLDM), Translational Immunology Groningen (TRIGR), and IRAS OH Epidemiology Chemical Agents
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Multidisciplinary ,Bacteria ,GENETICS ,ASSOCIATION ,Environment ,METAGENOMICS ,ENTEROTYPES ,Diet ,Gastrointestinal Microbiome ,ALIGNMENT ,Socioeconomic Factors ,POLLUTION ,MARKERS ,USE REGRESSION-MODELS ,AREAS ,Humans ,INTESTINAL MICROBIOME ,Life Style ,Netherlands - Abstract
The gut microbiome is associated with diverse diseases(1-3), but a universal signature of a healthy or unhealthy microbiome has not been identified, and there is a need to understand how genetics, exposome, lifestyle and diet shape the microbiome in health and disease. Here we profiled bacterial composition, function, antibiotic resistance and virulence factors in the gut microbiomes of 8,208 Dutch individuals from a three-generational cohort comprising 2,756 families. We correlated these to 241 host and environmental factors, including physical and mental health, use of medication, diet, socioeconomic factors and childhood and current exposome. We identify that the microbiome is shaped primarily by the environment and cohabitation. Only around 6.6% of taxa are heritable, whereas the variance of around 48.6% of taxa is significantly explained by cohabitation. By identifying 2,856 associations between the microbiome and health, we find that seemingly unrelated diseases share a common microbiome signature that is independent of comorbidities. Furthermore, we identify 7,519 associations between microbiome features and diet, socioeconomics and early life and current exposome, with numerous early-life and current factors being significantly associated with microbiome function and composition. Overall, this study provides a comprehensive overview of gut microbiome and the underlying impact of heritability and exposures that will facilitate future development of microbiome-targeted therapies.
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- 2022
6. Long-Term Exposure to Source-Specific Fine Particles and Mortality-A Pooled Analysis of 14 European Cohorts within the ELAPSE Project
- Author
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Jie Chen, Gerard Hoek, Kees de Hoogh, Sophia Rodopoulou, Zorana J. Andersen, Tom Bellander, Jørgen Brandt, Daniela Fecht, Francesco Forastiere, John Gulliver, Ole Hertel, Barbara Hoffmann, Ulla Arthur Hvidtfeldt, W. M. Monique Verschuren, Karl-Heinz Jöckel, Jeanette T. Jørgensen, Klea Katsouyanni, Matthias Ketzel, Diego Yacamán Méndez, Karin Leander, Shuo Liu, Petter Ljungman, Elodie Faure, Patrik K. E. Magnusson, Gabriele Nagel, Göran Pershagen, Annette Peters, Ole Raaschou-Nielsen, Debora Rizzuto, Evangelia Samoli, Yvonne T. van der Schouw, Sara Schramm, Gianluca Severi, Massimo Stafoggia, Maciej Strak, Mette Sørensen, Anne Tjønneland, Gudrun Weinmayr, Kathrin Wolf, Emanuel Zitt, Bert Brunekreef, and George D. Thurston
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Technology ,SOURCE-APPORTIONMENT ,Medizin ,Environmental Sciences & Ecology ,fine particulate matter (PM) ,HEART-DISEASE ,NO2 ,complex mixtures ,Cohort Studies ,Engineering ,absolute principal component analysis (APCA) ,USE REGRESSION-MODELS ,PARTICULATE MATTER ,Air Pollution ,Environmental Chemistry ,Humans ,SPATIAL VARIATION ,Air Pollutants ,Science & Technology ,COMPONENTS ,Engineering, Environmental ,source apportionment ,General Chemistry ,Environmental Exposure ,AIR-POLLUTION ,fine particulate matter (PM2.5) ,mortality ,Absolute Principal Component Analysis (apca) ,Fine Particulate Matter (pm2.5) ,Mortality ,Source Apportionment ,RISK-FACTORS ,HEALTH ,Life Sciences & Biomedicine ,Environmental Sciences - Abstract
We assessed mortality risks associated with source-specific fine particles (PM2.5) in a pooled European cohort of 323,782 participants. Cox proportional hazard models were applied to estimate mortality hazard ratios (HRs) for source-specific PM2.5identified through a source apportionment analysis. Exposure to 2010 annual average concentrations of source-specific PM2.5components was assessed at baseline residential addresses. The source apportionment resulted in the identification of five sources: traffic, residual oil combustion, soil, biomass and agriculture, and industry. In single-source analysis, all identified sources were significantly positively associated with increased natural mortality risks. In multisource analysis, associations with all sources attenuated but remained statistically significant with traffic, oil, and biomass and agriculture. The highest association per interquartile increase was observed for the traffic component (HR: 1.06; 95% CI: 1.04 and 1.08 per 2.86 μg/m3increase) across five identified sources. On a 1 μg/m3basis, the residual oil-related PM2.5had the strongest association (HR: 1.13; 95% CI: 1.05 and 1.22), which was substantially higher than that for generic PM2.5mass, suggesting that past estimates using the generic PM2.5exposure response function have underestimated the potential clean air health benefits of reducing fossil-fuel combustion. Source-specific associations with cause-specific mortality were in general consistent with findings of natural mortality.
- Published
- 2022
7. LongITools: Dynamic longitudinal exposome trajectories in cardiovascular and metabolic noncommunicable diseases
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Ronkainen, Justiina, Nedelec, Rozenn, Atehortua, Angelica, Balkhiyarova, Zhanna, Cascarano, Anna, Ngoc Dang, Vien, Elhakeem, Ahmed, van Enckevort, Esther, Goncalves Soares, Ana, Haakma, Sido, Halonen, Miia, Heil, Katharina F, Heiskala, Anni, Hyde, Eleanor, Jacquemin, Bénédicte, Keikkala, Elina, Kerckhoffs, Jules, Klåvus, Anton, Kopinska, Joanna A, Lepeule, Johanna, Marazzi, Francesca, Motoc, Irina, Näätänen, Mari, Ribbenstedt, Anton, Rundblad, Amanda, Savolainen, Otto, Simonetti, Valentina, de Toro Eadie, Nina, Tzala, Evangelia, Ulrich, Anna, Wright, Thomas, Zarei, Iman, d'Amico, Enrico, Belotti, Federico, Brunius, Carl, Castleton, Christopher, Charles, Marie-Aline, Gaillard, Romy, Hanhineva, Kati, Hoek, Gerard, Holven, Kirsten B, Jaddoe, Vincent W V, Kaakinen, Marika A, Kajantie, Eero, Kavousi, Maryam, Lakka, Timo, Matthews, Jason, Piano Mortari, Andrea, Vääräsmäki, Marja, Voortman, Trudy, Webster, Claire, Zins, Marie, Atella, Vincenzo, Bulgheroni, Maria, Chadeau-Hyam, Marc, Conti, Gabriella, Evans, Jayne, Felix, Janine F, Heude, Barbara, Järvelin, Marjo-Riitta, Kolehmainen, Marjukka, Landberg, Rikard, Lekadir, Karim, Parusso, Stefano, Prokopenko, Inga, de Rooij, Susanne R, Roseboom, Tessa, Swertz, Morris, Timpson, Nicholas, Ulven, Stine M, Vermeulen, Roel, Juola, Teija, Sebert, Sylvain, IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, dIRAS RA-I&I RA, IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, dIRAS RA-I&I RA, Pediatrics, Epidemiology, Epidemiology and Data Science, Amsterdam Reproduction & Development (AR&D), APH - Aging & Later Life, APH - Health Behaviors & Chronic Diseases, APH - Mental Health, ARD - Amsterdam Reproduction and Development, Obstetrics and Gynaecology, University of Oulu, Institut de recherche en santé, environnement et travail (Irset), Université d'Angers (UA)-Université de Rennes (UR)-École des Hautes Études en Santé Publique [EHESP] (EHESP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), Cohortes épidémiologiques en population (CONSTANCES), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Saclay-Université Paris Cité (UPCité), UMS 011, Institut National de la Santé et de la Recherche Médicale (INSERM), UFR Médecine [Santé] - Université Paris Cité (UFR Médecine UPCité), Université Paris Cité (UPCité), Centre de Recherche Épidémiologie et Statistique Sorbonne Paris Cité (CRESS (U1153 / UMR_A_1125 / UMR_S_1153)), Conservatoire National des Arts et Métiers [CNAM] (CNAM), HESAM Université - Communauté d'universités et d'établissements Hautes écoles Sorbonne Arts et métiers université (HESAM)-HESAM Université - Communauté d'universités et d'établissements Hautes écoles Sorbonne Arts et métiers université (HESAM)-Université Sorbonne Paris Cité (USPC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Utrecht University [Utrecht], Julius Center for Health Sciences and Primary Care, University Medical Center [Utrecht], HUS Children and Adolescents, Lastentautien yksikkö, Children's Hospital, Clinicum, University of Helsinki, and Groningen Institute for Gastro Intestinal Genetics and Immunology (3GI)
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Settore SECS-P/01 ,EUROPE ,Epidemiology ,[SDV]Life Sciences [q-bio] ,Health, Toxicology and Mutagenesis ,Omics ,PM2.5 ,NO2 ,Analytical Chemistry ,SDG 3 - Good Health and Well-being ,USE REGRESSION-MODELS ,AREAS ,Health Sciences ,SDG 13 - Climate Action ,Other Biological Topics ,COHORT ,Toxicology and Mutagenesis ,Cardio-metabolic and vascular health ,European research consortium ,Exposome ,Life-course pathways ,SDG 2 - Zero Hunger ,Global and Planetary Change ,Bioinformatics (Computational Biology) ,Mass spectrometry ,Environmental and Occupational Health ,Public Health, Environmental and Occupational Health ,Biochemistry and Molecular Biology ,Cohort ,Pollution ,Life sciences ,3142 Public health care science, environmental and occupational health ,SDG 11 - Sustainable Cities and Communities ,Health ,Settore MED/42 ,Public Health ,sense organs ,Social Sciences Interdisciplinary ,Exposomics - Abstract
International audience; The current epidemics of cardiovascular and metabolic noncommunicable diseases have emerged alongside dramatic modifications in lifestyle and living environments. These correspond to changes in our “modern” postwar societies globally characterized by rural-to-urban migration, modernization of agricultural practices, and transportation, climate change, and aging. Evidence suggests that these changes are related to each other, although the social and biological mechanisms as well as their interactions have yet to be uncovered. LongITools, as one of the 9 projects included in the European Human Exposome Network, will tackle this environmental health equation linking multidimensional environmental exposures to the occurrence of cardiovascular and metabolic noncommunicable diseases.
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- 2022
8. Ultrafine particles, particle components and lung function at age 16 years: The PIAMA birth cohort study
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Yu, Z., Koppelman, G.H., Hoek, G., Kerckhoffs, J., Vonk, J.M., Vermeulen, R., Gehring, U., IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, dIRAS RA-I&I RA, Organic geochemistry, IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, dIRAS RA-I&I RA, Organic geochemistry, and Groningen Research Institute for Asthma and COPD (GRIAC)
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Vital capacity ,Adolescent ,CHILDREN ,NO2 ,complex mixtures ,Cohort Studies ,FEV1/FVC ratio ,Animal science ,Interquartile range ,Environmental Science(all) ,USE REGRESSION-MODELS ,AREAS ,Air Pollution ,Linear regression ,Ultrafine particle ,medicine ,Humans ,GE1-350 ,EXPOSURE ,Prospective Studies ,Lung ,General Environmental Science ,Asthma ,Air Pollutants ,business.industry ,Confounding ,AIR-POLLUTION ,Environmental Exposure ,medicine.disease ,Confidence interval ,Lung function ,respiratory tract diseases ,Adolescence ,Environmental sciences ,Ultrafine particles ,Elemental composition ,RESPIRATORY HEALTH ,ASTHMA ,business ,Particulate matter - Abstract
Background: Particulate matter (PM) air pollution exposure has been linked to lung function in adolescents, but little is known about the relevance of specific PM components and ultrafine particles (UFP).Objectives: To investigate the associations of long-term exposure to PM elemental composition and UFP with lung function at age 16 years.Methods: For 706 participants of a prospective Dutch birth cohort, we assessed associations of forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC) at age 16 with average exposure to eight elemental components (copper, iron, potassium, nickel, sulfur, silicon, vanadium and zinc) in PM2.5 and PM10, as well as UFP during the preceding years (age 13-16 years) estimated by land-use regression models. After assessing associations for each pollutant individually using linear regression models with adjustment for potential confounders, independence of associations with different pollutants was assessed in two-pollutant models with PM mass and NO2, for which associations with lung function have been reported previously.Results: We observed that for most PM elemental components higher exposure was associated with lower FEV1, especially PM10 sulfur [e.g. adjusted difference -2.23% (95% confidence interval (CI) -3.70 to -0.74%) per interquartile range (IQR) increase in PM10 sulfur]. The association with PM10 sulfur remained after adjusting for PM10 mass. Negative associations of exposure to UFP with both FEV1 and FVC were observed [-1.06% (95% CI: -2.08 to -0.03%) and -0.65% (95% CI: -1.53 to 0.23%), respectively per IQR increase in UFP], but did not persist in two-pollutant models with NO2 or PM2.5.Conclusions: Long-term exposure to sulfur in PM10 may result in lower FEV1 at age 16. There is no evidence for an independent effect of UFP exposure.
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- 2021
9. Long-term exposure to air pollution and liver cancer incidence in six European cohorts
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Jeanette Therming Jørgensen, Alois Lang, Klea Katsouyanni, Massimo Stafoggia, Ulla Arthur Hvidtfeldt, Anton Lager, Matteo Renzi, Gerard Hoek, Anne Tjønneland, Marie-Christine Boutron-Ruault, Barbara Hoffmann, Ole Raaschou-Nielsen, Matthias Ketzel, Karin Leander, Hans Concin, Tom Bellander, Göran Pershagen, Nicole A.H. Janssen, Sophia Rodopoulou, John S. Gulliver, Raphael Simon Peter, Jochem O. Klompmaker, Evangelia Samoli, Gudrun Weinmayr, Mariska Bauwelinck, Youn-Hee Lim, Gabriele Nagel, Debora Rizzuto, Rina So, Bert Brunekreef, Amar Mehta, Torben Sigsgaard, Annette Peters, Giulia Cesaroni, Francesco Forastiere, Shuo Liu, Zorana Jovanovic Andersen, Patrik K. E. Magnusson, Petter Ljungman, Jie Chen, Maciej Strak, Mette Kildevæld Simonsen, Richard Atkinson, Danielle Vienneau, Kathrin Wolf, Carla H. van Gils, Daniela Fecht, Kees de Hoogh, Rudi G. J. Westendorp, Gianluca Severi, Jørgen Brandt, Ole Hertel, Faculty of Economic and Social Sciences and Solvay Business School, and Sociology
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Adult ,Male ,Cancer Research ,Liver cancer incidence ,PARTICIPATION ,air pollution ,Air pollution ,PM2.5 ,medicine.disease_cause ,PROFILE ,complex mixtures ,Liver disease ,USE REGRESSION-MODELS ,Environmental health ,HEPATOCELLULAR-CARCINOMA ,medicine ,cohort study ,Humans ,1112 Oncology and Carcinogenesis ,particulate matter ,Oncology & Carcinogenesis ,Particle Size ,Lung cancer ,liver cancer incidence ,POPULATION ,Proportional Hazards Models ,RISK ,Air Pollutants ,Science & Technology ,business.industry ,Proportional hazards model ,Incidence (epidemiology) ,Incidence ,Hazard ratio ,Liver Neoplasms ,Cancer ,MEN ,Environmental Exposure ,Middle Aged ,medicine.disease ,PREVALENCE ,Europe ,Oncology ,Female ,Liver cancer ,business ,Life Sciences & Biomedicine ,LUNG - Abstract
Particulate matter air pollution and diesel engine exhaust have been classified as carcinogenic for lung cancer, yet few studies have explored associations with liver cancer. We used six European adult cohorts which were recruited between 1985 and 2005, pooled within the “Effects of low-level air pollution: A study in Europe” (ELAPSE) project, and followed for the incidence of liver cancer until 2011 to 2015. The annual average exposure to nitrogen dioxide (NO 2), particulate matter with diameter 2.5), black carbon (BC), warm-season ozone (O 3), and eight elemental components of PM 2.5 (copper, iron, zinc, sulfur, nickel, vanadium, silicon, and potassium) were estimated by European-wide hybrid land-use regression models at participants' residential addresses. We analyzed the association between air pollution and liver cancer incidence by Cox proportional hazards models adjusting for potential confounders. Of 330 064 cancer-free adults at baseline, 512 developed liver cancer during a mean follow-up of 18.1 years. We observed positive linear associations between NO 2 (hazard ratio, 95% confidence interval: 1.17, 1.02-1.35 per 10 μg/m 3), PM 2.5 (1.12, 0.92-1.36 per 5 μg/m 3), and BC (1.15, 1.00-1.33 per 0.5 10 −5/m) and liver cancer incidence. Associations with NO 2 and BC persisted in two-pollutant models with PM 2.5. Most components of PM 2.5 were associated with the risk of liver cancer, with the strongest associations for sulfur and vanadium, which were robust to adjustment for PM 2.5 or NO 2. Our study suggests that ambient air pollution may increase the risk of liver cancer, even at concentrations below current EU standards.
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- 2021
10. Associations of traffic-related air pollution and greenery with academic outcomes among primary schoolchildren
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Miguel Alvarado Molina, Amanda J. Wheeler, Joep L.A. Claesen, Rachel Tham, Gonnie Klabbers, David Donaire Gonzalez, Alison Carver, Mark J. Nieuwenhuijsen, Metamedica, and RS: FHML non-thematic output
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Mediation (statistics) ,Traffic-Related Pollution ,MEDIATION ,STRESS ,media_common.quotation_subject ,education ,CHILDREN ,Academic achievement ,010501 environmental sciences ,01 natural sciences ,Biochemistry ,Literacy ,Proxy (climate) ,COGNITIVE PERFORMANCE ,03 medical and health sciences ,0302 clinical medicine ,Numeracy ,Traffic-related air pollution ,USE REGRESSION-MODELS ,Air Pollution ,Humans ,030212 general & internal medicine ,EXPOSURE ,Road traffic density ,GREENNESS ,Child ,0105 earth and related environmental sciences ,General Environmental Science ,media_common ,Primary school ,Schools ,Grammar ,Australia ,Moderation ,Punctuation ,Greenspace ,Cross-Sectional Studies ,PHYSICAL-ACTIVITY ,MODERATOR ,Cognitive development ,Psychology ,LANDSCAPES ,Demography - Abstract
Background There is preliminary evidence that greenery/greenspace around schools may be positively associated with children's cognitive development and academic outcomes, whereas traffic-related air pollution (TRAP) may have a detrimental effect. Few studies have examined pathways between both exposures and academic outcomes. This study aimed to assess associations between greenery, road traffic density (a proxy for TRAP) surrounding primary (elementary) schools, and academic achievement of primary schoolchildren in Melbourne, Australia. Methods This cross-sectional study examined mean academic scores in Years 3 and 5 for primary schools (n = 851) in Greater Melbourne. Scores were from the 2018 ‘National Assessment Program – Literacy and Numeracy’ (NAPLAN) in five domains: ‘Reading’; ‘Writing’; ‘Spelling’; ‘Grammar & Punctuation’ and ‘Numeracy’. Greenery was measured within school boundaries and surrounding Euclidean buffers (100, 300, 1000 and 2000 m) using the Normalized Difference Vegetation Index (NDVI). Measured TRAP proxies were weighted road density (WRD) within the buffers and distance to a major road. Generalised Linear Models were used to examine associations of greenery and TRAP with academic scores (adjusted for school socio-educational status), and to identify mediating pathways. Results Greenery was positively associated with Reading scores in Year 3 (all buffers except 2000 m) and in Year 5 (all buffers), with Numeracy in Years 3 and 5 (all buffers) and with Grammar & Punctuation in Year 5 (all buffers). WRD was inversely associated with Reading scores in Year 5 (all buffers), with Numeracy in Year 3 (all buffers) and Year 5 (300 and 1000 m buffers), and with Grammar & Punctuation in Year 3 (100 and 300 m buffers) and Year 5 (all buffers). Distance to a major road was not associated with any score. TRAP partially mediated associations of greenery within 300 m with Numeracy in Year 3 and Grammar & Punctuation in Year 5, and within 2000 m for Reading in Year 5. Conclusions Preliminary evidence indicated that greenery around primary schools was positively associated with Reading, Numeracy and Grammar & Punctuation scores, with TRAP mediating some associations. Further research is required to improve TRAP exposure assessment around schools to verify these findings and inform town/school planners and educators regarding optimal school locations and environments for promoting learning.
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- 2021
11. Vegetation and vehicle emissions around primary schools across urban Australia: associations with academic performance
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Alison Carver, Miguel Alvarado Molina, Joep L.A. Claesen, Gonnie Klabbers, David Donaire, null Gonzalez, Rachel Tham, Ester Cerin, Mark Nieuwenhuijsen, Amanda J. Wheeler, Metamedica, and RS: FHML non-thematic output
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ENVIRONMENT ,Schools ,STRESS ,Australia ,CHILDREN ,AIR-POLLUTION ,Biochemistry ,Vehicle emissions ,Cross-Sectional Studies ,Elementary school ,MODERATOR ,PHYSICAL-ACTIVITY ,COGNITIVE-DEVELOPMENT ,USE REGRESSION-MODELS ,Greenery ,Road density ,Academic Performance ,Humans ,Learning ,GREENNESS ,Child ,LANDSCAPES ,General Environmental Science - Abstract
BACKGROUND: Evolving evidence suggests that vegetation surrounding schools is beneficial to children's academic performance, however vehicle emissions are adversely related. Little is known about concurrent impacts of vegetation and vehicle emissions on academic performance. This study examined associations of vegetation and vehicle emissions near urban Australian primary schools with children's academic performance.METHODS: Vegetation within schoolyards and Euclidean buffers (100, 300 and 1000m) was assessed using the Normalised Difference Vegetation Index (NDVI). Weighted road density (WRD) was computed for each buffer as a vehicle emissions proxy. Cross-sectional associations and mediating pathways between vegetation and vehicle emissions and standardised average academic scores in Literacy (Reading, Writing, Language Conventions) and Mathematics for Grades 3 and 5 attending 3745 primary schools in urban areas (population ≥10,000) of Australia in 2018 were assessed using generalised linear models adjusted for school socio-educational status.RESULTS: Significant positive associations were found between vegetation and Reading in Grades 3 and 5, Mathematics in Grade 3 (all buffers), Writing in Grade 3 (100 and 300m), and Language Conventions in Grades 3 and 5 (most buffers). Increased vehicle emissions were negatively associated with Reading and Mathematics in Grades 3 and 5 (most buffers), and Language Conventions in Grade 3 (300 and 1000m) and Grade 5 (100-1000m). Within 300m, vehicle emissions partially mediated associations between vegetation with Mathematics in Grade 3 (proportion mediated, 21%), Reading and Language Conventions in Grade 5 (15%, 37% respectively).CONCLUSIONS: Our findings contribute to growing evidence that vegetation around primary schools is associated with higher achievement in Literacy and Mathematics, with partial mediation by vehicle emissions. Future studies should conduct on-site measurement of vehicle emissions and audit vegetation around schools to confirm findings and inform urban/school planners and school leaders on designing and modifying school environments to support learning.
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- 2022
12. Long-Term Exposure to Fine Particle Elemental Components and Natural and Cause-Specific Mortality-a Pooled Analysis of Eight European Cohorts within the ELAPSE Project
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Chen, Jie, Rodopoulou, Sophia, de Hoogh, Kees, Strak, Maciej, Andersen, Zorana J., Atkinson, Richard, Bauwelinck, Mariska, Bellander, Tom, Brandt, Jorgen, Cesaroni, Giulia, Concin, Hans, Fecht, Daniela, Forastiere, Francesco, Gulliver, John, Hertel, Ole, Hoffmann, Barbara, Hvidtfeldt, Ulla Arthur, Janssen, Nicole A. H., Joeckel, Karl-Heinz, Jorgensen, Jeanette, Katsouyanni, Klea, Ketzel, Matthias, Klompmaker, Jochem O., Lager, Anton, Leander, Karin, Liu, Shuo, Ljungman, Petter, MacDonald, Conor J., Magnusson, Patrik K. E., Mehta, Amar, Nagel, Gabriele, Oftedal, Bente, Pershagen, Goran, Peters, Annette, Raaschou-Nielsen, Ole, Renzi, Matteo, Rizzuto, Debora, Samoli, Evangelia, van der Schouw, Yvonne T., Schramm, Sara, Schwarze, Per, Sigsgaard, Torben, Sørensen, Mette, Stafoggia, Massimo, Tjonneland, Anne, Vienneau, Danielle, Weinmayr, Gudrun, Wolf, Kathrin, Brunekreef, Bert, Hoek, Gerard, Chen, Jie, Rodopoulou, Sophia, de Hoogh, Kees, Strak, Maciej, Andersen, Zorana J., Atkinson, Richard, Bauwelinck, Mariska, Bellander, Tom, Brandt, Jorgen, Cesaroni, Giulia, Concin, Hans, Fecht, Daniela, Forastiere, Francesco, Gulliver, John, Hertel, Ole, Hoffmann, Barbara, Hvidtfeldt, Ulla Arthur, Janssen, Nicole A. H., Joeckel, Karl-Heinz, Jorgensen, Jeanette, Katsouyanni, Klea, Ketzel, Matthias, Klompmaker, Jochem O., Lager, Anton, Leander, Karin, Liu, Shuo, Ljungman, Petter, MacDonald, Conor J., Magnusson, Patrik K. E., Mehta, Amar, Nagel, Gabriele, Oftedal, Bente, Pershagen, Goran, Peters, Annette, Raaschou-Nielsen, Ole, Renzi, Matteo, Rizzuto, Debora, Samoli, Evangelia, van der Schouw, Yvonne T., Schramm, Sara, Schwarze, Per, Sigsgaard, Torben, Sørensen, Mette, Stafoggia, Massimo, Tjonneland, Anne, Vienneau, Danielle, Weinmayr, Gudrun, Wolf, Kathrin, Brunekreef, Bert, and Hoek, Gerard
- Abstract
BACKGROUND: Inconsistent associations between long-term exposure to particles with an aerodynamic diameterOBJECTIVES: We investigated the associations between long-term exposure to PM2.5 elemental components and mortality in a large pooled European cohort; to compare health effects of PM2.5 components estimated with two exposure modeling approaches, namely, supervised linear regression (SLR) and random forest (RF) algorithms.METHODS: We pooled data from eight European cohorts with 323,782 participants, average age 49 y at baseline (1985-2005). Residential exposure to 2010 annual average concentration of eight PM2.5 components [copper (Cu), iron (Fe), potassium (K), nickel (Ni), sulfur (S), silicon (Si), vanadium (V), and zinc (Zn)] was estimated with Europe-wide SLR and RF models at a 100 X 100 m scale. We applied Cox proportional hazards models to investigate the associations between components and natural and cause-specific mortality. In addition, two-pollutant analyses were conducted by adjusting each component for PM2.5 mass and nitrogen dioxide (NO2) separately.RESULTS: We observed 46,640 natural-cause deaths with 6,317,235 person-years and an average follow-up of 19.5 y. All SLR-modeled components were statistically significantly associated with natural-cause mortality in single-pollutant models with hazard ratios (HRs) from 1.05 to 1.27. Similar HRs were observed for RE-modeled Cu, Fe, K, S, V, and Zn with wider confidence intervals (CIs). HRs for SLR-modeled Ni, S, Si, V, and Zn remained above unity and (almost) significant after adjustment for both PM2.5 and NO2. HRs only remained (almost) significant for RE-modeled K and V in two-pollutant models. The HRs for V were 1.03 (95% CI: 1.02, 1.05) and 1.06 (95% CI: 1.02, 1.10) for SLR- and RF-modeled exposures, respectively, per 2 ng/m(3), adjusting for PM2.5 mass. Associations with cause-specific mortality were less consistent in two-pollutant models.CONCLUSION: Long-term exposure
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- 2021
13. Multiple air pollutant exposure and lung cancer in Tehran, Iran
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Khorrami, Zahra, Pourkhosravani, Mohsen, Rezapour, Maysam, Etemad, Koorosh, Taghavi-Shahri, Seyed Mahmood, Kuenzli, Nino, Amini, Heresh, Khanjani, Narges, Khorrami, Zahra, Pourkhosravani, Mohsen, Rezapour, Maysam, Etemad, Koorosh, Taghavi-Shahri, Seyed Mahmood, Kuenzli, Nino, Amini, Heresh, and Khanjani, Narges
- Abstract
Lung cancer is the most rapidly increasing malignancy worldwide with an estimated 2.1 million cancer cases in the latest, 2018 World Health Organization (WHO) report. The objective of this study was to investigate the association of air pollution and lung cancer, in Tehran, Iran. Residential area information of the latest registered lung cancer cases that were diagnosed between 2014 and 2016 (N=1,850) were inquired from the population-based cancer registry of Tehran. Long-term average exposure to PM10, SO2, NO, NO2, NOX, benzene, toluene, ethylbenzene, m-xylene, p-xylene, o-xylene (BTEX), and BTEX in 22 districts of Tehran were estimated using land use regression models. Latent profile analysis (LPA) was used to generate multi-pollutant exposure profiles. Negative binomial regression analysis was used to examine the association between air pollutants and lung cancer incidence. The districts with higher concentrations for all pollutants were mostly in downtown and around the railway station. Districts with a higher concentration for NOx (IRR=1.05, for each 10 unit increase in air pollutant), benzene (IRR=3.86), toluene (IRR=1.50), ethylbenzene (IRR=5.16), p-xylene (IRR=9.41), o-xylene (IRR=7.93), m-xylene (IRR=2.63) and TBTEX (IRR=1.21) were significantly associated with higher lung cancer incidence. Districts with a higher multiple air-pollution profile were also associated with more lung cancer incidence (IRR=1.01). Our study shows a positive association between air pollution and lung cancer incidence. This association was stronger for, respectively, p-xylene, o-xylene, ethylbenzene, benzene, m-xylene and toluene.
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- 2021
14. Low-Cost Outdoor Air Quality Monitoring and Sensor Calibration: A Survey and Critical Analysis
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Concas, Francesco, Mineraud, Julien, Lagerspetz, Eemil, Varjonen, Samu, Liu, Xiaoli, Puolam��ki, Kai, Nurmi, Petteri, Tarkoma, Sasu, Department of Computer Science, Helsinki Institute for Information Technology, and Content-Centric Structures and Networking research group / Sasu Tarkoma
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Signal Processing (eess.SP) ,FOS: Computer and information sciences ,Computer Science - Machine Learning ,review ,Machine Learning (stat.ML) ,113 Computer and information sciences ,calibration ,LONG-TERM EXPOSURE ,AVAILABLE SENSORS ,Machine Learning (cs.LG) ,low-cost ,machine learning ,TIME-SERIES ANALYSIS ,POLLUTION ,Statistics - Machine Learning ,USE REGRESSION-MODELS ,PARTICULATE MATTER ,FOS: Electrical engineering, electronic engineering, information engineering ,FIELD CALIBRATION ,survey ,NETWORK ,Electrical Engineering and Systems Science - Signal Processing ,Air quality sensors ,GAS SENSORS ,NITROGEN-DIOXIDE - Abstract
arXiv:1912.06384 [eess.SP] The significance of air pollution and the problems associated with it are fueling deployments of air quality monitoring stations worldwide. The most common approach for air quality monitoring is to rely on environmental monitoring stations, which unfortunately are very expensive both to acquire and to maintain. Hence environmental monitoring stations are typically sparsely deployed, resulting in limited spatial resolution for measurements. Recently, low-cost air quality sensors have emerged as an alternative that can improve the granularity of monitoring. The use of low-cost air quality sensors, however, presents several challenges: they suffer from cross-sensitivities between different ambient pollutants; they can be affected by external factors, such as traffic, weather changes, and human behavior; and their accuracy degrades over time. Periodic re-calibration can improve the accuracy of low-cost sensors, particularly with machine-learning-based calibration, which has shown great promise due to its capability to calibrate sensors in-field. In this article, we survey the rapidly growing research landscape of low-cost sensor technologies for air quality monitoring and their calibration using machine learning techniques. We also identify open research challenges and present directions for future research.
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- 2021
15. Parkinson's disease and long-term exposure to outdoor air pollution
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Toro, Rosario, Downward, George S, van der Mark, Marianne, Brouwer, Maartje, Huss, Anke, Peters, Susan, Hoek, Gerard, Nijssen, Peter, Mulleners, Wim M, Sas, Antonetta, van Laar, Teus, Kromhout, Hans, Vermeulen, Roel, One Health Chemisch, dIRAS RA-2, LS IRAS EEPI EXAS (Arb.hyg+bl.st.kar.), dIRAS RA-I&I RA, Movement Disorder (MD), One Health Chemisch, dIRAS RA-2, LS IRAS EEPI EXAS (Arb.hyg+bl.st.kar.), and dIRAS RA-I&I RA
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Male ,long-term exposure ,Parkinson's disease ,010504 meteorology & atmospheric sciences ,air pollution ,Air pollution ,010501 environmental sciences ,medicine.disease_cause ,Particulate Matter/analysis ,01 natural sciences ,Environmental Science(all) ,USE REGRESSION-MODELS ,AREAS ,lcsh:Environmental sciences ,Netherlands ,General Environmental Science ,lcsh:GE1-350 ,RISK ,Air Pollutants ,education.field_of_study ,Parkinson Disease ,Middle Aged ,Particulates ,Nitrogen Oxides/analysis ,Multicenter Study ,Quartile ,Female ,Nitrogen Oxides ,Environmental Exposure/analysis ,Air Pollutants/analysis ,Population ,Netherlands/epidemiology ,Air Pollution/analysis ,Parkinson Disease/epidemiology ,Soot/analysis ,Soot ,Environmental health ,Journal Article ,medicine ,Humans ,education ,land-use regression ,Aged ,0105 earth and related environmental sciences ,Pollutant ,business.industry ,Long-term exposure ,Case-control study ,Environmental Exposure ,Odds ratio ,medicine.disease ,Land-use regression ,Case-Control Studies ,parkinson's disease ,Particulate Matter ,business - Abstract
Background: There is some evidence to suggest an association between ambient air pollution and development of Parkinson's disease (PD). However, the small number of studies published to date has reported inconsistent findings. Objectives: To assess the association between long-term exposure to ambient air pollution constituents and the development of PD. Methods: Air pollution exposures (particulate matter with aerodynamic diameter 30.4 μg/m3) was 0.87 (95% CI: 0.54, 1.41). For PM2.5 where the contrast in exposure was more limited, the OR associated with an increase from the first quartile PM2.5 (22.3 μg/m3) was 0.50 (95% CI: 0.24, 1.01). In a subset of the population with long-term residential stability (n = 632), an increased risk of PD was observed (e.g. OR for Q4 vs Q1 NO2:1.37, 95% CI: 0.71, 2.67). Conclusions: We found no clear association between 16 years of residential exposure to ambient air pollution and the development of PD in The Netherlands. Keywords: Air pollution, Parkinson's disease, Long-term exposure, Land-use regression
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- 2019
16. Multiple air pollutant exposure and lung cancer in Tehran, Iran
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Koorosh Etemad, Narges Khanjani, Seyed Mahmood Taghavi Shahri, Mohsen Pourkhosravani, Maysam Rezapour, Zahra Khorrami, Heresh Amini, and Nino Künzli
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Male ,Lung Neoplasms ,Air pollution ,Diseases ,BTEX ,Iran ,010501 environmental sciences ,medicine.disease_cause ,01 natural sciences ,DISEASE ,0302 clinical medicine ,USE REGRESSION-MODELS ,Benzene Derivatives ,030212 general & internal medicine ,Cancer ,ASSOCIATIONS ,General Environmental Science ,Air Pollutants ,education.field_of_study ,Multidisciplinary ,Incidence (epidemiology) ,Middle Aged ,LONG-TERM EXPOSURE ,Medicine ,population characteristics ,Female ,EASTERN MEGACITY TEHRAN ,HEALTH ,Science ,Population ,AMBIENT AIR ,Xylenes ,Malignancy ,Risk Assessment ,Article ,World health ,03 medical and health sciences ,Environmental health ,parasitic diseases ,medicine ,Humans ,COHORT ,Lung cancer ,education ,Aged ,0105 earth and related environmental sciences ,Pollutant ,business.industry ,MORTALITY ,Natural hazards ,Benzene ,Environmental Exposure ,medicine.disease ,Cancer registry ,Environmental sciences ,Risk factors ,RESPIRATORY HOSPITAL ADMISSIONS ,General Earth and Planetary Sciences ,business ,Toluene - Abstract
Lung cancer is the most rapidly increasing malignancy worldwide with an estimated 2.1 million cancer cases in the latest, 2018 World Health Organization (WHO) report. The objective of this study was to investigate the association of air pollution and lung cancer, in Tehran, Iran. Residential area information of the latest registered lung cancer cases that were diagnosed between 2014 and 2016 (N = 1,850) were inquired from the population-based cancer registry of Tehran. Long-term average exposure to PM10, SO2, NO, NO2, NOX, benzene, toluene, ethylbenzene, m-xylene, p-xylene, o-xylene (BTEX), and BTEX in 22 districts of Tehran were estimated using land use regression models. Latent profile analysis (LPA) was used to generate multi-pollutant exposure profiles. Negative binomial regression analysis was used to examine the association between air pollutants and lung cancer incidence. The districts with higher concentrations for all pollutants were mostly in downtown and around the railway station. Districts with a higher concentration for NOx (IRR = 1.05, for each 10 unit increase in air pollutant), benzene (IRR = 3.86), toluene (IRR = 1.50), ethylbenzene (IRR = 5.16), p-xylene (IRR = 9.41), o-xylene (IRR = 7.93), m-xylene (IRR = 2.63) and TBTEX (IRR = 1.21) were significantly associated with higher lung cancer incidence. Districts with a higher multiple air-pollution profile were also associated with more lung cancer incidence (IRR = 1.01). Our study shows a positive association between air pollution and lung cancer incidence. This association was stronger for, respectively, p-xylene, o-xylene, ethylbenzene, benzene, m-xylene and toluene.
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- 2021
17. Long-Term Exposure to Fine Particle Elemental Components and Natural and Cause-Specific Mortality-a Pooled Analysis of Eight European Cohorts within the ELAPSE Project
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Daniela Fecht, Klea Katsouyanni, Ole Hertel, Anton Lager, Danielle Vienneau, Sophia Rodopoulou, Ulla Arthur Hvidtfeldt, Matteo Renzi, Torben Sigsgaard, Francesco Forastiere, Karl-Heinz Jöckel, Jørgen Brandt, Jochem O. Klompmaker, Gabriele Nagel, Per E. Schwarze, Gudrun Weinmayr, Kathrin Wolf, Bert Brunekreef, Amar Mehta, Tom Bellander, Annette Peters, Hans Concin, Sara Schramm, Bente Oftedal, Conor James MacDonald, Matthias Ketzel, Massimo Stafoggia, John S. Gulliver, Göran Pershagen, Mette Sørensen, Shuo Liu, Ole Raaschou-Nielsen, Jie Chen, Maciej Strak, Richard Atkinson, Jeanette Therming Jørgensen, Karin Leander, Debora Rizzuto, Yvonne T. van der Schouw, Giulia Cesaroni, Gerard Hoek, Evangelia Samoli, Kees de Hoogh, Anne Tjønneland, Petter Ljungman, Nicole A.H. Janssen, Barbara Hoffmann, Zorana Jovanovic Andersen, Patrik K. E. Magnusson, Mariska Bauwelinck, Faculty of Economic and Social Sciences and Solvay Business School, and Sociology
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Fine particulate ,Health, Toxicology and Mutagenesis ,05 Environmental Sciences ,Medizin ,PM2.5 ,010501 environmental sciences ,Atmospheric sciences ,Toxicology ,PROFILE ,ESCAPE ,complex mixtures ,01 natural sciences ,Cohort Studies ,03 medical and health sciences ,0302 clinical medicine ,USE REGRESSION-MODELS ,PARTICULATE MATTER ,Air Pollution ,Cause of Death ,Humans ,Aerodynamic diameter ,030212 general & internal medicine ,11 Medical and Health Sciences ,0105 earth and related environmental sciences ,RISK ,Air Pollutants ,Research ,Public Health, Environmental and Occupational Health ,Cause specific mortality ,MEN ,Environmental Exposure ,Middle Aged ,Particulates ,Term (time) ,Pooled analysis ,Particle ,Environmental science ,Particulate Matter - Abstract
BACKGROUND: Inconsistent associations between long-term exposure to particles with an aerodynamic diameter ≤ 2.5 μ m [fine particulate matter ( PM 2.5 )] components and mortality have been reported, partly related to challenges in exposure assessment. OBJECTIVES: We investigated the associations between long-term exposure to PM 2.5 elemental components and mortality in a large pooled European cohort; to compare health effects of PM 2.5 components estimated with two exposure modeling approaches, namely, supervised linear regression (SLR) and random forest (RF) algorithms. METHODS: We pooled data from eight European cohorts with 323,782 participants, average age 49 y at baseline (1985-2005). Residential exposure to 2010 annual average concentration of eight PM 2.5 components [copper (Cu), iron (Fe), potassium (K), nickel (Ni), sulfur (S), silicon (Si), vanadium (V), and zinc (Zn)] was estimated with Europe-wide SLR and RF models at a 100 × 100 m scale. We applied Cox proportional hazards models to investigate the associations between components and natural and cause-specific mortality. In addition, two-pollutant analyses were conducted by adjusting each component for PM 2.5 mass and nitrogen dioxide ( NO 2 ) separately. RESULTS: We observed 46,640 natural-cause deaths with 6,317,235 person-years and an average follow-up of 19.5 y. All SLR-modeled components were statistically significantly associated with natural-cause mortality in single-pollutant models with hazard ratios (HRs) from 1.05 to 1.27. Similar HRs were observed for RF-modeled Cu, Fe, K, S, V, and Zn with wider confidence intervals (CIs). HRs for SLR-modeled Ni, S, Si, V, and Zn remained above unity and (almost) significant after adjustment for both PM 2.5 and NO 2 . HRs only remained (almost) significant for RF-modeled K and V in two-pollutant models. The HRs for V were 1.03 (95% CI: 1.02, 1.05) and 1.06 (95% CI: 1.02, 1.10) for SLR- and RF-modeled exposures, respectively, per 2 ng / m 3 , adjusting for PM 2.5 mass. Associations with cause-specific mortality were less consistent in two-pollutant models. CONCLUSION: Long-term exposure to V in PM 2.5 was most consistently associated with increased mortality. Associations for the other components were weaker for exposure modeled with RF than SLR in two-pollutant models. https://doi.org/10.1289/EHP8368.
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- 2021
18. A comparison of associations with childhood lung function between air pollution exposure assessment methods with and without accounting for time-activity patterns
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Ntarladima, Anna Maria, Karssenberg, Derek, Vaartjes, Ilonca, Grobbee, Diederick E., Schmitz, Oliver, Lu, Meng, Boer, Jolanda, Koppelman, Gerard, Vonk, Judith, Vermeulen, Roel, Hoek, Gerard, Gehring, Ulrike, Landscape functioning, Geocomputation and Hydrology, Landdegradatie en aardobservatie, Hydrologie, Organic geochemistry, IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, dIRAS RA-I&I RA, Groningen Research Institute for Asthma and COPD (GRIAC), Landscape functioning, Geocomputation and Hydrology, Landdegradatie en aardobservatie, Hydrologie, Organic geochemistry, IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, and dIRAS RA-I&I RA
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medicine.medical_specialty ,Activity patterns ,IMPACT ,Air pollution exposure ,Air pollution ,Accounting ,PM2.5 ,medicine.disease_cause ,PROFILE ,complex mixtures ,Biochemistry ,Cohort Studies ,RELEVANCE ,USE REGRESSION-MODELS ,Environmental Science(all) ,AREAS ,Air Pollution ,Epidemiology ,medicine ,Humans ,Child ,Lung ,Lung function ,General Environmental Science ,Exposure assessment ,Air Pollutants ,business.industry ,Time activity ,Environmental Exposure ,Cross-Sectional Studies ,MOBILITY ,Assessment methods ,Environmental science ,Particulate Matter ,Birth cohort ,business - Abstract
BACKGROUND: To investigate associations between annual average air pollution exposures and health, most epidemiological studies rely on estimated residential exposures because information on actual time-activity patterns can only be collected for small populations and short periods of time due to costs and logistic constraints. In the current study, we aim to compare exposure assessment methodologies that use data on time-activity patterns of children with residence-based exposure assessment. We compare estimated exposures and associations with lung function for residential exposures and exposures accounting for time activity patterns.METHODS: We compared four annual average air pollution exposure assessment methodologies; two rely on residential exposures only, the other two incorporate estimated time activity patterns. The time-activity patterns were based on assumptions about the activity space and make use of available external data sources for the duration of each activity. Mapping of multiple air pollutants (NO2, NOX, PM2.5, PM2.5absorbance, PM10) at a fine resolution as input to exposure assessment was based on land use regression modelling. First, we assessed the correlations between the exposures from the four exposure methods. Second, we compared estimates of the cross-sectional associations between air pollution exposures and lung function at age 8 within the PIAMA birth cohort study for the four exposure assessment methodologies.RESULTS: The exposures derived from the four exposure assessment methodologies were highly correlated (R > 0.95) for all air pollutants. Similar statistically significant decreases in lung function were found for all four methods. For example, for NO2 the decrease in FEV1 was -1.40% (CI; -2.54, -0.24%) per IQR (9.14 μg/m3) for front door exposure, and -1.50% (CI; -2.68, -0.30%) for the methodology which incorporates time activity pattern and actual school addresses.CONCLUSIONS: Exposure estimates from methods based on the residential location only and methods including time activity patterns were highly correlated and associated with similar decreases in lung function. Our study illustrates that the annual average exposure to air pollution for 8-year-old children in the Netherlands is sufficiently captured by residential exposures.
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- 2021
19. Prenatal air pollution exposure and growth and cardio-metabolic risk in preschoolers
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Medicina preventiva y salud pública, Prebentzio medikuntza eta osasun publikoa, Fossati, Serena, Valvi, Damaskini, Martínez, David, Cirach, Marta, Estarlich, Marisa, Fernández Somoano, Ana, Guxens, Mónica, Iñíguez, Carmen, Irizar, Amaia, Lertxundi Manterola, Aitana, Nieuwenhuijsen, Mark J., Tamayo, Ibon, Vioque, Jesús, Tardón, Adonina, Sunyer, Jordi, Vrijheid, Martine, Medicina preventiva y salud pública, Prebentzio medikuntza eta osasun publikoa, Fossati, Serena, Valvi, Damaskini, Martínez, David, Cirach, Marta, Estarlich, Marisa, Fernández Somoano, Ana, Guxens, Mónica, Iñíguez, Carmen, Irizar, Amaia, Lertxundi Manterola, Aitana, Nieuwenhuijsen, Mark J., Tamayo, Ibon, Vioque, Jesús, Tardón, Adonina, Sunyer, Jordi, and Vrijheid, Martine
- Abstract
Objectives: We investigated the association between outdoor air pollutants exposure in the first trimester of pregnancy, and growth and cardio-metabolic risk at four years of age, and evaluated the mediating role of birth weight. Methods: We included mother-child pairs (N = 1,724) from the Spanish INMA birth cohort established in 2003-2008. First trimester of pregnancy nitrogen dioxide (NO2) and fine particles (PM2.5) exposure levels were estimated. Height, weight, waist circumference, blood pressure, and lipids were measured at four years of age. Body mass index (BMI) trajectories from birth to four years were identified. Results: Increased PM2.5 exposure in the first trimester of pregnancy was associated with decreased z-scores of weight (zWeight) and BMI (zBMI) (zWeight change per interquartile range increase in PM2.5 exposure = -0.12; 95% CI: -0.23, -0.01; zBMI change = -0.12; 95% CI: -0.23, -0.01). Higher NO2 and PM2.5 exposure was associated to a reduced risk of being in a trajectory with accelerated BMI gain, compared to children with the average trajectory. Birth weight partially mediated the association between PM2.5 and zWeight and zBMI. PM2.5 and NO2 were not associated with the other cardio-metabolic risk factors. Conclusions: This comprehensive study of many growth and cardio-metabolic risk related outcomes suggests that air pollution exposure during pregnancy may be associated with delays in physical growth in the early years after birth. These findings imply that pregnancy exposure to air pollutants has a lasting effect on growth after birth and require follow-up at later child ages.
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- 2020
20. Prenatal air pollution exposure and growth and cardio-metabolic risk in preschoolers
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Adonina Tardón, Amaia Irizar, Jordi Sunyer, Aitana Lertxundi, Jesús Vioque, Serena Fossati, David Martinez, Damaskini Valvi, Martine Vrijheid, Marisa Estarlich, Ana Fernández-Somoano, Marta Cirach, Ibon Tamayo, Mònica Guxens, Carmen Iñiguez, Mark J. Nieuwenhuijsen, European Commission, and Child and Adolescent Psychiatry / Psychology
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obesity ,010504 meteorology & atmospheric sciences ,air pollution ,prenatal exposure ,use regression-models ,010501 environmental sciences ,Malalties neonatals ,01 natural sciences ,Pregnancy ,Interquartile range ,Prenatal exposure ,Childhood obesity ,Child ,lcsh:Environmental sciences ,General Environmental Science ,lcsh:GE1-350 ,2. Zero hunger ,Air Pollutants ,Obstetrics ,Childhood growth ,health ,traffic pollution ,fetal ,Pollution ,Maternal Exposure ,Child, Preschool ,Contaminació ,maternal smoking ,Female ,Neonatal diseases ,childhood obesity ,pregnant-women ,medicine.medical_specialty ,Waist ,Birth weight ,Nitrogen Dioxide ,Air pollution ,complex mixtures ,childhood growth ,early-childhood ,medicine ,Humans ,mediation analysis ,0105 earth and related environmental sciences ,particulate matter ,Fetus ,business.industry ,medicine.disease ,Particulate matter ,Obesity ,business ,Body mass index - Abstract
Objectives: We investigated the association between outdoor air pollutants exposure in the first trimester of pregnancy, and growth and cardio-metabolic risk at four years of age, and evaluated the mediating role of birth weight. Methods: We included mother-child pairs (N = 1,724) from the Spanish INMA birth cohort established in 2003-2008. First trimester of pregnancy nitrogen dioxide (NO2) and fine particles (PM2.5) exposure levels were estimated. Height, weight, waist circumference, blood pressure, and lipids were measured at four years of age. Body mass index (BMI) trajectories from birth to four years were identified. Results: Increased PM2.5 exposure in the first trimester of pregnancy was associated with decreased z-scores of weight (zWeight) and BMI (zBMI) (zWeight change per interquartile range increase in PM2.5 exposure = -0.12; 95% CI: -0.23, -0.01; zBMI change = -0.12; 95% CI: -0.23, -0.01). Higher NO2 and PM2.5 exposure was associated to a reduced risk of being in a trajectory with accelerated BMI gain, compared to children with the average trajectory. Birth weight partially mediated the association between PM2.5 and zWeight and zBMI. PM2.5 and NO2 were not associated with the other cardio-metabolic risk factors. Conclusions: This comprehensive study of many growth and cardio-metabolic risk related outcomes suggests that air pollution exposure during pregnancy may be associated with delays in physical growth in the early years after birth. These findings imply that pregnancy exposure to air pollutants has a lasting effect on growth after birth and require follow-up at later child ages. This study was funded by grants from the Eulji University (grant numbers ESCAPE project FP7-ENV-2007-1-211250, DENAMIC project FP7-ENV-2011-282957, HELIX project FP7-ENV-2012-308333, and MEDALL project HEALTH.2010.2.4.5-1), from the Spanish Instituto de Salud Carlos III (grant numbers Red INMA G03/176; CB06/02/0041; PI03/1615 incl. FEDER funds, PI04/1112 incl. FEDER funds, PI041436, PI04/1509 incl. FEDER funds, PI04/1931 incl. FEDER funds, PI042018 incl. FEDER funds, PI05/1079 incl. FEDER funds, PI05/1052 incl. FEDER funds, FIS-PI06/0867, PI06/1213 incl. FEDER funds, PI07/0314 incl. FEDER funds, PI081151 incl. FEDER funds, FIS-PI09/00090, PI09/02311 incl. FEDER funds, PI09/02647 incl. FEDER funds, PI11/01007 incl. FEDER funds, PI11/02591 incl. FEDER funds, PI11/02038 incl. FEDER funds, PI13/1944 incl. FEDER funds, PI13/2032 incl. FEDER funds, PI13/02429 incl. FEDER funds, PI14/00891 incl. FEDER funds, PI14/01687 incl. FEDER funds, PI15/00118 incl. FEDER funds, PI16/1288 incl. FEDER funds, and PI17/00663 incl. FEDER funds, PI18/00547 incl. FEDER funds, PI18/00909 incl. FEDER funds; CP11/00178, CP15/00025, and CPII16/00051; MS13/00054 incl. FEDER funds), CIBERESP, Department of Health of the Basque Government (grant numbers 2005111093, 2013111089), Generalitat de Catalunya-CIRIT (grant numbers 1999SGR 00241), Generalitat Valenciana: FISABIO (grant numbers UGP 15-230, UGP-15-244, and UGP-15-249), Provincial Government of Gipuzkoa (grant number DFG06/002), Alicia Koplowitz Foundation 2017, Fundacio La marato de TV3 (grant number 090430), Obra Social Cajastur/Fundacion Liberbank, Universidad de Oviedo, and annual agreements with the municipalities of the study area of the Gipuzkoa sub-cohort (Zumarraga, Urretxu, Legazpi, Azkoitia, Azpeitia and Beasain). ISGlobal is a member of the Agency for the Research Centres of Catalonia (CERCA) Programme, Generalitat de Catalunya.
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- 2020
21. microRNA expression profiles and personal monitoring of exposure to particulate matter
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Mancini, F.R., Laine, J.E., Tarallo, S., Vlaanderen, J., Vermeulen, R., van Nunen, E., Hoek, G., Probst-Hensch, N., Imboden, M., Jeong, A., Gulliver, J., Chadeau-Hyam, M., Nieuwenhuijsen, M., de Kok, T.M., Piepers, J., Krauskopf, J., Kleinjans, J.C.S., Vineis, P., Naccarati, A., IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, LS IRAS EEPI GRA (Gezh.risico-analyse), dIRAS RA-I&I RA, Toxicogenomics, RS: FSE MaCSBio, RS: FPN MaCSBio, RS: FHML MaCSBio, RS: MHeNs - R3 - Neuroscience, RS: GROW - R1 - Prevention, IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, LS IRAS EEPI GRA (Gezh.risico-analyse), dIRAS RA-I&I RA, and Commission of the European Communities
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Exposome ,010504 meteorology & atmospheric sciences ,Health, Toxicology and Mutagenesis ,Personal monitoring ,air pollution ,Air pollution ,Physiology ,010501 environmental sciences ,Toxicology ,medicine.disease_cause ,01 natural sciences ,USE REGRESSION-MODELS ,Gene expression ,microRNA ,fine and ultrafine particles ,medicine ,Fine and ultrafine particles ,Humans ,personal monitoring ,0105 earth and related environmental sciences ,Netherlands ,Pollutant ,Gene Expression Profiling ,General Medicine ,AIR-POLLUTION ,Pollution ,United Kingdom ,microRNAs ,Gene expression profiling ,Europe ,Circulating MicroRNA ,MicroRNAs ,Italy ,Gene chip analysis ,Particulate Matter ,Environmental Sciences ,Switzerland - Abstract
An increasing number of findings from epidemiological studies support associations between exposure to air pollution and the onset of several diseases, including pulmonary, cardiovascular and neurodegenerative diseases, and malignancies. However, intermediate, and potentially mediating, biological mechanisms associated with exposure to air pollutants are largely unknown. Previous studies on the human exposome have shown that the expression of certain circulating microRNAs (miRNAs), regulators of gene expression, are altered upon exposure to traffic-related air pollutants. In the present study, we investigated the relationship between particulate matter (PM) smaller than 2.5 mm (PM2.5), PM2.5 absorbance (as a proxy of black carbon and soot), and ultrafine-particles (UFP, smaller than 0.1 mm), measured in healthy volunteers by 24 h personal monitoring (PEM) sessions and global expression levels of peripheral blood miRNAs. The PEM sessions were conducted in four European countries, namely Switzerland (Basel), United Kingdom (Norwich), Italy (Turin), and The Netherlands (Utrecht). miRNAs expression levels were analysed using microarray technology on blood samples from 143 participants. Seven miRNAs, hsa-miR-24-3p, hsa-miR-4454, hsa-miR-4763-3p, hsa-miR-425-5p, hsa-let-7d-5p, hsa-miR502-5p, and hsa-miR-505-3p were significantly (FDR corrected) expressed in association with PM2.5 personal exposure, while no significant association was found between miRNA expression and the other pollutants. The results obtained from this investigation suggest that personal exposure to PM2.5 is associated with miRNA expression levels, showing the potential for these circulating miRNAs as novel biomarkers for air pollution health risk assessment. (C) 2020 Elsevier Ltd. All rights reserved.
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- 2020
22. Long-term air pollution exposure is associated with increased severity of rhinitis in 2 European cohorts
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Roberto Bono, Kees de Hoogh, Meriem Benmerad, Bénédicte Jacquemin, Valérie Siroux, Emilie Burte, Jordi Sunyer, Deborah Jarvis, Mark J. Nieuwenhuijsen, Jean Bousquet, Alessandro Marcon, Anne-Elie Carsin, Rachel Nadif, Nino Künzli, Bertil Forsberg, Bénédicte Leynaert, Isabelle Pin, Frédéric Gormand, Jocelyne Just, Simona Villani, Morgane Stempfelet, Joachim Heinrich, Vieillissement et Maladies chroniques : approches épidémiologique et de santé publique (VIMA), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Versailles Saint-Quentin-en-Yvelines (UVSQ), Universitat Pompeu Fabra [Barcelona] (UPF), Instituto de Salud Global - Institute For Global Health [Barcelona] (ISGlobal), Physiopathologie et Epidémiologie des Maladies Respiratoires (PHERE (UMR_S_1152 / U1152)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP), University of Verona (UNIVR), CHU Montpellier, Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Contre les MAladies Chroniques pour un VIeillissement Actif en Languedoc-Roussillon (MACVIA-LR), Université Montpellier 1 (UM1)-Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre Hospitalier Universitaire de Nîmes (CHU Nîmes)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS)-European Innovation Partnership on Active and Healthy Ageing Reference Site (EIP on AHA), Commission Européenne-Commission Européenne-Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO), Institute for Advanced Biosciences / Institut pour l'Avancée des Biosciences (Grenoble) (IAB), Centre Hospitalier Universitaire [Grenoble] (CHU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Etablissement français du sang - Auvergne-Rhône-Alpes (EFS)-Centre National de la Recherche Scientifique (CNRS)-Université Grenoble Alpes (UGA), University of Turin, University of Basel (Unibas), Umeå University, Hôpital Edouard Herriot [CHU - HCL], Hospices Civils de Lyon (HCL), Ludwig-Maximilians-Universität München (LMU), CHU Trousseau [APHP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), CIBER de Epidemiología y Salud Pública (CIBERESP), CHU Grenoble, Santé publique France - French National Public Health Agency [Saint-Maurice, France], Università degli Studi di Pavia, Imperial College London, European CommissionEuropean Commission Joint Research Centre, local studies in ECRHS III, National Institute for Health Research through the Primary Care Research Network, PHRC-Paris, PHRC-Grenoble, ANRFrench National Research Agency (ANR) [05-SEST-020-02/05-9-97, ANR-06-CEBS, ANR-CES-2009], Merck Sharp DohmeMerck and Company, Region Nord Pas-de-CalaisRegion Hauts-de-France, European Study of Cohorts for Air Pollution Effects Funding, Belgium Antwerp South, Antwerp City Research Foundation Flanders (FWO) [G.0.410.08], European CommunityEuropean Community (EC) [211250], Ministere de la Sante, Programme Hospitalier de Recherche Clinique (PHRC), Paris Agence Nationale de la SanteFrench National Research Agency (ANR), Region Ile de FranceRegion Ile-de-France, Spain Fondo de Investigacion Sanitaria [PS09/02457, PS09/00716 09/01511, PS09/02185, PS09/03190], Germany Erfurt German Research Foundation - Cariverona Foundation, Education Ministry, Sociedad Espanola de Neumologia y Cirurgia Toracica [FIS PS09/00716], Swedish Heart and Lung FoundationSwedish Heart-Lung Foundation, Galdakao Fondo de Investigacion Sanitaria [FIS 09/01511, FIS PS09/02185], Swedish Asthma and Allergy Association, Heart Disease, Swedish Research Council for health, working life and welfare (FORTE), United Kingdom Medical Research CouncilMedical Research Council UK (MRC) [92091], European Project: 211250,EC:FP7:ENV,FP7-ENV-2007-1,ESCAPE(2008), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), Università degli studi di Verona = University of Verona (UNIVR), Università degli studi di Torino = University of Turin (UNITO), Università degli Studi di Pavia = University of Pavia (UNIPV), ANR-06-CEBS-0009,CRB CHU Grenoble,Centre de ressources biologiques tumorales du CHU de Grenoble(2006), Medical Research Council (MRC), CCSD, Accord Elsevier, Collection d'Échantillons Biologiques de la Santé (CEBS) : Valorisation et Certification - Centre de ressources biologiques tumorales du CHU de Grenoble - - CRB CHU Grenoble2006 - ANR-06-CEBS-0009 - CEBS - VALID, and European Study of Cohorts for Air Pollution Effects - ESCAPE - - EC:FP7:ENV2008-06-01 - 2012-11-30 - 211250 - VALID
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Male ,Allergy ,IMPACT ,Air pollution exposure ,[SDV]Life Sciences [q-bio] ,air pollution ,severity ,010501 environmental sciences ,Logistic regression ,01 natural sciences ,Cohort Studies ,0302 clinical medicine ,USE REGRESSION-MODELS ,Epidemiology ,Immunology and Allergy ,Medicine ,POLLUTANTS ,Rinitis ,Rhinitis ,CLIMATE-CHANGE ,Aire -- Contaminació ,Respiratory disease ,Regression analysis ,Middle Aged ,respiratory disease ,3. Good health ,[SDV] Life Sciences [q-bio] ,ALLERGIC RHINITIS ,Europe ,Quartile ,1107 Immunology ,BRONCHIAL HYPERRESPONSIVENESS ,Female ,allergic sensitization ,environment ,Life Sciences & Biomedicine ,Adult ,medicine.medical_specialty ,GENETICS ,Immunology ,ESCAPE ,complex mixtures ,03 medical and health sciences ,Humans ,0105 earth and related environmental sciences ,Asthma ,Science & Technology ,business.industry ,Odds ratio ,Environmental Exposure ,medicine.disease ,Cross-Sectional Studies ,030228 respiratory system ,13. Climate action ,ASTHMA ,Particulate Matter ,business ,Demography - Abstract
Background: Very few studies have examined the association between long-term outdoor air pollution and rhinitis severity in adults. Objective: We sought to assess the cross-sectional association between individual long-term exposure to air pollution and severity of rhinitis. Methods: Participants with rhinitis from 2 multicenter European cohorts (Epidemiological Study on the Genetics and Environment on Asthma and the European Community Respiratory Health Survey) were included. Annual exposure to NO2, PM10, PM2.5, and PMcoarse (calculated by subtracting PM2.5 from PM10) was estimated using land-use regression models derived from the European Study of Cohorts for Air Pollution Effects project, at the participants' residential address. The score of rhinitis severity (range, 0-12), based on intensity of disturbance due to symptoms reported by questionnaire, was categorized into low (reference), mild, moderate, and high severity. Polytomous logistic regression models with a random intercept for city were used. Results: A total of 1408 adults with rhinitis (mean age, 52 years; 46% men, 81% from the European Community Respiratory Health Survey) were included. The median (1st quartile-3rd quartile) score of rhinitis severity was 4 (2-6). Higher exposure to PM10 was associated with higher rhinitis severity (adjusted odds ratio [95% CI] for a 10 μg/m3 increase in PM10: for mild: 1.20 [0.88-1.64], moderate: 1.53 [1.07-2.19], and high severity: 1.72 [1.23-2.41]). Similar results were found for PM2.5. Higher exposure to NO2 was associated with an increased severity of rhinitis, with similar adjusted odds ratios whatever the level of severity. Adjusted odds ratios were higher among participants without allergic sensitization than among those with, but interaction was found only for NO2. CONCLUSIONS: People with rhinitis who live in areas with higher levels of pollution are more likely to report more severe nasal symptoms. Further work is required to elucidate the mechanisms of this association. The following bodies funded the local studies in ECRHS III in this article: Belgium: Antwerp South, Antwerp City: Research Foundation Flanders (FWO), grant code G.0.410.08.N.10 (both sites); France: Ministère de la Santé , Programme Hospitalier de Recherche Clinique (PHRC) national 2010; Germany: Erfurt: German Research Foundation ( HE 3294/10-1 ); Spain: Fondo de Investigación Sanitaria ( PS09/02457 , PS09/00716 09/01511 , PS09/02185 , and PS09/03190 ), Servicio Andaluz de Salud, Sociedad Española de Neumología y Cirurgía Torácica ( SEPAR 1001/2010 ); Barcelona: Fondo de Investigación Sanitaria ( FIS PS09/00716 ); Galdakao: Fondo de Investigación Sanitaria ( FIS 09/01511 ); Huelva: Fondo de Investigación Sanitaria ( FIS PS09/02185 ) and Servicio Andaluz de Salud ; Oviedo: Fondo de Investigación Sanitaria ( FIS PS09/03190 ); United Kingdom: Medical Research Council (grant no. 92091 ). The Epidemiological Study on the Genetics and Environment on Asthma is funded in part by PHRC-Paris, PHRC-Grenoble, ANR 05-SEST-020-02/05-9-97, ANR-06-CEBS, ANR-CES-2009, Région Nord Pas-de-Calais, and Merck Sharp & Dohme. European Study of Cohorts for Air Pollution Effects Funding: The research leading to these results has received funding from the European Community’s Seventh Framework Program ( FP7/2007-2011 ; under grant agreement no. 211250 )
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- 2020
23. The association of air pollution with congenital anomalies
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Salavati, N, Strak, M, Burgerhof, J G M, de Walle, H E K, Erwich, J J H M, Bakker, M K, One Health Chemisch, dIRAS RA-2, Sub Mathematics Education, One Health Chemisch, dIRAS RA-2, Sub Mathematics Education, Life Course Epidemiology (LCE), and Reproductive Origins of Adult Health and Disease (ROAHD)
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Adult ,Male ,Congenital anomalies ,Adolescent ,Air pollution exposure ,Exploratory research ,Genital anomalies ,Air pollution ,010501 environmental sciences ,Land use regression ,medicine.disease_cause ,NO2 ,01 natural sciences ,Land use regression model ,Major Congenital Anomaly ,Congenital Abnormalities ,03 medical and health sciences ,Young Adult ,0302 clinical medicine ,Air pollutants ,USE REGRESSION-MODELS ,Environmental health ,AREAS ,BIRTH-DEFECTS ,Medicine ,Humans ,030212 general & internal medicine ,EXPOSURE ,METAANALYSIS ,0105 earth and related environmental sciences ,Netherlands ,RISK ,Air Pollutants ,business.industry ,Anomaly (natural sciences) ,Public Health, Environmental and Occupational Health ,Infant, Newborn ,ESCAPE PROJECT ,Maternal Exposure ,Particulate matter pregnancy outcome ,Case-Control Studies ,Female ,Nitrogen Oxides ,Particulate Matter ,business - Abstract
Background: There are a growing number of reports on the association between air pollution and the risk of congenital anomalies. However, the results are inconsistent and most studies have only focused on the association of air pollution with congenital heart defects and orofacial clefts.Objectives: Using an exploratory study design, we aimed to identify congenital anomalies that may be sensitive to maternal exposure to specific air pollutants during the periconceptional period.Methods: We conducted a case-control study of 7426 subjects born in the 15 years between 1999 and 2014 and registered in the European Registration of Congenital Anomalies and Twins Northern Netherlands (EUROCAT NNL). Concentrations of various air pollutants (PM10, PM2.5, PM10-2.5, NO2, NOx, absorbance) were obtained using land use regression models from the European Study of Cohorts for Air Pollution Effects (ESCAPE). We linked these data to every subject in the EUROCAT NNL registry via their full postal code. Cases were classified as children or fetuses born in the 15-year period with a major congenital anomaly that was not associated with a known monogenic or chromosomal anomaly. Cases were divided into anomaly subgroups and compared with two different control groups: control group 1 comprised children or fetuses with a known monogenic or chromosomal anomaly, while control group 2 comprised all other non-monogenic and non-chromosomal registrations.Results: Using control group 1 (n = 1618) for analysis, we did not find any significant associations, but when we used control group 2 (ranges between n = 4299 and n = 5771) there were consistent positive associations between several air pollutants (NO2, PM2.5, PM10-2.5, absorbance) and the genital anomalies subgroup.Conclusion: We examined various congenital anomalies and their possible associations with a number of air pollutants in order to generate hypotheses for future research. We found that air pollution exposure was positively associated with genital anomalies, mainly driven by hypospadias. These results broaden the evidence of associations between air pollution exposure during gestation and congenital anomalies in the child. They warrant further research, which should also focus on possible underlying mechanisms.
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- 2018
24. DNA methylation and exposure to ambient air pollution in two prospective cohorts
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EXPRESSION ,Illumina 450 k human methylation array ,CARCINOGENESIS ,Air pollution ,ESCAPE PROJECT ,NOx ,ASSOCIATION ,PERIPHERAL-BLOOD ,GENE-SPECIFIC METHYLATION ,LUNG-CANCER ,MARKERS ,USE REGRESSION-MODELS ,Epigenome-wide DNA methylation ,SMOKING ,Particulate matter ,EPIC - Abstract
Long-term exposure to air pollution has been associated with several adverse health effects including cardiovascular, respiratory diseases and cancers. However, underlying molecular alterations remain to be further investigated. The aim of this study is to investigate the effects of long-term exposure to air pollutants on (a) average DNA methylation at functional regions and, (b) individual differentially methylated CpG sites. An assumption is that omic measurements, including the methylome, are more sensitive to low doses than hard health outcomes. This study included blood-derived DNA methylation (Illumina-HM450 methylation) for 454 Italian and 159 Dutch participants from the European Prospective Investigation into Cancer and Nutrition (EPIC). Long-term air pollution exposure levels, including NO2, NOx, PM2.5, PMcoarse, PM10, PM2.5 absorbance (soot) were estimated using models developed within the ESCAPE project, and back-extrapolated to the time of sampling when possible. We meta-analysed the associations between the air pollutants and global DNA methylation, methylation in functional regions and epigenome-wide methylation. CpG sites found differentially methylated with air pollution were further investigated for functional interpretation in an independent population (EnviroGenoMarkers project), where (N= 613) participants had both methylation and gene expression data available. Exposure to NO2 was associated with a significant global somatic hypomethylation (p-value = 0.014). Hypomethylation of CpG island's shores and shelves and gene bodies was significantly associated with higher exposures to NO2 and NOx. Meta-analysing the epigenome-wide findings of the 2 cohorts did not show genome-wide significant associations at single CpG site level. However, several significant CpG were found if the analyses were separated by countries. By regressing gene expression levels against methylation levels of the exposure-related CpG sites, we identified several significant CpG-transcript pairs and highlighted 5 enriched pathways for NO2 and 9 for NOx mainly related to the immune system and its regulation. Our findings support results on global hypomethylation associated with air pollution, and suggest that the shores and shelves of CpG islands and gene bodies are mostly affected by higher exposure to NO2 and NOx. Functional differences in the immune system were suggested by transcriptome analyses.
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- 2017
25. Air pollution and cardiovascular mortality with over 25 years follow-up: A combined analysis of two British cohorts
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Therese Tillin, Hakim-Moulay Dehbi, Marta Blangiardo, Rebecca Hardy, Anna Hansell, John S. Gulliver, Zaina Al-Kanaani, Nish Chaturvedi, Daniela Fecht, and Kees de Hoogh
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Male ,Air pollution ,010501 environmental sciences ,medicine.disease_cause ,01 natural sciences ,DISEASE ,0302 clinical medicine ,USE REGRESSION-MODELS ,Environmental Science(all) ,Smoke ,London ,030212 general & internal medicine ,lcsh:Environmental sciences ,General Environmental Science ,ASSOCIATIONS ,lcsh:GE1-350 ,Air Pollutants ,Hazard ratio ,ESCAPE PROJECT ,Middle Aged ,3. Good health ,Particles ,Quartile ,Cardiovascular Diseases ,Cohort ,Female ,HEALTH ,Gases ,Life Sciences & Biomedicine ,Adult ,GREAT-BRITAIN ,Environmental Sciences & Ecology ,Black smoke ,PM2.5 ,Follow-up studies ,complex mixtures ,Article ,03 medical and health sciences ,Air Pollution ,MD Multidisciplinary ,medicine ,Humans ,Adverse effect ,METAANALYSIS ,0105 earth and related environmental sciences ,Aged ,Proportional Hazards Models ,Science & Technology ,Proportional hazards model ,business.industry ,Long-term exposure ,United Kingdom ,13. Climate action ,Particulate Matter ,Environmental epidemiology ,business ,Environmental Sciences ,Demography - Abstract
Background Adverse effects of air pollution on cardiovascular disease (CVD) mortality are well established. There are comparatively fewer studies in Europe, and in the UK particularly, than in North America. We examined associations in two British cohorts with > 25 years of follow-up. Methods Annual average NO2, SO2 and black smoke (BS) air pollution exposure estimates for 1991 were obtained from land use regression models using contemporaneous monitoring data. From the European Study of Cohorts and Air Pollution (ESCAPE), air pollution estimates in 2010–11 were obtained for NO2, NOx, PM10, PMcoarse and PM2.5. The exposure estimates were assigned to place of residence 1989 for participants in a national birth cohort born in 1946, the MRC National Study of Health and Development (NSHD), and an adult multi-ethnic London cohort, Southall and Brent Revisited (SABRE) recruited 1988–91. The combined median follow-up was 26 years. Single-pollutant competing risk models were employed, adjusting for individual risk factors. Results Elevated non-significant hazard ratios for CVD mortality were seen with 1991 BS and SO2 and with ESCAPE PM10 and PM2.5 in fully adjusted linear models. Per 10 μg/m3 increase HRs were 1.11 [95% CI: 0.76–1.61] for BS, 1.05 [95% CI: 0.91–1.22] for SO2, 1.16 [95% CI: 0.70–1.92] for PM10 and 1.30 [95% CI: 0.39–4.34] for PM2.5, with largest effects seen in the fourth quartile of BS and PM2.5 compared to the first with HR 1.24 [95% CI: 0.91–1.61] and 1.21 [95% CI: 0.88–1.66] respectively. There were no consistent associations with other ESCAPE pollutants, or with 1991 NO2. Modelling using Cox regression led to similar results. Conclusion Our results support a detrimental long-term effect for air pollutants on cardiovascular mortality., Highlights • Adverse effects of air pollution on cardiovascular mortality are well established. • There are comparatively fewer studies in the UK compared to North America. • In two British cohort studies, we investigated associations between gases, particulates and cardiovascular mortality. • Detrimental associations, non-statistically significant, between cardiovascular mortality and particulates were found.
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- 2017
26. The Influence of Meteorological Factors and Atmospheric Pollutants on the Risk of Preterm Birth
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Giorgis-Allemand, Lise, Pedersen, Marie, Bernard, Claire, Aguilera, Inmaculada, Beelen, Rob M J, Chatzi, Leda, Cirach, Marta, Danileviciute, Asta, Dedele, Audrius, van Eijsden, Manon, Estarlich, Marisa, Fernández-Somoano, Ana, Fernández, Mariana F, Forastiere, Francesco, Gehring, Ulrike, Grazuleviciene, Regina, Gruzieva, Olena, Heude, Barbara, Hoek, Gerard, de Hoogh, Kees, van den Hooven, Edith H, Håberg, Siri E, Iñiguez, Carmen, Jaddoe, Vincent W V, Korek, Michal, Lertxundi, Aitana, Lepeule, Johanna, Nafstad, Per, Nystad, Wenche, Patelarou, Evridiki, Porta, Daniela, Postma, Dirkje, Raaschou-Nielsen, Ole, Rudnai, Peter, Siroux, Valérie, Sunyer, Jordi, Stephanou, Euripides, Sørensen, Mette, Eriksen, Kirsten Thorup, Tuffnell, Derek, Varró, Mihály J, Vrijkotte, Tanja G M, Wijga, Alet, Wright, John, Nieuwenhuijsen, Mark J, Pershagen, Göran, Brunekreef, Bert, Kogevinas, Manolis, Slama, Rémy, LS IRAS EEPI ME (Milieu epidemiologie), Dep IRAS, dIRAS RA-2, dI&I RA-I&I I&I, LS IRAS EEPI ME (Milieu epidemiologie), Dep IRAS, dIRAS RA-2, dI&I RA-I&I I&I, Dermatology, Epidemiology, Erasmus MC other, Pediatrics, Groningen Research Institute for Asthma and COPD (GRIAC), APH - Methodology, APH - Health Behaviors & Chronic Diseases, ARD - Amsterdam Reproduction and Development, Public and occupational health, and APH - Aging & Later Life
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Pediatrics ,meteorological conditions ,pooled ,Meteorological Concepts ,Epidemiology ,analysis ,Air pollution ,BLOOD-PRESSURE ,010501 environmental sciences ,medicine.disease_cause ,01 natural sciences ,0302 clinical medicine ,atmospheric pressure ,cohort studies ,USE REGRESSION-MODELS ,Medicine ,030212 general & internal medicine ,NITROGEN-DIOXIDE ,Air Pollutants ,atmospheric pollution ,MATERNAL EXPOSURE ,Regression analysis ,ESCAPE PROJECT ,Europe ,pooledanalysis ,PREGNANCY ,Premature birth ,Premature Birth ,FINE PARTICULATE MATTER ,pooled analysis ,Cohort study ,medicine.medical_specialty ,03 medical and health sciences ,Environmental health ,Humans ,Proportional Hazards Models ,0105 earth and related environmental sciences ,Pregnancy ,business.industry ,Proportional hazards model ,Urban Health ,humidity ,preterm birth ,temperature ,Odds ratio ,medicine.disease ,Confidence interval ,AMBIENT AIR-POLLUTION ,13. Climate action ,WEIGHT ,business - Abstract
Atmospheric pollutants and meteorological conditions are suspected to be causes of preterm birth. We aimed to characterize their possible association with the risk of preterm birth (defined as birth occurring before 37 completed gestational weeks). We pooled individual data from 13 birth cohorts in 11 European countries (71,493 births from the period 1994-2011, European Study of Cohorts for Air Pollution Effects (ESCAPE)). City-specific meteorological data from routine monitors were averaged over time windows spanning from 1 week to the whole pregnancy. Atmospheric pollution measurements (nitrogen oxides and particulate matter) were combined with data from permanent monitors and land-use data into seasonally adjusted land-use regression models. Preterm birth risks associated with air pollution and meteorological factors were estimated using adjusted discrete-time Cox models. The frequency of preterm birth was 5.0%. Preterm birth risk tended to increase with first-trimester average atmospheric pressure (odds ratio per 5-mbar increase = 1.06, 95% confidence interval: 1.01, 1.11), which could not be distinguished from altitude. There was also some evidence of an increase in preterm birth risk with first-trimester average temperature in the-5 degrees C to 15 degrees C range, with a plateau afterwards (spline coding, P = 0.08). No evidence of adverse association with atmospheric pollutants was observed. Our study lends support for an increase in preterm birth risk with atmospheric pressure.
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- 2017
27. Prenatal and Childhood Traffic-Related Air Pollution Exposure and Telomere Length in European Children: The HELIX Project
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Mark J. Nieuwenhuijsen, Marina Vafeiadi, Diana B.P. Clemente, Rémy Slama, Tim S. Nawrot, Ibon Tamayo, Regina Grazuleviciene, Léa Maitre, Martine Vrijheid, Mariona Bustamante, John Wright, Per E. Schwarze, Rosie McEachan, Johanna Lepeule, Kristine B. Gutzkow, Leda Chatzi, Asta Danileviciute, Dries S. Martens, Oliver Robinson, Montserrat de Castro, Complexe Genetica, RS: NUTRIM - R3 - Respiratory & Age-related Health, and Medical Research Council (MRC)
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Male ,Traffic-Related Pollution ,Health, Toxicology and Mutagenesis ,Air pollution exposure ,05 Environmental Sciences ,010501 environmental sciences ,Toxicology ,01 natural sciences ,Cohort Studies ,0302 clinical medicine ,USE REGRESSION-MODELS ,PARTICULATE MATTER ,CHAINED EQUATIONS ,11. Sustainability ,Leukocytes ,Medicine ,Ion-Models ,030212 general & internal medicine ,11 Medical and Health Sciences ,Telomere Shortening ,media_common ,Public, Environmental & Occupational Health ,2. Zero hunger ,RISK ,Air Pollutants ,Environmental exposure ,3. Good health ,Europe ,PREGNANCY ,Maternal Exposure ,Child, Preschool ,Female ,HEALTH ,Life Sciences & Biomedicine ,Pollution ,media_common.quotation_subject ,Nitrogen Dioxide ,Environmental Sciences & Ecology ,03 medical and health sciences ,MULTIPLE IMPUTATION ,Environmental health ,Air Pollution ,Humans ,CELL ,0105 earth and related environmental sciences ,Science & Technology ,business.industry ,Research ,MORTALITY ,Public Health, Environmental and Occupational Health ,Infant ,Environmental Exposure ,Telomere ,Multicenter study ,13. Climate action ,COHORT PROFILE ,business ,Environmental Sciences - Abstract
Background: Telomere length is a molecular marker of biological aging. Objective: Here we investigated whether early-life exposure to residential air pollution was associated with leukocyte telomere length (LTL) at 8 y of age. Methods: In a multicenter European birth cohort study, HELIX (Human Early Life Exposome) ([Formula: see text]), we estimated prenatal and 1-y childhood exposure to nitrogen dioxide ([Formula: see text]), particulate matter with aerodynamic diameter [Formula: see text] ([Formula: see text]), and proximity to major roads. Average relative LTL was measured using quantitative real-time polymerase chain reaction (qPCR). Effect estimates of the association between LTL and prenatal, 1-y childhood air pollution, and proximity to major roads were calculated using multiple linear mixed models with a random cohort effect and adjusted for relevant covariates. Results: LTL was inversely associated with prenatal and 1-y childhood [Formula: see text] and [Formula: see text] exposures levels. Each standard deviation (SD) increase in prenatal [Formula: see text] was associated with a [Formula: see text] (95% CI: [Formula: see text], [Formula: see text]) change in LTL. Prenatal [Formula: see text] was nonsignificantly associated with LTL ([Formula: see text] per SD increase; 95% CI: [Formula: see text], 0.6). For each SD increment in 1-y childhood [Formula: see text] and [Formula: see text] exposure, LTL shortened by [Formula: see text] (95% CI: [Formula: see text], [Formula: see text]) and [Formula: see text] (95% CI: [Formula: see text], 0.1), respectively. Each doubling in residential distance to nearest major road during childhood was associated with a 1.6% (95% CI: 0.02, 3.1) lengthening in LTL. Conclusion: Lower exposures to air pollution during pregnancy and childhood were associated with longer telomeres in European children at 8 y of age. These results suggest that reductions in traffic-related air pollution may promote molecular longevity, as exemplified by telomere length, from early life onward. https://doi.org/10.1289/EHP4148. The research leading to these results has received funding from the European Community’s Seventh Framework Programme (FP7/2007–2013) under grant agreement no. 308333 (the HELIX project) and from Instituto de Salud Carlos III (PI15/00118, including The European Regional Development Fund (FEDER)). T.S.N. was funded by the EU Program “Ideas” (ERC-2012-StG 310898). ISGlobal is a member of the Centres de Recerca de Catalunya (CERCA) Programme, Generalitat de Catalunya. We are grateful to all the participating families in the six countries who took part in this study.
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- 2019
28. The associations of air pollution, traffic noise and green space with overweight throughout childhood: The PIAMA birth cohort study
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Henriette A. Smit, Nicole A.H. Janssen, Alet H. Wijga, Erik Lebret, Gerard H. Koppelman, Lizan D. Bloemsma, Bert Brunekreef, Jochem O. Klompmaker, Gerard Hoek, Ulrike Gehring, and Groningen Research Institute for Asthma and COPD (GRIAC)
- Subjects
Traffic-Related Pollution ,Air pollution ,CHILDREN ,010501 environmental sciences ,Overweight ,01 natural sciences ,Biochemistry ,Normalized Difference Vegetation Index ,Odds ,Cohort Studies ,03 medical and health sciences ,0302 clinical medicine ,MARKERS ,Environmental Science(all) ,Pregnancy ,USE REGRESSION-MODELS ,Environmental health ,Journal Article ,Medicine ,Humans ,030212 general & internal medicine ,EXPOSURE ,Child ,0105 earth and related environmental sciences ,General Environmental Science ,Green space ,Air Pollutants ,business.industry ,Air ,Traffic noise ,Odds ratio ,Environmental Exposure ,medicine.disease ,Obesity ,Childhood ,PREVENTION ,Confidence interval ,BODY-MASS INDEX ,Noise, Transportation ,OBESITY ,ASTHMA ,Female ,WEIGHT ,medicine.symptom ,business ,Body mass index ,WAIST CIRCUMFERENCE - Abstract
BACKGROUND: Air pollution, traffic noise and absence of green space may contribute to the development of overweight in children.OBJECTIVES: To investigate the combined associations of air pollution, traffic noise and green space with overweight throughout childhood.METHODS: We used data for 3680 participants of the Dutch PIAMA birth cohort. We estimated exposure to air pollution, traffic noise and green space (i.e. the average Normalized Difference Vegetation Index (NDVI) and percentages of green space in circular buffers of 300 m and 3000 m) at the children's home addresses at the time of parental reported weight and height measurements. Associations of these exposures with overweight from age 3 to 17 years were analyzed by generalized linear mixed models, adjusting for potential confounders. Odds ratios (OR's) are presented for an interquartile range increase in exposure.RESULTS: odds of being overweight increased with increasing exposure to NO2 (adjusted OR 1.40 [95% confidence interval (CI) 1.12-1.74] per 8.90 µg/m3) and tended to decrease with increasing exposure to green space in a 3000 m buffer (adjusted OR 0.86 [95% CI 0.71-1.04] per 0.13 increase in the NDVI; adjusted OR 0.86 [95% CI 0.71-1.03] per 29.5% increase in the total percentage of green space). After adjustment for NO2, the associations with green space in a 3000 m buffer weakened. No associations of traffic noise with overweight throughout childhood were found. In children living in an urban area, living further away from a park was associated with a lower odds of being overweight (adjusted OR 0.67 [95% CI 0.52-0.85] per 359.6 m).CONCLUSIONS: Exposure to traffic-related air pollution, but not traffic noise or green space, may contribute to childhood overweight. Future studies examining the associations of green space with childhood overweight should account for air pollution exposure.
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- 2019
29. Influence of the Urban Exposome on Birth Weight
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Per E. Schwarze, Audrius Dedele, Léa Maitre, Payam Dadvand, Rosie McEachan, Valérie Siroux, Ibon Tamayo-Uria, Lise Giorgis-Allemand, Oliver Robinson, Martine Vrijheid, Norun Hjertager Krog, Jose Urquiza, Leda Chatzi, Antonia Valentin, Gunn Marit Aasvang, Sandra Andrusaityte, Xavier Basagaña, David Donaire, Rémy Slama, John Wright, Mark J. Nieuwenhuijsen, Ferran Ballester, Jane West, Lydiane Agier, Montserrat de Castro, Jesús Ibarluzea, Regina Grazuleviciene, Instituto de Salud Global - Institute For Global Health [Barcelona] (ISGlobal), Institute for Advanced Biosciences / Institut pour l'Avancée des Biosciences (Grenoble) (IAB), Centre Hospitalier Universitaire [Grenoble] (CHU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Etablissement français du sang - Auvergne-Rhône-Alpes (EFS)-Université Grenoble Alpes [2016-2019] (UGA [2016-2019]), CIBER de Epidemiología y Salud Pública (CIBERESP), Department of Statistics, Faculty of Arts and Sciences, Harvard University, Unité Mixte de Recherche Epidémiologique et de Surveillance Transport Travail Environnement (UMRESTTE UMR_T9405), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Université Gustave Eiffel, MRC-PHE Centre for Environment and Health, School of Public Health, Imperial College London, Norwegian Institute of Public Health [Oslo] (NIPH), Vytautas Magnus University - Vytauto Didziojo Universitetas (VDU), Bradford Institute for Health Research Bradford, Universitat Pompeu Fabra [Barcelona] (UPF), Complexe Genetica, RS: NUTRIM - R3 - Respiratory & Age-related Health, Cadic, Ifsttar, Centre Hospitalier Universitaire [Grenoble] (CHU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Etablissement français du sang - Auvergne-Rhône-Alpes (EFS)-Centre National de la Recherche Scientifique (CNRS)-Université Grenoble Alpes [2016-2019] (UGA [2016-2019]), and Medical Research Council (MRC)
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Health, Toxicology and Mutagenesis ,05 Environmental Sciences ,010501 environmental sciences ,Toxicology ,01 natural sciences ,Cohort Studies ,0302 clinical medicine ,USE REGRESSION-MODELS ,Pregnancy ,11. Sustainability ,SANTE ,WIDE ASSOCIATION ,Birth Weight ,Research article ,030212 general & internal medicine ,reproductive and urinary physiology ,11 Medical and Health Sciences ,media_common ,Europe ,Geography ,Female ,HEALTH ,medicine.symptom ,Cohort study ,Pollution ,Exposome ,PRETERM BIRTH ,Birth weight ,media_common.quotation_subject ,03 medical and health sciences ,POLLUTION ,Environmental health ,medicine ,Humans ,RESIDENTIAL GREENNESS ,Cities ,0105 earth and related environmental sciences ,Land use ,LAND-USE ,Research ,EXPOSOME ,Public Health, Environmental and Occupational Health ,Infant, Newborn ,Environmental Exposure ,AMBIENT AIR-POLLUTION ,CHILD COHORT ,13. Climate action ,[SDV.SPEE] Life Sciences [q-bio]/Santé publique et épidémiologie ,COHORT PROFILE ,[SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie ,VEGETATION ,Vegetation (pathology) - Abstract
Background: The exposome is defined as the totality of environmental exposures from conception onwards. It calls for providing a holistic view of environmental exposures and their effects on human health by evaluating multiple environmental exposures simultaneously during critical periods of life. Objective: We evaluated the association of the urban exposome with birth weight. Methods: We estimated exposure to the urban exposome, including the built environment, air pollution, road traffic noise, meteorology, natural space, and road traffic (corresponding to 24 environmental indicators and 60 exposures) for nearly 32,000 pregnant women from six European birth cohorts. To evaluate associations with either continuous birth weight or term low birth weight (TLBW) risk, we primarily relied on the Deletion-Substitution-Addition (DSA) algorithm, which is an extension of the stepwise variable selection method. Second, we used an exposure-by-exposure exposome-wide association studies (ExWAS) method accounting for multiple hypotheses testing to report associations not adjusted for coexposures. Results: The most consistent statistically significant associations were observed between increasing green space exposure estimated as Normalized Difference Vegetation Index (NDVI) and increased birth weight and decreased TLBW risk. Furthermore, we observed statistically significant associations among presence of public bus line, land use Shannon's Evenness Index, and traffic density and birth weight in our DSA analysis. Conclusion: This investigation is the first large urban exposome study of birth weight that tests many environmental urban exposures. It confirmed previously reported associations for NDVI and generated new hypotheses for a number of built-environment exposures. The study has received funding from the European Community’s Seventh Framework Programme (FP7/2007–2013) under Grant Agreement No. 308333—the HELIX project—for data collection and analyses. The HELIX program built on six existing cohorts that received previous funding, including the major cohorts listed here. INMA data collections were supported by grants from the Instituto de Salud Carlos III, CIBERESP, the Conselleria de Sanitat, Generalitat Valenciana, Department of Health of the Basque Government; the Provincial Government of Gipuzkoa, and the Generalitat de Catalunya-CIRIT. KANC was funded by the grant of the Lithuanian Agency for Science Innovation and Technology (6-04-2014_31V-66). MoBa (Norwegian Mother and Child Cohort Study) is supported by the Norwegian Ministry of Health and the Ministry of Education and Research, NIH/NIEHS (Contract No. N01-ES-75558), and the U.S. National Institutes of Health (NIH) National Institute of Environmental Health Sciences (NIEHS; Contract No. N01-ES-75558), and National Institute of Neurological Disorders and Stroke (Grant No. 1 UO1 NS 047537-01 and Grant No. 2 UO1 NS 047537-06A1). The Rhea project was financially supported by European projects (EU FP6–2003-Food-3-NewGeneris, EU FP6.STREP Hiwate, EU FP7 ENV.2007·1.2.2.2, Project No. 211250 Escape, EU FP7–2008-ENV-1·2.1·4 Envirogenomarkers, EU FP7-HEALTH-2009-single stage CHICOS, EU FP7 ENV.2008.1.2.1.6, Proposal No. 226285 ENRIECO, EUFP7-HEALTH-2012 Proposal No. 308333 HELIX, FP7 European Union Project No. 264357 MeDALL), and the Greek Ministry of Health (Program of Prevention of Obesity and Neurodevelopmental Disorders in Preschool Children, in Heraklion district, Crete, Greece: 2011–2014; “Rhea Plus”: Primary Prevention Program of Environmental Risk Factors for Reproductive Health, and Child Health: 2012–15). L.C. received additional funding from the Southern California Environmental Health Sciences Center (Grant No. P30ES007048) funded by NIEHS. We acknowledge the support of the program for international scientific collaborations of Région Rhône-Alpes-Auvergne.
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- 2019
30. Associations of Residential Long-Term Air Pollution Exposures and Satellite-Derived Greenness with Insulin Resistance in German Adolescents
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Andrea von Berg, Elaine Fuertes, Dietrich Berdel, Jürgen Kratzsch, Irene Brüske, Joachim Heinrich, Iana Markevych, Elisabeth Thiering, Dorothea Sugiri, Sibylle Koletzko, Carl-Peter Bauer, and Barbara Hoffmann
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Male ,Health, Toxicology and Mutagenesis ,05 Environmental Sciences ,Air pollution ,CHILDREN ,Type 2 diabetes ,010501 environmental sciences ,medicine.disease_cause ,Toxicology ,NO2 ,01 natural sciences ,German ,0302 clinical medicine ,USE REGRESSION-MODELS ,Germany ,Epidemiology ,030212 general & internal medicine ,Public, Environmental & Occupational Health ,RISK ,Air Pollutants ,ESCAPE PROJECT ,Environmental exposure ,11 Medical And Health Sciences ,Geography ,Children's Health ,language ,Female ,FINE PARTICULATE MATTER ,Life Sciences & Biomedicine ,medicine.medical_specialty ,Adolescent ,Nitrogen Dioxide ,TYPE-2 DIABETES-MELLITUS ,Environmental Sciences & Ecology ,03 medical and health sciences ,Insulin resistance ,Air pollutants ,Environmental health ,Air Pollution ,medicine ,Humans ,COHORT ,METAANALYSIS ,0105 earth and related environmental sciences ,Science & Technology ,Public Health, Environmental and Occupational Health ,Environmental Exposure ,medicine.disease ,language.human_language ,PHYSICAL-ACTIVITY ,Diabetes Mellitus, Type 2 ,Particulate Matter ,Insulin Resistance ,Environmental Sciences - Abstract
Background: Epidemiological studies have identified associations between air pollution and green space access with type 2 diabetes in adults. However, it remains unclear to what extent associations with greenness are attributable to air pollution exposure. Objectives: We aimed to investigate associations between long-term exposure to air pollution and satellite-derived greenness with insulin resistance in adolescents. Methods: A total of 837 participants of two German birth cohorts (LISAplus and GINIplus) were included in the analysis. Generalized additive models were used to determine the association of individual satellite-derived greenness defined by the Normalized Difference Vegetation Index (NDVI), long-term air pollution exposure estimated by land-use regression (LUR) models with insulin resistance (HOMA-IR) in 15-year-old adolescents. Models were adjusted for study area, cohort, socioeconomic, and individual characteristics such as body mass index, physical activity, and smoking. Results: Increases of 2 SDs in nitrogen dioxide (NO2; 8.9 μg/m3) and particulate matter ≤ 10 μm in diameter (PM10; 6.7 μg/m3) were significantly associated with 11.4% (95% CI: 4.4, 18.9) and 11.4% (95% CI: 0.4, 23.7) higher HOMA-IR. A 2-SD increase in NDVI in a 1,000-m buffer (0.2 units) was significantly associated with a lower HOMA-IR (–7.4%; 95% CI: –13.3, –1.1). Associations tended to be stronger in adolescents who spent more time outside and in those with lower socioeconomic status. In combined models including both air pollution and greenness, only NO2 remained significantly associated with HOMA-IR, whereas effect estimates for all other exposures attenuated after adjustment for NO2. Conclusions: NO2, often considered as a marker of traffic, was independently associated with insulin resistance. The observed association between higher greenness exposure and lower HOMA-IR in adolescents might thus be attributable mainly to the lower co-exposure to traffic-related air pollution. Citation: Thiering E, Markevych I, Brüske I, Fuertes E, Kratzsch J, Sugiri D, Hoffmann B, von Berg A, Bauer CP, Koletzko S, Berdel D, Heinrich J. 2016. Associations of residential long-term air pollution exposures and satellite-derived greenness with insulin resistance in German adolescents. Environ Health Perspect 124:1291–1298; http://dx.doi.org/10.1289/ehp.1509967
- Published
- 2016
31. Human Early Life Exposome (HELIX) study: a European population-based exposome cohort
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Procesos psicológicos básicos y su desarrollo, Oinarrizko psikologia prozesuak eta haien garapena, Maitre, Léa, De Bont, Jeroen, Casas, Maribel, Robinson, Oliver, Aasvang, Gunn Marit, Agier, Lydiane, Andrušaitytė, Sandra, Ballester, Ferrán, Basagaña, Xavier, Borrás, Eva, Brochot, Céline, Bustamante, Mariona, Carracedo, Angel, De Castro, Montserrat, Dedele, Audrius, Donaire González, David, Estivill, Xavier, Evandt, Jorunn, Fossati, Serena, Giorgis Allemand, Lise, Granum, Berit, Grazuleviciene, Regina, Gützkow, Kristine Bjerve, Småstuen Haug, Line, Hernández Ferrer, Carles, Heude, Barbara, Ibarluzea Maurolagoitia, Jesús María, Julvez, Jordi, Karachaliou, Marianna, Keun, Hector C, Hjertager Krog, Norun, Lau, Chung-Ho E., Leventakou, Vasiliki, Lyon Caen, Sarah, Manzano, Cyntia, Mason, Dan, McEachan, Rosemary, Meltzer, Helle Margrete, Petraviciene, Inga, Quentin, Joane, Roumeliotaki, Theano, Sabido, Eduard, Saulnier, Pierre-Jean, Siskos, Alexandros P, Siroux, Valérie, Sunyer, Jordi, Tamayo, Ibon, Urquiza, Jose, Vafeiadi, Marina, Van Gent, Diana, Vives Usano, Marta, Waiblinger, Dagmar, Warembourg, Charline, Chatzi, Leda, Coen, Muireann, Van den Hazel, Peter, Nieuwenhuijsen, Mark J., Slama, Rémy, Thomsen, Cathrine, Wright, John, Vrijheid, Martine, Procesos psicológicos básicos y su desarrollo, Oinarrizko psikologia prozesuak eta haien garapena, Maitre, Léa, De Bont, Jeroen, Casas, Maribel, Robinson, Oliver, Aasvang, Gunn Marit, Agier, Lydiane, Andrušaitytė, Sandra, Ballester, Ferrán, Basagaña, Xavier, Borrás, Eva, Brochot, Céline, Bustamante, Mariona, Carracedo, Angel, De Castro, Montserrat, Dedele, Audrius, Donaire González, David, Estivill, Xavier, Evandt, Jorunn, Fossati, Serena, Giorgis Allemand, Lise, Granum, Berit, Grazuleviciene, Regina, Gützkow, Kristine Bjerve, Småstuen Haug, Line, Hernández Ferrer, Carles, Heude, Barbara, Ibarluzea Maurolagoitia, Jesús María, Julvez, Jordi, Karachaliou, Marianna, Keun, Hector C, Hjertager Krog, Norun, Lau, Chung-Ho E., Leventakou, Vasiliki, Lyon Caen, Sarah, Manzano, Cyntia, Mason, Dan, McEachan, Rosemary, Meltzer, Helle Margrete, Petraviciene, Inga, Quentin, Joane, Roumeliotaki, Theano, Sabido, Eduard, Saulnier, Pierre-Jean, Siskos, Alexandros P, Siroux, Valérie, Sunyer, Jordi, Tamayo, Ibon, Urquiza, Jose, Vafeiadi, Marina, Van Gent, Diana, Vives Usano, Marta, Waiblinger, Dagmar, Warembourg, Charline, Chatzi, Leda, Coen, Muireann, Van den Hazel, Peter, Nieuwenhuijsen, Mark J., Slama, Rémy, Thomsen, Cathrine, Wright, John, and Vrijheid, Martine
- Abstract
Purpose Essential to exposome research is the collection of data on many environmental exposures from different domains in the same subjects. The aim of the Human Early Life Exposome (HELIX) study was to measure and describe multiple environmental exposures during early life (pregnancy and childhood) in a prospective cohort and associate these exposures with molecular omics signatures and child health outcomes. Here, we describe recruitment, measurements available and baseline data of the HELIX study populations. Participants The HELIX study represents a collaborative project across six established and ongoing longitudinal population-based birth cohort studies in six European countries (France, Greece, Lithuania, Norway, Spain and the UK). HELIX used a multilevel study design with the entire study population totalling 31472 mother-child pairs, recruited during pregnancy, in the six existing cohorts (first level); a subcohort of 1301 mother-child pairs where biomarkers, omics signatures and child health outcomes were measured at age 6-11 years (second level) and repeat-sampling panel studies with around 150 children and 150 pregnant women aimed at collecting personal exposure data (third level). Findings to date Cohort data include urban environment, hazardous substances and lifestyle-related exposures for women during pregnancy and their offspring from birth until 6-11 years. Common, standardised protocols were used to collect biological samples, measure exposure biomarkers and omics signatures and assess child health across the six cohorts. Baseline data of the cohort show substantial variation in health outcomes and determinants between the six countries, for example, in family affluence levels, tobacco smoking, physical activity, dietary habits and prevalence of childhood obesity, asthma, allergies and attention deficit hyperactivity disorder. Future plans HELIX study results will inform on the early life exposome and its association with molecular omics signatur
- Published
- 2018
32. Air pollution exposure and lung function until age 16 years
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Milanzi, Edith B, Koppelman, Gerard H, Smit, Henriette A, Wijga, Alet H, Oldenwening, Marieke, Vonk, Judith M, Brunekreef, Bert, Gehring, Ulrike, One Health Chemisch, dIRAS RA-2, LS IRAS EEPI ME (Milieu epidemiologie), One Health Chemisch, dIRAS RA-2, LS IRAS EEPI ME (Milieu epidemiologie), and Groningen Research Institute for Asthma and COPD (GRIAC)
- Subjects
Male ,Vital capacity ,Cross-sectional study ,CHILDREN ,NO2 ,chemistry.chemical_compound ,0302 clinical medicine ,Interquartile range ,USE REGRESSION-MODELS ,Forced Expiratory Volume ,AREAS ,Medicine ,Lung volumes ,030212 general & internal medicine ,Longitudinal Studies ,Child ,Netherlands ,Air Pollutants ,ASSOCIATION ,respiratory system ,FUNCTION GROWTH ,Respiratory Function Tests ,PM2.5 ABSORBENCY ,Female ,HEALTH ,Pulmonary and Respiratory Medicine ,Adolescent ,Nitrogen Dioxide ,03 medical and health sciences ,FEV1/FVC ratio ,PM10 ,Soot ,Humans ,Nitrogen dioxide ,Particle Size ,Asthma ,STABILITY ,business.industry ,Environmental Exposure ,Airway obstruction ,Models, Theoretical ,medicine.disease ,respiratory tract diseases ,Cross-Sectional Studies ,030228 respiratory system ,chemistry ,Linear Models ,Particulate Matter ,business ,Demography - Abstract
Evidence for the effects of air pollution exposure on lung function growth into adolescence is scarce. We investigated associations of air pollution exposure with lung function and lung function growth until age 16.We conducted both longitudinal (n=915) and cross-sectional (n=721) analyses of associations of air pollution exposure with forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC) growth from ages eight to 16 and FEV1 and FVC at age 16. We estimated residential concentrations of nitrogen dioxide (NO2), “soot” and particulate matter (PMx, where x is the 50% cut-off aerodynamic diameter in µm) with diameters of 2.5), 10) and 2.5–10 µm (PMcoarse) during the preschool, primary school and secondary school time windows by land use regression models. Associations with (growth in) FEV1 and FVC were analysed by linear (mixed effects) regression.Higher air pollution exposure was associated with reduced FEV1 growth (e.g. adjusted difference −0.26% (95% CI −0.49 to −0.03%) per interquartile range increase in secondary school PM2.5) and lower FEV1 (adjusted difference −2.36% (95% CI −3.76 to −0.94%)), but was not adversely associated with FVC. Associations with FEV1 were stronger in boys than girls and were not modified by asthma status.Higher air pollution exposure may lead to increased airway obstruction, but not reduced lung volume in adolescence.
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- 2018
33. The Urban Exposome during Pregnancy and Its Socioeconomic Determinants
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Xavier Basagaña, Rosie McEachan, Johanna Lepeule, Jesús Ibarluzea, Valérie Siroux, Jose Urquiza, Mark J. Nieuwenhuijsen, Regina Gražuleviciene, Mariza Kampouri, Jordi Sunyer, Audrius Dėdelė, Léa Maitre, Oliver Robinson, Kjell Vegard Fjeldheim Weyde, Rémy Slama, Martine Vrijheid, David Donaire-Gonzalez, Marta Cirach, Montserrat de Castro, Ibon Tamayo, Norun Hjertager Krog, Antònia Valentín, Pippa Bird, Euripides G. Stephanou, Lise Giorgis-Allemand, Minas Iakovidis, Leda Chatzi, Bente Oftedal, Albert Ambros, Gunn Marit Aasvang, Ferran Ballester, John Wright, RS: NUTRIM - R3 - Respiratory & Age-related Health, Complexe Genetica, RS: NUTRIM - R4 - Gene-environment interaction, Medical Research Council (MRC), Imperial College London, Instituto de Salud Global - Institute For Global Health [Barcelona] (ISGlobal), Universitat Pompeu Fabra [Barcelona] (UPF), CIBER de Epidemiología y Salud Pública (CIBERESP), Institute for Advanced Biosciences / Institut pour l'Avancée des Biosciences (Grenoble) (IAB), Centre Hospitalier Universitaire [Grenoble] (CHU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Etablissement français du sang - Auvergne-Rhône-Alpes (EFS)-Université Grenoble Alpes [2016-2019] (UGA [2016-2019]), Norwegian Institute of Public Health [Oslo] (NIPH), Fundación para el Fomento de la Investigación Sanitaria y Biomédica de la Comunitat Valenciana [Espagne] (FISABIO), Universitat Jaume I, Universitat de València (UV), Bradford Institute for Health Research [Bradford, UK], Bradford Teaching Hospitals NHS Foundation Trust [Bradford, UK] (BTHFT), University of Crete [Heraklion] (UOC), University of Southern California (USC), Maastricht University [Maastricht], Vytautas Magnus University - Vytauto Didziojo Universitetas (VDU), Biodonostia Institute [San Sebastian, Espagne], University of the Basque Country [Bizkaia] (UPV/EHU), Basque Government [San Sebastien, Spain], Université Grenoble Alpes (UGA), Siroux, Valérie, Centre Hospitalier Universitaire [Grenoble] (CHU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Etablissement français du sang - Auvergne-Rhône-Alpes (EFS)-Centre National de la Recherche Scientifique (CNRS)-Université Grenoble Alpes [2016-2019] (UGA [2016-2019]), and University of the Basque Country/Euskal Herriko Unibertsitatea (UPV/EHU)
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[SDE] Environmental Sciences ,Urban Population ,Health, Toxicology and Mutagenesis ,05 Environmental Sciences ,NEIGHBORHOOD WALKABILITY ,010501 environmental sciences ,Toxicology ,01 natural sciences ,0302 clinical medicine ,USE REGRESSION-MODELS ,11. Sustainability ,030212 general & internal medicine ,NITROGEN-DIOXIDE ,11 Medical And Health Sciences ,3. Good health ,Europe ,MESH: Urban Population ,Geography ,GREEN SPACES ,MESH: Environmental Pollutants ,MESH: Young Adult ,[SDE]Environmental Sciences ,ENVIRONMENTAL JUSTICE ,Environmental Pollutants ,Female ,Adult ,Exposome ,medicine.medical_specialty ,MESH: Socioeconomic Factors ,Adolescent ,MESH: Environmental Exposure ,Young Adult ,03 medical and health sciences ,Environmental health ,medicine ,MESH: Cities ,Humans ,Cities ,Socioeconomic status ,0105 earth and related environmental sciences ,Environmental justice ,MESH: Adolescent ,Pregnancy ,MESH: Humans ,Land use ,LAND-USE ,Research ,Public health ,Public Health, Environmental and Occupational Health ,MESH: Adult ,Environmental Exposure ,medicine.disease ,Child development ,AMBIENT AIR-POLLUTION ,ROAD TRAFFIC NOISE ,RESIDENTIAL EXPOSURE ,Socioeconomic Factors ,[SDV.SPEE] Life Sciences [q-bio]/Santé publique et épidémiologie ,13. Climate action ,COHORT PROFILE ,[SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie ,MESH: Europe ,MESH: Female - Abstract
Background: The urban exposome is the set of environmental factors that are experienced in the outdoor urban environment and that may influence child development. Objective: The authors’ goal was to describe the urban exposome among European pregnant women and understand its socioeconomic determinants. Methods: Using geographic information systems, remote sensing and spatio-temporal modeling we estimated exposure during pregnancy to 28 environmental indicators in almost 30,000 women from six population-based birth cohorts, in nine urban areas from across Europe. Exposures included meteorological factors, air pollutants, traffic noise, traffic indicators, natural space, the built environment, public transport, facilities, and walkability. Socioeconomic position (SEP), assessed at both the area and individual level, was related to the exposome through an exposome-wide association study and principal component (PC) analysis. Results: Mean±standard deviation (SD) NO2 levels ranged from 13.6±5.1 μg/m3 (in Heraklion, Crete) to 43.2±11 μg/m3 (in Sabadell, Spain), mean±SD walkability score ranged from 0.22±0.04 (Kaunas, Lithuania) to 0.32±0.07 (Valencia, Spain) and mean±SD Normalized Difference Vegetation Index ranged from 0.21±0.05 in Heraklion to 0.51±0.1 in Oslo, Norway. Four PCs explained more than half of variation in the urban exposome. There was considerable heterogeneity in social patterning of the urban exposome across cities. For example, high-SEP (based on family education) women lived in greener, less noisy, and less polluted areas in Bradford, UK (0.39 higher PC1 score, 95% confidence interval (CI): 0.31, 0.47), but the reverse was observed in Oslo (−0.57 PC1 score, 95% CI: −0.73, −0.41). For most cities, effects were stronger when SEP was assessed at the area level: In Bradford, women living in high SEP areas had a 1.34 higher average PC1 score (95% CI: 1.21, 1.48). Conclusions: The urban exposome showed considerable variability across Europe. Pregnant women of low SEP were exposed to higher levels of environmental hazards in some cities, but not others, which may contribute to inequities in child health and development. The research leading to these results received funding from the European Community’s Seventh Framework Programme (FP7/2007-2013) under grant agreement no 308333 – the HELIX project.
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- 2018
34. Air pollution and airway resistance at age 8 years – the PIAMA birth cohort study
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Finke, Isabelle, de Jongste, Johan C, Smit, Henriette A, Wijga, Alet H, Koppelman, Gerard H, Vonk, Judith, Brunekreef, Bert, Gehring, Ulrike, One Health Chemisch, dIRAS RA-2, LS IRAS EEPI ME (Milieu epidemiologie), Pediatrics, Groningen Research Institute for Asthma and COPD (GRIAC), One Health Chemisch, dIRAS RA-2, and LS IRAS EEPI ME (Milieu epidemiologie)
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Vital capacity ,Health, Toxicology and Mutagenesis ,Air pollution ,010501 environmental sciences ,NO2 ,medicine.disease_cause ,01 natural sciences ,Interrupter resistance ,Cohort Studies ,chemistry.chemical_compound ,0302 clinical medicine ,Airway resistance ,USE REGRESSION-MODELS ,Interquartile range ,Child ,Children ,Netherlands ,Nitrogen dioxide ,Air Pollutants ,medicine.diagnostic_test ,lcsh:Public aspects of medicine ,ESCAPE PROJECT ,respiratory system ,LUNG-FUNCTION ,Health ,PM2.5 ABSORBENCY ,lcsh:Industrial medicine. Industrial hygiene ,Nitrogen Oxides ,Public Health ,Spirometry ,complex mixtures ,EARLY-LIFE ,lcsh:RC963-969 ,03 medical and health sciences ,Soot ,Environmental health ,medicine ,Humans ,Toxicology and Mutagenesis ,EXPOSURE ,0105 earth and related environmental sciences ,Asthma ,business.industry ,Airway Resistance ,Research ,Environmental and Occupational Health ,Public Health, Environmental and Occupational Health ,lcsh:RA1-1270 ,medicine.disease ,Confidence interval ,respiratory tract diseases ,030228 respiratory system ,chemistry ,ASTHMA ,Particulate matter ,business - Abstract
Background Air pollution has been found to adversely affect children’s lung function. Forced expiratory volume in 1 s and forced vital capacity from spirometry have been studied most frequently, but measurements of airway resistance may provide additional information. We assessed associations of long-term air pollution exposure with airway resistance. Methods We measured airway resistance at age 8 with the interrupter resistance technique (Rint) in participants of the Dutch PIAMA birth cohort study. We linked Rint with estimated annual average air pollution concentrations [nitrogen oxides (NO2, NOx), PM2.5 absorbance (“soot”), and particulate matter
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- 2018
35. Error in air pollution exposure model determinants and bias in health estimates
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Bert Brunekreef, Roel Vermeulen, Jelle Vlaanderen, Marc Chadeau-Hyam, Lützen Portengen, Adam A. Szpiro, Gerard Hoek, Ulrike Gehring, and Commission of the European Communities
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Epidemiology ,Air pollution exposure ,05 Environmental Sciences ,Nitrogen Dioxide ,Air pollution ,Model parameters ,Environmental Sciences & Ecology ,UNCERTAINTY ,030501 epidemiology ,medicine.disease_cause ,Land use regression ,Toxicology ,ESCAPE ,Exposure modeling ,Cohort Studies ,03 medical and health sciences ,USE REGRESSION-MODELS ,AREAS ,Air Pollution ,Statistics ,medicine ,Aerodynamic diameter ,Humans ,11 Medical and Health Sciences ,Public, Environmental & Occupational Health ,ASSOCIATIONS ,Air Pollutants ,Science & Technology ,Models, Statistical ,Spatially resolved ,Public Health, Environmental and Occupational Health ,NOX ,COHORTS ,Pollution ,LONG-TERM EXPOSURE ,LUNG-FUNCTION ,PM2.5 ABSORBENCY ,Environmental science ,Regression Analysis ,Particulate Matter ,Seasons ,Empirical/statistical models ,0305 other medical science ,03 Chemical Sciences ,Life Sciences & Biomedicine ,Environmental Sciences ,Environmental epidemiology ,Environmental Monitoring - Abstract
BACKGROUND: Land use regression (LUR) models are commonly used in environmental epidemiology to assign spatially resolved estimates of air pollution to study participants. In this setting, estimated LUR model parameters are assumed to be transportable to a main study (the ''transportability assumption''). We provide an empirical illustration of how violation of this assumption can affect exposure predictions and bias health-effect estimates. METHODS: We based our simulation on two existing LUR models, one for nitrogen dioxide, the other for particulate matter with aerodynamic diameter
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- 2018
36. Long-term Air Pollution Exposure, Genome-wide DNA Methylation and Lung Function in the LifeLines Cohort Study
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de F C Lichtenfels, Ana Julia, van der Plaat, Diana A, de Jong, Kim, van Diemen, Cleo C, Postma, Dirkje S, Nedeljkovic, Ivana, van Duijn, Cornelia M, Amin, Najaf, la Bastide-van Gemert, Sacha, de Vries, Maaike, Ward-Caviness, Cavin K, Wolf, Kathrin, Waldenberger, Melanie, Peters, Annette, Stolk, Ronald P, Brunekreef, Bert, Boezen, H Marike, Vonk, Judith M, One Health Chemisch, dIRAS RA-2, Epidemiology, One Health Chemisch, dIRAS RA-2, Groningen Research Institute for Asthma and COPD (GRIAC), Life Course Epidemiology (LCE), and Lifestyle Medicine (LM)
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0301 basic medicine ,Male ,Time Factors ,Health, Toxicology and Mutagenesis ,Air pollution exposure ,05 Environmental Sciences ,Genome-wide association study ,BLOOD-PRESSURE ,010501 environmental sciences ,Bioinformatics ,Toxicology ,01 natural sciences ,Genome ,ARTERY ENDOTHELIAL-CELLS ,Cohort Studies ,USE REGRESSION-MODELS ,Lung function ,NITROGEN-DIOXIDE ,media_common ,Public, Environmental & Occupational Health ,ASSOCIATIONS ,Air Pollutants ,ESCAPE PROJECT ,11 Medical And Health Sciences ,Middle Aged ,Respiratory Function Tests ,EPIGENETIC MEDIATION ,DNA methylation ,Female ,FINE PARTICULATE MATTER ,Life Sciences & Biomedicine ,Cohort study ,Pollution ,Adult ,media_common.quotation_subject ,Nitrogen Dioxide ,Environmental Sciences & Ecology ,Biology ,OBSTRUCTIVE PULMONARY-DISEASE ,03 medical and health sciences ,Negatively associated ,Air Pollution ,Humans ,0105 earth and related environmental sciences ,Science & Technology ,Research ,Public Health, Environmental and Occupational Health ,Environmental Exposure ,DNA Methylation ,PHOSPHOLIPASE-D ,030104 developmental biology ,Linear Models ,CpG Islands ,Particulate Matter ,Environmental Sciences ,Genome-Wide Association Study - Abstract
BACKGROUND: Long-term air pollution exposure is negatively associated with lung function, yet the mechanisms underlying this association are not fully clear. Differential DNA methylation may explain this association. OBJECTIVES: Our main aim was to study the association between long-term air pollution exposure and DNA methylation. METHODS: We performed a genome-wide methylation study using robust linear regression models in 1,017 subjects from the LifeLines cohort study to analyze the association between exposure to nitrogen dioxide (NO 2 ) and particulate matter (PM 2.5 , fine particulate matter with aerodynamic diameter ≤2.5 lm; PM 10 , particulate matter with aerodynamic diameter ≤10 lm) and PM 2.5absorbance , indicator of elemental carbon content (estimated with land-use-regression models) with DNA methylation in whole blood (Illumina® HumanMethylation450K BeadChip). Replication of the top hits was attempted in two independent samples from the population-based Cooperative Health Research in the Region of Augsburg studies (KORA). RESULTS: Depending on the p-value threshold used, we found significant associations between NO 2 exposure and DNA methylation for seven CpG sites (Bonferroni corrected threshold p < 1.19 × 10 −7 ) or for 4,980 CpG sites (False Discovery Rate < 0.05). The top associated CpG site was annotated to the PSMB9 gene (i.e., cg04908668). None of the seven Bonferroni significant CpG-sites were significantly replicated in the two KORA-cohorts. No associations were found for PM exposure. CONCLUSIONS: Long-term NO 2 exposure was genome-wide significantly associated with DNA methylation in the identification cohort but not in the replication cohort. Future studies are needed to further elucidate the potential mechanisms underlying NO 2 -exposure–related respiratory disease.
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- 2018
37. Human Early Life Exposome (HELIX) study: a European population-based exposome cohort
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Maitre, Léa, De Bont, Jeroen, Casas, Maribel, Robinson, Oliver, Aasvang, Gunn Marit, Agier, Lydiane, Andrušaitytė, Sandra, Ballester, Ferrán, Basagaña, Xavier, Borrás, Eva, Brochot, Céline, Bustamante, Mariona, Carracedo, Angel, De Castro, Montserrat, Dedele, Audrius, Donaire González, David, Estivill, Xavier, Evandt, Jorunn, Fossati, Serena, Giorgis Allemand, Lise, Granum, Berit, Grazuleviciene, Regina, Gützkow, Kristine Bjerve, Småstuen Haug, Line, Hernández Ferrer, Carles, Heude, Barbara, Ibarluzea Maurolagoitia, Jesús María, Julvez, Jordi, Karachaliou, Marianna, Keun, Hector C, Hjertager Krog, Norun, Lau, Chung-Ho E., Leventakou, Vasiliki, Lyon Caen, Sarah, Manzano, Cyntia, Mason, Dan, McEachan, Rosemary, Meltzer, Helle Margrete, Petraviciene, Inga, Quentin, Joane, Roumeliotaki, Theano, Sabido, Eduard, Saulnier, Pierre-Jean, Siskos, Alexandros P, Siroux, Valérie, Sunyer, Jordi, Tamayo, Ibon, Urquiza, Jose, Vafeiadi, Marina, Van Gent, Diana, Vives Usano, Marta, Waiblinger, Dagmar, Warembourg, Charline, Chatzi, Leda, Coen, Muireann, Van den Hazel, Peter, Nieuwenhuijsen, Mark J., Slama, Rémy, Thomsen, Cathrine, Wright, John, Vrijheid, Martine, Instituto de Salud Global - Institute For Global Health [Barcelona] (ISGlobal), Universitat Pompeu Fabra [Barcelona] (UPF), CIBER de Epidemiología y Salud Pública (CIBERESP), Norwegian Institute of Public Health [Oslo] (NIPH), Institute for Advanced Biosciences / Institut pour l'Avancée des Biosciences (Grenoble) (IAB), Centre Hospitalier Universitaire [Grenoble] (CHU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Etablissement français du sang - Auvergne-Rhône-Alpes (EFS)-Centre National de la Recherche Scientifique (CNRS)-Université Grenoble Alpes [2016-2019] (UGA [2016-2019]), Vytautas Magnus University - Vytauto Didziojo Universitetas (VDU), Universitat de València (UV), Fundación para el Fomento de la Investigación Sanitaria y Biomédica de la Comunitat Valenciana [Espagne] (FISABIO), Centre for Genomic Regulation [Barcelona] (CRG), Universitat Pompeu Fabra [Barcelona] (UPF)-Centro Nacional de Analisis Genomico [Barcelona] (CNAG), Institut National de l'Environnement Industriel et des Risques (INERIS), Universidade de Santiago de Compostela [Spain] (USC ), CIBER de Enfermedades Raras (CIBERER), Sidra Medicine [Doha, Qatar], Centre de Recherche Épidémiologie et Statistique Sorbonne Paris Cité (CRESS (U1153 / UMR_A_1125 / UMR_S_1153)), Conservatoire National des Arts et Métiers [CNAM] (CNAM)-Université Sorbonne Paris Cité (USPC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), University of the Basque Country/Euskal Herriko Unibertsitatea (UPV/EHU), BIODonostia Research Institute, Public Health Division of Gipuzkoa, University of Crete [Heraklion] (UOC), Imperial College London, CIC - Poitiers, Université de Poitiers-Centre hospitalier universitaire de Poitiers (CHU Poitiers)-Direction Générale de l'Organisation des Soins (DGOS)-Institut National de la Santé et de la Recherche Médicale (INSERM), Harvard University [Cambridge], Keck School of Medicine [Los Angeles], University of Southern California (USC), Maastricht University [Maastricht], Veiligheids-en Gezondheidsregio Gelderland Midden [Arnhem, the Netherlands] (VGGM), Civs, Gestionnaire, Institut National de la Recherche Agronomique (INRA)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Université Sorbonne Paris Cité (USPC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Commission of the European Communities, Universidade de Santiago de Compostela. Departamento de Ciencias Forenses, Anatomía Patolóxica, Xinecoloxía e Obstetricia, e Pediatría, Universidade de Santiago de Compostela. Instituto de Ciencias Forenses 'Luis Concheiro'(INCIFOR), RS: NUTRIM - R3 - Respiratory & Age-related Health, and Complexe Genetica
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Male ,Urban Population ,Epidemiology ,Blood Pressure ,01 natural sciences ,0302 clinical medicine ,USE REGRESSION-MODELS ,Prospective Studies ,profile ,education.field_of_study ,Anthropometry ,public health ,birth cohort ,General Medicine ,3. Good health ,MOTHER ,Child, Preschool ,Prenatal Exposure Delayed Effects ,[SDV.TOX]Life Sciences [q-bio]/Toxicology ,Cohort ,Body Composition ,HEALTH ,Food Hypersensitivity ,Birth cohort ,medicine.medical_specialty ,Exposome ,exposome ,03 medical and health sciences ,land-use ,[SDV.EE.SANT] Life Sciences [q-bio]/Ecology, environment/Health ,Humans ,education ,Psychological Tests ,child cohort ,Public health ,areas ,Infant ,Environmental Exposure ,AIR-POLLUTION ,DNA Methylation ,Omics ,medicine.disease ,CHILD COHORT ,exposure ,Attention Deficit Disorder with Hyperactivity ,Biomarkers ,Proteome ,Salut Pública ,Neurodevelopment ,use regression-models ,010501 environmental sciences ,AREAS ,11. Sustainability ,030212 general & internal medicine ,Prospective cohort study ,mother ,Smoking ,Community child health ,health ,omics ,Respiratory Function Tests ,[SDV.TOX] Life Sciences [q-bio]/Toxicology ,Europe ,PREGNANCY ,Exposoma ,Blood pressure ,Metabolome ,epidemiology ,Female ,pregnancy ,community child health ,Adult ,Population ,Mothers ,PROFILE ,Childhood obesity ,Hazardous Substances ,Young Adult ,Environmental health ,medicine ,air-pollution ,Body Weights and Measures ,EXPOSURE ,0105 earth and related environmental sciences ,[SDV.EE.SANT]Life Sciences [q-bio]/Ecology, environment/Health ,LAND-USE ,business.industry ,Respiratory health ,Infant, Newborn ,HELIX ,Socioeconomic Factors ,[SDV.SPEE] Life Sciences [q-bio]/Santé publique et épidémiologie ,Gene-Environment Interaction ,[SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie ,European population ,business ,Transcriptome - Abstract
Purpose Essential to exposome research is the collection of data on many environmental exposures from different domains in the same subjects. The aim of the Human Early Life Exposome (HELIX) study was to measure and describe multiple environmental exposures during early life (pregnancy and childhood) in a prospective cohort and associate these exposures with molecular omics signatures and child health outcomes. Here, we describe recruitment, measurements available and baseline data of the HELIX study populations. Participants The HELIX study represents a collaborative project across six established and ongoing longitudinal population-based birth cohort studies in six European countries (France, Greece, Lithuania, Norway, Spain and the UK). HELIX used a multilevel study design with the entire study population totalling 31472 mother-child pairs, recruited during pregnancy, in the six existing cohorts (first level); a subcohort of 1301 mother-child pairs where biomarkers, omics signatures and child health outcomes were measured at age 6-11 years (second level) and repeat-sampling panel studies with around 150 children and 150 pregnant women aimed at collecting personal exposure data (third level). Findings to date Cohort data include urban environment, hazardous substances and lifestyle-related exposures for women during pregnancy and their offspring from birth until 6-11 years. Common, standardised protocols were used to collect biological samples, measure exposure biomarkers and omics signatures and assess child health across the six cohorts. Baseline data of the cohort show substantial variation in health outcomes and determinants between the six countries, for example, in family affluence levels, tobacco smoking, physical activity, dietary habits and prevalence of childhood obesity, asthma, allergies and attention deficit hyperactivity disorder. Future plans HELIX study results will inform on the early life exposome and its association with molecular omics signatures and child health outcomes. Cohort data are accessible for future research involving researchers external to the project. The research leading to these results has received funding from the European Community's Seventh Framework Programme (FP7/2007-206) under grant agreement no 308333-the HELIX project. Dr Maribel Casas and Dr Jordi Julvez received funding from Instituto de Salud Carlos III (Ministry of Economy and Competitiveness) (MS16/00128, MS14/00108). INMA data collections were supported by grants from the Instituto de Salud Carlos III, CIBERESP, the Conselleria de Sanitat, Generalitat Valenciana, Department of Health of the Basque Government; the Provincial Government of Gipuzkoa, and the Generalitat de Catalunya-CIRIT. KANC was funded by the grant of the Lithuanian Agency for Science Innovation and Technology (6-04-2014_31V-66). The Norwegian Mother and Child Cohort Study (MoBa) is supported by the Norwegian Ministry of Health and the Ministry of Education and Research, NIH/NIEHS (contract no. N01-ES-75558), and NIH/NINDS (grant no. 1 UO1 NS 047537-01 and grant no. 2 UO1 NS 047537-06A1). The Rhea project was financially supported by European projects, and the Greek Ministry of Health (Program of Prevention of Obesity and Neurodevelopmental Disorders in Preschool Children, in Heraklion district, Crete, Greece: 2011-2014; 'Rhea Plus': Primary Prevention Program of Environmental Risk Factors for Reproductive Health, and Child Health: 2012-2015). The work was also supported by MICINN (MTM2015-68140-R) and Centro Nacional de Genotipado-CEGEN-PRB2-ISCIII. CW received funding from the Fondation de France.
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- 2018
38. DNA methylation and exposure to ambient air pollution in two prospective cohorts
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Michelle Plusquin, Florence Guida, Silvia Polidoro, Roel Vermeulen, Ole Raaschou-Nielsen, Gianluca Campanella, Gerard Hoek, Soterios A. Kyrtopoulos, Panagiotis Georgiadis, Alessio Naccarati, Carlotta Sacerdote, Vittorio Krogh, H. Bas Bueno-de-Mesquita, W.M. Monique Verschuren, Sergi Sayols-Baixeras, Tommaso Panni, Annette Peters, Dennie G.A.J. Hebels, Jos Kleinjans, Paolo Vineis, Marc Chadeau-Hyam, LS IRAS EEPI ME (Milieu epidemiologie), dIRAS RA-2, dIRAS RA-I&I RA, CBITE, RS: MERLN - Cell Biology - Inspired Tissue Engineering (CBITE), Toxicogenomics, RS: GROW - R1 - Prevention, PLUSQUIN, Michelle, Guida, Florence, Polidoro, Silvia, Vermeulen, Roel, Raaschou-Nielsen, Ole, Campanella, Gianluca, Hoek, Gerard, Kyrtopoulos, Soterios A., Georgiadis, Panagiotis, Naccarati, Alessio, Sacerdote, Carlotta, Krogh, Vittorio, Bueno-de-Mesquita, H. Bas, Verschuren, W. M. Monique, Sayols-Baixeras, Sergi, Panni, Tommaso, Peters, Annette, Hebels, Dennie G. A. J., KLEINJANS, J., Vineis, Paolo, and Chadeau-Hyam, Marc
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Epigenomics ,Male ,EXPRESSION ,air pollution ,epigenome-wide DNA methylation ,Illumina 450 k human methylation array ,particulate matter ,NOx ,EPIC ,Illumina 450k human methylation array ,European Continental Ancestry Group ,Air pollution ,Gene Expression ,Environmental Sciences & Ecology ,PERIPHERAL-BLOOD ,White People ,NO ,Cohort Studies ,NO(x) ,LUNG-CANCER ,Soot ,MARKERS ,USE REGRESSION-MODELS ,Environmental Science(all) ,MD Multidisciplinary ,Epigenome-wide ,Humans ,Prospective Studies ,lcsh:Environmental sciences ,lcsh:GE1-350 ,Air Pollutants ,Science & Technology ,DNA methylation ,CARCINOGENESIS ,ESCAPE PROJECT ,Environmental Exposure ,ASSOCIATION ,DNA Methylation ,Middle Aged ,GENE-SPECIFIC METHYLATION ,Cardiovascular Diseases ,Epigenome-wide DNA methylation ,Female ,SMOKING ,Particulate matter ,Life Sciences & Biomedicine ,Environmental Sciences ,Genome-Wide Association Study - Abstract
Long-term exposure to air pollution has been associated with several adverse health effects including cardiovascular, respiratory diseases and cancers. However, underlying molecular alterations remain to be further investigated. The aim of this study is to investigate the effects of long-term exposure to air pollutants on (a) average DNA methylation at functional regions and, (b) individual differentially methylated CpG sites. An assumption is that omic measurements, including the methylome, are more sensitive to low doses than hard health outcomes. This study included blood-derived DNA methylation (Illumina-HM450 methylation) for 454 Italian and 159 Dutch participants from the European Prospective Investigation into Cancer and Nutrition (EPIC). Long-term air pollution exposure levels, including NO2, NOx, PM2.5, PMcoarse, PM10, PM2.5 absorbance (soot) were estimated using models developed within the ESCAPE project, and back-extrapolated to the time of sampling when possible. We meta-analysed the associations between the air pollutants and global DNA methylation, methylation in functional regions and epigenome-wide methylation. CpG sites found differentially methylated with air pollution were further investigated for functional interpretation in an independent population (EnviroGenoMarkers project), where (N= 613) participants had both methylation and gene expression data available. Exposure to NO2 was associated with a significant global somatic hypomethylation (p-value = 0.014). Hypomethylation of CpG island's shores and shelves and gene bodies was significantly associated with higher exposures to NO2 and NOx. Meta-analysing the epigenome-wide findings of the 2 cohorts did not show genome-wide significant associations at single CpG site level. However, several significant CpG were found if the analyses were separated by countries. By regressing gene expression levels against methylation levels of the exposure-related CpG sites, we identified several significant CpG-transcript pairs and highlighted 5 enriched pathways for NO2 and 9 for NOx mainly related to the immune system and its regulation. Our findings support results on global hypomethylation associated with air pollution, and suggest that the shores and shelves of CpG islands and gene bodies are mostly affected by higher exposure to NO2 and NOx. Functional differences in the immune system were suggested by transcriptome analyses. EPIC-Italy was financially supported by the Italian Association for Cancer Research (AIRC). Genome-wide DNA methylation profiling of EPIC-Italy samples was financially supported by the Human Genetics Foundation (HuGeF) and Compagnia di San Paolo. EPIC-Netherlands was financially supported by the Dutch Ministry of Public Health, Welfare, and Sports (VWS), by the Netherlands Cancer Registry, by LK Research Funds, by Dutch Prevention Funds, by the Netherlands Organisation for Health Research and Development (ZON), and by the World Cancer Research Fund (WCRF). Genome-wide DNA methylation profiling of EPIC-Netherlands samples was financially supported by internal Imperial College funds. The REGICOR study was supported by the Spanish Ministry of Economy and Innovation through the Carlos III Health Institute [Red HERACLES RD12/0042, PI12/00232, PI09/90506], European Funds for Development (ERDF-FEDER), and by the Catalan Research and Technology Innovation Interdepartmental Commission [SGR 1195]. Michelle Plusquin was supported by the People Program (Marie Curie Actions) of the European Union's Seventh Framework Program FP7/2007-2013/under REA grant agreement n [628858]. Florence Guida was supported by the COLT foundation. Support for this work was also provided by the project EXPOSOMICS, grant agreement 308610-FP7 European Commission. Sergi Sayols-Baixeras was funded by a contract from Instituto de Salud Carlos III FEDER [IFI14/00007].
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- 2017
39. Inflammatory markers in relation to long-term air pollution
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Mostafavi Montazeri, Nahid, Vlaanderen, Jelle, Chadeau-Hyam, Marc, Beelen, Rob, Modig, Lars, Palli, Domenico, Bergdahl, Ingvar A, Vineis, Paolo, Hoek, Gerard, Kyrtopoulos, Soterios Α, Vermeulen, Roel, Risk Assessment of Toxic and Immunomodulatory Agents, IRAS RATIA2, IRAS RATIA-SIB, LS IRAS EEPI ME (Milieu epidemiologie), LS IRAS EEPI GRA (Gezh.risico-analyse), Risk Assessment of Toxic and Immunomodulatory Agents, IRAS RATIA2, IRAS RATIA-SIB, LS IRAS EEPI ME (Milieu epidemiologie), and LS IRAS EEPI GRA (Gezh.risico-analyse)
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Male ,SYSTEMIC INFLAMMATION ,BLOOD ,Air pollution ,Inflammatory markers ,Physiology ,NO2 ,Systemic inflammation ,medicine.disease_cause ,USE REGRESSION-MODELS ,AREAS ,PARTICIPANTS ,Prospective Studies ,Prospective cohort study ,lcsh:Environmental sciences ,General Environmental Science ,lcsh:GE1-350 ,Air Pollutants ,Respiratory disease ,Confounding ,Interleukin ,ESCAPE PROJECT ,Middle Aged ,CANCER ,Italy ,Cytokines ,Female ,Nitrogen Oxides ,medicine.symptom ,Life Sciences & Biomedicine ,Adult ,Environmental Sciences & Ecology ,Inflammation ,CYTOKINE LEVELS ,MD Multidisciplinary ,medicine ,Humans ,EXPOSURE ,NOx ,Aged ,Sweden ,Science & Technology ,business.industry ,medicine.disease ,Immunology ,Linear Models ,Gene expression ,business ,Chronic health effects ,Environmental Sciences ,Biomarkers - Abstract
Long-term exposure to ambient air pollution can lead to chronic health effects such as cancer, cardiovascular and respiratory disease. Systemic inflammation has been hypothesized as a putative biological mechanism contributing to these adverse health effects. We evaluated the effect of long-term exposure to air pollution on blood markers of systemic inflammation.We measured a panel of 28 inflammatory markers in peripheral blood samples from 587 individuals that were biobanked as part of a prospective study. Participants were from Varese and Turin (Italy) and Umea (Sweden). Long-term air pollution estimates of nitrogen oxides (NOx) were available from the European Study of Cohorts for Air Pollution Effects (ESCAPE). Linear mixed models adjusted for potential confounders were applied to assess the association between NOx and the markers of inflammation.Long-term exposure to NOx was associated with decreased levels of interleukin (IL)-2, IL-8, IL-10 and tumor necrosis factor-α in Italy, but not in Sweden. NOx exposure levels were considerably lower in Sweden than in Italy (Sweden: median (5th, 95th percentiles) 6.65 μg/m3 (4.8, 19.7); Italy: median (5th, 95th percentiles) 94.2 μg/m3 (7.8, 124.5)). Combining data from Italy and Sweden we only observed a significant association between long-term exposure to NOx and decreased levels of circulating IL-8.We observed some indication for perturbations in the inflammatory markers due to long-term exposure to NOx. Effects were stronger in Italy than in Sweden, potentially reflecting the difference in air pollution levels between the two cohorts. Keywords: Air pollution, Inflammatory markers, Gene expression, Chronic health effects
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- 2015
40. Air Pollution and Atherosclerosis: A Cross-Sectional Analysis of Four European Cohort Studies in the ESCAPE Study
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Perez, Laura, Wolf, Kathrin, Hennig, Frauke, Penell, Johanna, Basagaña, Xavier, Aguilera, Inmaculada, Agis, David, Beelen, Rob, Brunekreef, Bert, Cyrys, Josef, Fuks, Kateryna B, Adam, Martin, Baldassare, Damiano, Cirach, Marta, Elosua, Roberto, Dratva, Julia, Hampel, Regina, Koenig, Wolfgang, Marrugat, Jaume, De Faire, Ulf, Pershagen, Göran, Probst-Hensch, Nicole M, de Nazelle, Audrey, Nieuwenhuijsen, Mark J, Rathmann, Wolfgang, Rivera, Marcela, Seissler, Jochen, Schindler, Christian, Thierry, Joachim, Hoffmann, Barbara, Peters, Annette, Künzli, Nino, LS IRAS EEPI ME (Milieu epidemiologie), Dep IRAS, Risk Assessment of Toxic and Immunomodulatory Agents, IRAS RATIA2, LS IRAS EEPI ME (Milieu epidemiologie), Dep IRAS, Risk Assessment of Toxic and Immunomodulatory Agents, IRAS RATIA2, Universitat Politècnica de Catalunya. Doctorat en Matemàtica Aplicada, and Universitat Politècnica de Catalunya. CoDAlab - Control, Modelització, Identificació i Aplicacions
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Male ,Pathology ,Cross-sectional study ,Health, Toxicology and Mutagenesis ,05 Environmental Sciences ,Air pollution ,030204 cardiovascular system & hematology ,010501 environmental sciences ,medicine.disease_cause ,Medi ambient -- Anàlisi d'impacte ,Toxicology ,SUBCLINICAL ATHEROSCLEROSIS ,NO2 ,01 natural sciences ,INTIMA-MEDIA THICKNESS ,Carotid Intima-Media Thickness ,Cohort Studies ,0302 clinical medicine ,USE REGRESSION-MODELS ,PARTICULATE MATTER ,11. Sustainability ,YOUNG-ADULTS ,OXIDATIVE STRESS ,Public, Environmental & Occupational Health ,Aire -- Contaminació ,Matemàtiques i estadística [Àrees temàtiques de la UPC] ,Environmental exposure ,11 Medical And Health Sciences ,Middle Aged ,LONG-TERM EXPOSURE ,Europe ,Meta-analysis ,Female ,Life Sciences & Biomedicine ,Cohort study ,Air -- Pollution ,Malalties cerebrovasculars ,Adult ,medicine.medical_specialty ,Environmental Sciences & Ecology ,complex mixtures ,03 medical and health sciences ,Environmental health ,Statistical significance ,Air Pollution ,Linear regression ,medicine ,Humans ,ddc:610 ,Ciències de la salut::Impacte ambiental [Àrees temàtiques de la UPC] ,METAANALYSIS ,0105 earth and related environmental sciences ,Aged ,Science & Technology ,Research ,Public Health, Environmental and Occupational Health ,Environmental Exposure ,Atherosclerosis ,Cross-Sectional Studies ,Intima-media thickness ,Environmental impact analysis ,13. Climate action ,CAROTID-ARTERY ,Environmental Sciences ,Biomarkers - Abstract
Background: In four European cohorts, we investigated the cross-sectional association between long-term exposure to air pollution and intima-media thickness of the common carotid artery (CIMT), a preclinical marker of atherosclerosis. Methods: Individually assigned levels of nitrogen dioxide, nitrogen oxides, particulate matter ≤ 2.5 μm (PM2.5), absorbance of PM2.5 (PM2.5abs), PM10, PMcoarse, and two indicators of residential proximity to highly trafficked roads were obtained under a standard exposure protocol (European Study of Cohorts for Air Pollution Effects—ESCAPE study) in the Stockholm area (Sweden), the Ausburg and Ruhr area (Germany), and the Girona area (Spain). We used linear regression and meta-analyses to examine the association between long-term exposure to air pollution and CIMT. Results: The meta-analysis with 9,183 individuals resulted in an estimated increase in CIMT (geometric mean) of 0.72% (95% CI: –0.65%, 2.10%) per 5-μg/m3 increase in PM2.5 and 0.42% (95% CI: –0.46%, 1.30%) per 10–5/m increase in PM2.5abs. Living in proximity to high traffic was also positively but not significantly associated with CIMT. Meta-analytic estimates for other pollutants were inconsistent. Results were similar across different adjustment sets and sensitivity analyses. In an extended meta-analysis for PM2.5 with three other previously published studies, a 0.78% (95% CI: –0.18%, 1.75%) increase in CIMT was estimated for a 5-μg/m3 contrast in PM2.5. Conclusions: Using a standardized exposure and analytical protocol in four European cohorts, we found that cross-sectional associations between CIMT and the eight ESCAPE markers of long-term residential air pollution exposure did not reach statistical significance. The additional meta-analysis of CIMT and PM2.5 across all published studies also was positive but not significant. Citation: Perez L, Wolf K, Hennig F, Penell J, Basagaña X, Foraster M, Aguilera I, Agis D, Beelen R, Brunekreef B, Cyrys J, Fuks KB, Adam M, Baldassarre D, Cirach M, Elosua R, Dratva J, Hampel R, Koenig W, Marrugat J, de Faire U, Pershagen G, Probst-Hensch NM, de Nazelle A, Nieuwenhuijsen MJ, Rathmann W, Rivera M, Seissler J, Schindler C, Thiery J, Hoffmann B, Peters A, Künzli N. 2015. Air pollution and atherosclerosis: a cross-sectional analysis of four European cohort studies in the ESCAPE Study. Environ Health Perspect 123:597–605; http://dx.doi.org/10.1289/ehp.1307711
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- 2015
41. Long-term Exposure to Ambient Air Pollution and Incidence of Postmenopausal Breast Cancer in 15 European Cohorts within the ESCAPE Project
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Bente Oftedal, Gunn Marit Aasvang, Ole Raaschou-Nielsen, Kirsten Thorup Eriksen, Gabriele Nagel, Anna Oudin, Bert Brunekreef, Paolo Vineis, Ming-Yi Tsai, Claes-Göran Östenson, Petra H.M. Peeters, Gudrun Weinmayr, Andrei Pyko, Göran Pershagen, Ibon Tamayo-Uria, Nancy L. Pedersen, Bas Bueno-de-Mesquita, Sara Grioni, Jeanette Therming Jørgensen, Anne Tjønneland, Rob Beelen, Laura Baglietto, Michal Korek, Andrea Jaensch, Fulvio Ricceri, Meng Wang, Ulf de Faire, Pilar Amiano, Enrica Migliore, Marie Pedersen, Alois Lang, Timothy J. Key, Laura Fratiglioni, Miren Dorronsoro, Geir Aamodt, Agnès Fournier, Alessandro Marcon, Massimo Stafoggia, David Olsson, Roel Vermeulen, Zorana Jovanovic Andersen, Bertil Forsberg, Gerard Hoek, Marie-Christine Boutron-Ruault, Claudia Galassi, Ranjeet S. Sokhi, Menno Keuken, Giulia Cesaroni, Kees de Hoogh, Carlotta Sacerdote, Michelle Plusquin, Vittorio Krogh, LS IRAS EEPI GRA (Gezh.risico-analyse), LS IRAS EEPI ME (Milieu epidemiologie), and dIRAS RA-2
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2016 Urban Mobility & Environment ,Health, Toxicology and Mutagenesis ,05 Environmental Sciences ,polycyclic aromatic hydrocarbons ,Air pollution ,010501 environmental sciences ,Toxicology ,NO2 ,medicine.disease_cause ,01 natural sciences ,Cohort Studies ,0302 clinical medicine ,Nickel ,USE REGRESSION-MODELS ,PARTICULATE MATTER ,skin and connective tissue diseases ,RISK ,Air Pollutants ,Aged ,Air Pollution ,Breast Neoplasms ,Environmental Exposure ,Europe ,Female ,Humans ,Incidence ,Middle Aged ,Postmenopause ,ENVIRONMENTAL-POLLUTANTS ,air pollution ,cancer ,breast ,epidemiology ,ESCAPE ,women ,Particulate matter ,PM10 ,PM2.5 ,Nitrogen dioxides ,Incidence (epidemiology) ,Hazard ratio ,Great Britain ,11 Medical And Health Sciences ,use regression models ,Environmental exposure ,3. Good health ,Health ,PM2.5 ABSORBENCY ,030220 oncology & carcinogenesis ,Public Health ,Healthy Living ,Cohort study ,Silicon ,Iron ,GREAT-BRITAIN ,California teachers ,New York ,POLYCYCLIC AROMATIC-HYDROCARBONS ,Arbetsmedicin och miljömedicin ,03 medical and health sciences ,LUNG-CANCER ,Breast cancer ,Environmental health ,Journal Article ,medicine ,environmental pollutants ,Toxicology and Mutagenesis ,Element ,0105 earth and related environmental sciences ,business.industry ,Environmental and Occupational Health ,Public Health, Environmental and Occupational Health ,Cancer ,Nitrogen oxide ,Occupational Health and Environmental Health ,medicine.disease ,Confidence interval ,lung cancer ,NEW-YORK ,13. Climate action ,SUMS - Sustainable Urban Mobility and Safety ,Potassium ,ELSS - Earth, Life and Social Sciences ,Healthy for Life ,business ,Copper ,Sulfur ,CALIFORNIA-TEACHERS - Abstract
BACKGROUND: Epidemiological evidence on the association between ambient air pollution and breast cancer risk is inconsistent. OBJECTIVE: We examined the association between long-term exposure to ambient air pollution and incidence of postmenopausal breast cancer in European women. METHODS: In 15 cohorts from nine European countries, individual estimates of air pollution levels at the residence were estimated by standardized land-use regression models developed within the European Study of Cohorts for Air Pollution Effects (ESCAPE) and Transport related Air Pollution and Health impacts - Integrated Methodologies for Assessing Particulate Matter (TRANSPHORM) projects: particulate matter (PM) ≤2:5 μm, ≤10 μm, and 2:5–10 μm in diameter (PM2:5, PM10, and PMcoarse, respectively); PM2:5 absorbance; nitrogen oxides (NO2 and NOx); traffic intensity; and elemental composition of PM. We estimated cohort-specific associations between breast cancer and air pollutants using Cox regression models, adjusting for major lifestyle risk factors, and pooled cohort-specific estimates using random-effects meta-analyses. RESULTS: Of 74,750 postmenopausal women included in the study, 3,612 developed breast cancer during 991,353 person-years of follow-up. We found positive and statistically insignificant associations between breast cancer and PM2:5 {hazard ratio (HR) =1:08 [95% confidence interval (CI): 0.77, 1.51] per 5 μg/m3 }, PM10 [1.07 (95% CI: 0.89, 1.30) per 10 μg/m3 ], PMcoarse [1.20 (95% CI: 0.96, 1.49 per 5 μg/m3 ], and NO2 [1.02 (95% CI: 0.98, 1.07 per 10 μg/m3 ], and a statistically significant association with NOx [1.04 (95% CI: 1.00, 1.08) per 20 μg/m3, p =0:04]. CONCLUSIONS: We found suggestive evidence of an association between ambient air pollution and incidence of postmenopausal breast cancer in European women. © 2017, Public Health Services, US Dept of Health and Human Services. All rights reserved. Chemicals/CAS: copper, 15158-11-9, 7440-50-8; iron, 14093-02-8, 53858-86-9, 7439-89-6; nickel, 7440-02-0; nitrogen oxide, 11104-93-1; potassium, 7440-09-7; silicon, 7440-21-3; sulfur, 13981-57-2, 7704-34-9; vanadium, 7440-62-2; zinc, 7440-66-6, 14378-32-6
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- 2017
42. An association of particulate air pollution and traffic exposure with mortality after lung transplantation in Europe
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Bart Luijk, Christian Benden, Ellen Winckelmans, Danielle Vienneau, Nikolaus Kneidinger, Walter Klepetko, Andrew J. Fisher, Erik A M Verschuuren, Claus Neurohr, Hannelore Bellon, Geert Verleden, Barbara Hoffmann, Jens Gottlieb, Robin Vos, Esmée M. Bijnens, Gregor Warnecke, Johanna M. Kwakkel-van Erp, Tim S. Nawrot, Martin Iversen, Hans Henrik Schultz, Benoit Nemery, G. Meachery, Elly Vandermeulen, Paul A. Corris, James Lordan, Antonio Roman, Gerard Hoek, Markus Kamler, Wim van der Bij, David Ruttens, Peter Jaksch, Davide Piloni, Gerhard Weinreich, Urte Sommerwerck, Bart M. Vanaudenaerde, Federica Meloni, Stijn E. Verleden, Are Martin Holm, Cristina Berastegui, Monica Morosini, Susana Gómez-Ollés, Kees de Hoogh, Erik Jan D Oudijk, RUTTENS, David, Verleden, Stijn E., BIJNENS, Esmee, WINCKELMANS, Ellen, Gottlieb, Jens, Warnecke, Gregor, Meloni, Federica, Morosini, Monica, Van Der Bij, Wim, Verschuuren, Erik A., Sommerwerck, Urte, Weinreich, Gerhard, Kamler, Markus, Roman, Antonio, Gomez-Olles, Susana, Berastegui, Cristina, Benden, Christian, Holm, AreMartin, Iversen, Martin, Schultz, Hans Henrik, Luijk, Bart, Oudijk, Erik-Jan, Erp, Johanna M. Kwakkel-van, Jaksch, Peter, Klepetko, Walter, Kneidinger, Nikolaus, Neurohr, Claus, Corris, Paul, Fisher, Andrew J., Lordan, James, Meachery, Gerard, Piloni, Davide, Vandermeulen, Elly, Bellon, Hannelore, Hoffmann, Barbara, Vienneau, Danielle, Hoek, Gerard, de Hoogh, Kees, Nemery, Benoit, Verleden, Geert M., Vos, Robin, NAWROT, Tim, Vanaudenaerde, Bart M., and Groningen Institute for Organ Transplantation (GIOT)
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Pulmonary and Respiratory Medicine ,medicine.medical_specialty ,medicine.medical_treatment ,Medizin ,AZITHROMYCIN ,Air pollution ,030204 cardiovascular system & hematology ,PLACEBO-CONTROLLED TRIAL ,NO2 ,medicine.disease_cause ,DOUBLE-BLIND ,03 medical and health sciences ,0302 clinical medicine ,USE REGRESSION-MODELS ,Environmental health ,medicine ,Lung transplantation ,Proportional hazards model ,business.industry ,BRONCHIOLITIS OBLITERANS SYNDROME ,Hazard ratio ,Confounding ,RANDOMIZED CONTROLLED-TRIAL ,Particulates ,PREVENTION ,Surgery ,ALLOGRAFT DYSFUNCTION ,EXACERBATIONS ,030228 respiratory system ,Cohort ,Human medicine ,business ,Cohort study - Abstract
Air pollution from road traffic is a serious health risk, especially for susceptible individuals. Single-centre studies showed an association with chronic lung allograft dysfunction (CLAD) and survival after lung transplantation, but there are no large studies.13 lung transplant centres in 10 European countries created a cohort of 5707 patients. For each patient, we quantified residential particulate matter with aerodynamic diameter ≤10 µm (PM10) by land use regression models, and the traffic exposure by quantifying total road length within buffer zones around the home addresses of patients and distance to a major road or freeway.After correction for macrolide use, we found associations between air pollution variables and CLAD/mortality. Given the important interaction with macrolides, we stratified according to macrolide use. No associations were observed in 2151 patients taking macrolides. However, in 3556 patients not taking macrolides, mortality was associated with PM10 (hazard ratio 1.081, 95% CI 1.000–1.167); similarly, CLAD and mortality were associated with road lengths in buffers of 200–1000 and 100–500 m, respectively (hazard ratio 1.085– 1.130). Sensitivity analyses for various possible confounders confirmed the robustness of these associations.Long-term residential air pollution and traffic exposure were associated with CLAD and survival after lung transplantation, but only in patients not taking macrolides.
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- 2017
43. Outdoor air pollution and risk for kidney parenchyma cancer in 14 European cohorts
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Raaschou-Nielsen, Ole, Pedersen, Marie, Stafoggia, Massimo, Weinmayr, Gudrun, Andersen, Zorana J., Galassi, Claudia, Sommar, Johan, Forsberg, Bertil, Olsson, David, Oftedal, Bente, Krog, Norun H., Aasvang, Gunn Marit, Pyko, Andrei, Pershagen, Göran, Korek, Michal, De Faire, Ulf, Pedersen, Nancy L., Östenson, Claes Göran, Fratiglioni, Laura, Sørensen, Mette, Eriksen, Kirsten T., Tjønneland, Anne, Peeters, Petra H., Bueno-de-Mesquita, Bas, Plusquin, Michelle, Key, Timothy J., Jaensch, Andrea, Nagel, Gabriele, Föger, Bernhard, Wang, Meng, Tsai, Ming Yi, Grioni, Sara, Marcon, Alessandro, Krogh, Vittorio, Ricceri, Fulvio, Sacerdote, Carlotta, Migliore, Enrica, Tamayo, Ibon, Amiano, Pilar, Dorronsoro, Miren, Sokhi, Ranjeet, Kooter, Ingeborg, de Hoogh, Kees, Beelen, Rob, Eeftens, Marloes, Vermeulen, Roel, Vineis, Paolo, Brunekreef, Bert, Hoek, Gerard, Commission of the European Communities, dIRAS RA-2, LS IRAS EEPI ME (Milieu epidemiologie), and dIRAS RA-I&I RA
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Adult ,Male ,Cancer Research ,Lung Neoplasms ,NO2 ,Cohort Studies ,kidney parenchyma ,Arbetsmedicin och miljömedicin ,LUNG-CANCER ,RENAL-CELL CARCINOMA ,Risk Factors ,USE REGRESSION-MODELS ,PARTICULATE MATTER ,Air Pollution ,Journal Article ,cancer ,Humans ,Oncology & Carcinogenesis ,EXPOSURE ,Particle Size ,Vehicle Emissions ,Medicine(all) ,Air Pollutants ,Cancer och onkologi ,Science & Technology ,MORTALITY ,ESCAPE PROJECT ,cohort ,Environmental Exposure ,Occupational Health and Environmental Health ,Middle Aged ,INHALED ULTRAFINE PARTICLES ,Kidney Neoplasms ,Europe ,Oncology ,PM2.5 ABSORBENCY ,Cancer and Oncology ,Female ,Gasoline ,Particulate Matter ,Life Sciences & Biomedicine ,1112 Oncology And Carcinogenesis ,air pollution, kidney parenchyma, cancer, cohort ,Meta-Analysis - Abstract
Several studies have indicated weakly increased risk for kidney cancer among occupational groups exposed to gasoline vapors, engine exhaust, polycyclic aromatic hydrocarbons and other air pollutants, although not consistently. It was the aim to investigate possible associations between outdoor air pollution at the residence and the incidence of kidney parenchyma cancer in the general population. We used data from 14 European cohorts from the ESCAPE study. We geocoded and assessed air pollution concentrations at baseline addresses by land-use regression models for particulate matter (PM10 , PM2.5 , PMcoarse , PM2.5 absorbance (soot)) and nitrogen oxides (NO2 , NOx ), and collected data on traffic. We used Cox regression models with adjustment for potential confounders for cohort-specific analyses and random effects models for meta-analyses to calculate summary hazard ratios (HRs). The 289,002 cohort members contributed 4,111,908 person-years at risk. During follow-up (mean 14.2 years) 697 incident cancers of the kidney parenchyma were diagnosed. The meta-analyses showed higher HRs in association with higher PM concentration, e.g. HR=1.57 (95%CI: 0.81-3.01) per 5μg/m(3) PM2.5 and HR=1.36 (95%CI: 0.84-2.19) per 10(-5) m(-1) PM2.5 absorbance, albeit never statistically significant. The HRs in association with nitrogen oxides and traffic density on the nearest street were slightly above one. Sensitivity analyses among participants who did not change residence during follow-up showed stronger associations, but none were statistically significant. This study provides suggestive evidence that exposure to outdoor PM at the residence may be associated with higher risk for kidney parenchyma cancer; the results should be interpreted cautiously as associations may be due to chance. This article is protected by copyright. All rights reserved.
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- 2017
44. Ambient air pollution and primary liver cancer incidence in four European cohorts within the ESCAPE project
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Roel Vermeulen, Vittorio Krogh, Hans Concin, Mette Sørensen, Rob Beelen, Kirsten Thorup Eriksen, Ole Raaschou-Nielsen, Fulvio Ricceri, Alessandro Marcon, Ming-Yi Tsai, Paolo Vineis, Meng Wang, Gabriele Nagel, Massimo Stafoggia, Bert Brunekreef, Zorana Jovanovic Andersen, Gerard Hoek, Sara Grioni, Andrea Jaensch, Marie Pedersen, Steffen Loft, Anne Tjønneland, Kees de Hoogh, Claudia Galassi, Ranjeet S. Sokhi, Carlotta Sacerdote, Andrea Ranzi, Gudrun Weinmayr, dIRAS RA-2, LS IRAS EEPI ME (Milieu epidemiologie), and dIRAS RA-I&I RA
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Male ,Denmark ,010501 environmental sciences ,01 natural sciences ,Biochemistry ,DISEASE ,Cohort Studies ,0302 clinical medicine ,USE REGRESSION-MODELS ,HEPATOCELLULAR-CARCINOMA ,Motorized vehicle traffic ,Medicine ,NITROGEN-DIOXIDE ,General Environmental Science ,Vehicle Emissions ,Air Pollutants ,Incidence (epidemiology) ,Incidence ,Hazard ratio ,Confounding ,Liver Neoplasms ,Cohort ,Environmental exposure ,ASSOCIATION ,cohort ,Italy ,030220 oncology & carcinogenesis ,Austria ,Female ,Nitrogen Oxides ,Ambient air pollution ,environment ,Liver cancer ,Cohort study ,motorized vehicle traffic ,Meteorology ,ambient air poluution ,Environment ,complex mixtures ,liver cancer ,03 medical and health sciences ,LUNG-CANCER ,Statistical significance ,Environmental health ,Air Pollution ,Humans ,EXPOSURE ,METAANALYSIS ,0105 earth and related environmental sciences ,business.industry ,MORTALITY ,Environmental Exposure ,Confidence interval ,RISK-FACTORS ,Particulate Matter ,business - Abstract
Background Tobacco smoke exposure increases the risk of cancer in the liver, but little is known about the possible risk associated with exposure to ambient air pollution. Objectives We evaluated the association between residential exposure to air pollution and primary liver cancer incidence. Methods We obtained data from four cohorts with enrolment during 1985–2005 in Denmark, Austria and Italy. Exposure to nitrogen oxides (NO 2 and NO X ), particulate matter (PM) with diameter of less than 10 µm (PM 10 ), less than 2.5 µm (PM 2.5 ), between 2.5 and 10 µm (PM 2.5–10 ) and PM 2.5 absorbance (soot) at baseline home addresses were estimated using land-use regression models from the ESCAPE project. We also investigated traffic density on the nearest road. We used Cox proportional-hazards models with adjustment for potential confounders for cohort-specific analyses and random-effects meta-analyses to estimate summary hazard ratios (HRs) and 95% confidence intervals (CIs). Results Out of 174,770 included participants, 279 liver cancer cases were diagnosed during a mean follow-up of 17 years. In each cohort, HRs above one were observed for all exposures with exception of PM 2.5 absorbance and traffic density. In the meta-analysis, all exposures were associated with elevated HRs, but none of the associations reached statistical significance. The summary HR associated with a 10-μg/m 3 increase in NO 2 was 1.10 (95% confidence interval (CI): 0.93, 1.30) and 1.34 (95% CI: 0.76, 2.35) for a 5-μg/m 3 increase in PM 2.5 . Conclusions The results provide suggestive evidence that ambient air pollution may increase the risk of liver cancer. Confidence intervals for associations with NO 2 and NO X were narrower than for the other exposures.
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- 2017
45. Effects of long-term exposure to air pollution on natural-cause mortality: an analysis of 22 European cohorts within the multicentre ESCAPE project
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Laura Fratiglioni, Françoise Clavel-Chapelon, Christian Schindler, Wei W. Xun, Bertil Forsberg, Gerard Hoek, Nino Künzli, Göran Pershagen, Michal Korek, Gabriele Nagel, Petra H.M. Peeters, Bert Brunekreef, Timo Lanki, Nicole Probst-Hensch, Paul Fischer, Annette Peters, Massimo Stafoggia, Francesco Forastiere, Chiara Badaloni, Marloes Eeftens, Ibon Tamayo, Kees de Hoogh, Ole Raaschou-Nielsen, Dorothea Sugiri, Giulia Cesaroni, Bas Bueno-de-Mesquita, Timothy J. Key, Antonia Trichopoulou, Johanna Penell, Rob Beelen, Regina Hampel, Emmanuel Schaffner, Barbara Hoffmann, Kees Meliefste, Enrica Migliore, Lars Modig, Miren Dorronsoro, Michail Katsoulis, Fulvio Ricceri, Thomas Ellermann, Kirsten Thorup Eriksen, Vittorio Krogh, Hans Concin, Meng Wang, Anu W. Turunen, Konstantina Dimakopoulou, Claes-Göran Östenson, Pilar Amiano, Zorana Jovanovic Andersen, Ulf de Faire, Ming-Yi Tsai, Alex Ineichen, Joachim Heinrich, Martin Adam, Evangelia Samoli, Aki S. Havulinna, Alice Vilier, Nancy L. Pedersen, Gudrun Weinmayr, Sara Grioni, Carlotta Sacerdote, Paolo Vineis, Christophe Declercq, Mark J. Nieuwenhuijsen, Kim Overvad, Per Nafstad, Klea Katsouyanni, Kathrin Wolf, Wenche Nystad, Bente Oftedal, Harish C. Phuleria, Tamara Schikowski, Ursula Krämer, Anna Oudin, Andrea Ranzi, C Galassi, Dep IRAS, LS IRAS EEPI ME (Milieu epidemiologie), Risk Assessment of Toxic and Immunomodulatory Agents, IRAS RATIA2, and IRAS RATIA-SIB
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Adult ,Male ,Adolescent ,Population ,Air pollution ,NO2 ,medicine.disease_cause ,AIRBORNE PARTICLES ,Cohort Studies ,Toxicology ,Young Adult ,LUNG-CANCER ,PM10 ,USE REGRESSION-MODELS ,Air Pollution ,Cause of Death ,AREAS ,medicine ,Humans ,Multicenter Studies as Topic ,Child ,education ,Aged ,Pollutant ,Air Pollutants ,education.field_of_study ,business.industry ,Hazard ratio ,Infant ,Environmental Exposure ,General Medicine ,Environmental exposure ,Middle Aged ,3. Good health ,Europe ,Cohort effect ,CARDIOVASCULAR-DISEASE ,13. Climate action ,Child, Preschool ,PM2.5 ABSORBENCY ,BLACK CARBON ,Population study ,Female ,Particulate Matter ,HEALTH ,business ,Demography ,Cohort study - Abstract
BACKGROUND: Few studies on long-term exposure to air pollution and mortality have been reported from Europe. Within the multicentre European Study of Cohorts for Air Pollution Effects (ESCAPE), we aimed to investigate the association between natural-cause mortality and long-term exposure to several air pollutants. METHODS: We used data from 22 European cohort studies, which created a total study population of 367,251 participants. All cohorts were general population samples, although some were restricted to one sex only. With a strictly standardised protocol, we assessed residential exposure to air pollutants as annual average concentrations of particulate matter (PM) with diameters of less than 2.5 μm (PM2.5), less than 10 μm (PM10), and between 10 μm and 2.5 μm (PMcoarse), PM2.5 absorbance, and annual average concentrations of nitrogen oxides (NO2 and NOx), with land use regression models. We also investigated two traffic intensity variables-traffic intensity on the nearest road (vehicles per day) and total traffic load on all major roads within a 100 m buffer. We did cohort-specific statistical analyses using confounder models with increasing adjustment for confounder variables, and Cox proportional hazards models with a common protocol. We obtained pooled effect estimates through a random-effects meta-analysis. FINDINGS: The total study population consisted of 367,251 participants who contributed 5,118,039 person-years at risk (average follow-up 13.9 years), of whom 29,076 died from a natural cause during follow-up. A significantly increased hazard ratio (HR) for PM2.5 of 1.07 (95% CI 1.02-1.13) per 5 μg/m(3) was recorded. No heterogeneity was noted between individual cohort effect estimates (I(2) p value=0.95). HRs for PM2.5 remained significantly raised even when we included only participants exposed to pollutant concentrations lower than the European annual mean limit value of 25 μg/m(3) (HR 1.06, 95% CI 1.00-1.12) or below 20 μg/m(3) (1.07, 1.01-1.13). INTERPRETATION: Long-term exposure to fine particulate air pollution was associated with natural-cause mortality, even within concentration ranges well below the present European annual mean limit value. FUNDING: European Community's Seventh Framework Program (FP7/2007-2011).
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- 2014
46. Long-term exposure to elemental constituents of particulate matter and cardiovascular mortality in 19 European cohorts: Results from the ESCAPE and TRANSPHORM projects
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Wang, Meng, Beelen, Rob, Stafoggia, Massimo, Raaschou-Nielsen, Ole, Andersen, Zorana Jovanovic, Hoffmann, Barbara, Fischer, Paul, Houthuijs, Danny, Nieuwenhuijsen, Mark, Weinmayr, Gudrun, Vineis, Paolo, Xun, Wei W., Dimakopoulou, Konstantina, Samoli, Evangelia, Laatikainen, Tiina, Lanki, Timo, Turunen, Anu W., Oftedal, Bente, Schwarze, Per, Aamodt, Geir, Penell, Johanna, De Faire, Ulf, Korek, Michal, Leander, Karin, Pershagen, Goran, Pedersen, Nancy L., Ostenson, Claes-Goran, Fratiglioni, Laura, Eriksen, Kirsten Thorup, Sorensen, Mette, Tjonneland, Anne, Bueno-de-Mesquita, Bas, Eeftens, Marloes, Bots, Michiel L., Meliefste, Kees, Kraemer, Ursula, Heinrich, Joachim, Sugiri, Dorothea, Key, Timothy, de Hoogh, Kees, Wolf, Kathrin, Peters, Annette, Cyrys, Josef, Jaensch, Andrea, Concin, Hans, Nagel, Gabriele, Tsai, Ming-Yi, Phuleria, Harish, Ineichen, Alex, Kuenzli, Nino, Probst-Hensch, Nicole, Schaffner, Emmanuel, Vilier, Alice, Clavel-Chapelon, Francoise, Declerq, Christophe, Ricceri, Fulvio, Sacerdote, Carlotta, Marcon, Alessandro, Galassi, Claudia, Migliore, Enrica, Ranzi, Andrea, Cesaroni, Giulia, Badaloni, Chiara, Forastiere, Francesco, Katsoulis, Michail, Trichopoulou, Antonia, Keuken, Menno, Jedynska, Aleksandra, Kooter, Ingeborg M., Kukkonen, Jaakko, Sokhi, Ranjeet S., Brunekreef, Bert, Katsouyanni, Klea, Hoek, Gerard, Dep IRAS, LS IRAS EEPI ME (Milieu epidemiologie), Risk Assessment of Toxic and Immunomodulatory Agents, IRAS RATIA2, IRAS RATIA-SIB, Dep IRAS, LS IRAS EEPI ME (Milieu epidemiologie), Risk Assessment of Toxic and Immunomodulatory Agents, IRAS RATIA2, and IRAS RATIA-SIB
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Male ,Air pollution ,Total population ,Joint analysis ,medicine.disease_cause ,NO2 ,DISEASE ,Cohort Studies ,HARVARD 6 CITIES ,USE REGRESSION-MODELS ,11. Sustainability ,Medicine ,Adult Aged Cardiovascular Diseases Cohort Studies Environmental Exposure Europe Female Humans Male Middle Aged Particulate Matter Proportional Hazards Models ,lcsh:Environmental sciences ,General Environmental Science ,lcsh:GE1-350 ,Hazard ratio ,Particulate matter air pollution ,cardiovascular mortality ,epidemiology ,Middle Aged ,Particulates ,3. Good health ,Europe ,Pooled analysis ,Cardiovascular Diseases ,Constituents ,Female ,EXTENDED FOLLOW-UP ,MOUSE LUNG ,Adult ,Cardiovascular mortality ,TIME-SERIES ,ESCAPE ,CHEMICAL-COMPOSITION ,Environmental health ,Humans ,PARTICLES ,Aged ,Proportional Hazards Models ,Proportional hazards model ,business.industry ,Long-term exposure ,Environmental engineering ,Environmental Exposure ,AIR-POLLUTION ,TRANSPHORM ,13. Climate action ,business ,Particulate matter - Abstract
Background: Associations between long-term exposure to ambient particulate matter (PM) and cardiovascular (CVD) mortality have been widely recognized. However, health effects of long-term exposure to constituents of PM on total CVD mortality have been explored in a single study only. Aims: The aim of this study was to examine the association of PM composition with cardiovascular mortality. Methods: We used data from 19 European ongoing cohorts within the framework of the ESCAPE (European Study of Cohorts for Air Pollution Effects) and TRANSPHORM (Transport related Air Pollution and Health impacts — Integrated Methodologies for Assessing Particulate Matter) projects. Residential annual average exposure to elemental constituents within particle matter smaller than 2.5 and 10 μm (PM2.5 and PM10) was estimated using Land Use Regression models. Eight elements representing major sources were selected a priori (copper, iron, potassium, nickel, sulfur, silicon, vanadium and zinc). Cohort-specific analyses were conducted using Cox proportional hazards models with a standardized protocol. Random-effects meta-analysis was used to calculate combined effect estimates. Results: The total population consisted of 322,291 participants, with 9545 CVD deaths. We found no statistically significant associations between any of the elemental constituents in PM2.5 or PM10 and CVD mortality in the pooled analysis. Most of the hazard ratios (HRs) were close to unity, e.g. for PM10 Fe the combined HR was 0.96 (0.84–1.09). Elevated combined HRs were found for PM2.5 Si (1.17, 95% CI: 0.93–1.47), and S in PM2.5 (1.08, 95% CI: 0.95–1.22) and PM10 (1.09, 95% CI: 0.90–1.32). Conclusion: In a joint analysis of 19 European cohorts, we found no statistically significant association between long-term exposure to 8 elemental constituents of particles and total cardiovascular mortality. Keywords: Long-term exposure, Particulate matter, Constituents, Cardiovascular mortality, ESCAPE, TRANSPHORM
- Published
- 2014
- Full Text
- View/download PDF
47. Air pollution and childhood leukaemia: a nationwide case-control study in Italy
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Badaloni, C., Ranucci, A., Cesaroni, G., Zanini, G., Vienneau, D., Al Aidrous, F., De Hoogh, K., Magnani, C., Forastiere, F., Mattioli, Stefano, Miligi, L., Rondelli, R., Salvan, A., Masera, G., Rizzari, C., Bisanti, L., Zambon, P., Greco, A., Cannizzaro, S., Gafa, L., Luzzatto, L. L., Benvenuti, A., Michelozzi, P., Kirchmayer, U., Cocco, P., Galassi, C., Celentano, E., Guarino, E., Assennato, G., de Nichilo, G., Merlo, D. F., Bocchini, V., Mosciatti, P., Minelli, L., Chiavarini, M., Cuttini, M., Casotto, V., Torregrossa, M. V., Valenti, R. M., Haupt, R., Lagorio, S., Risica, S., Polichetti, A., Bochicchio, F., Nuccetelli, C., Biddau, P., Arico, M., De Salvo, G. L., Locatelli, F., Pession, Andrea, Varotto, S., Poggi, V., Massaglia, P., Monetti, D., Targhetta, R., Bernini, G., Pannelli, F., Sampietro, G., Schiliro, G., Pulsoni, A., Badaloni, C., Ranucci, A., Cesaroni, G., Zanini, G., Vienneau, D., Al-Aidrous, F., De Hoogh, K., Magnani, C., Forastiere, F., C. Badaloni, A. Ranucci, G. Cesaroni, G. Zanini, D. Vienneau, F. Al-Aidrou, K. De Hoogh, C. Magnani, F. Forastiere, S. Mattioli, L. Miligi, R. Rondelli, A. Salvan, G. Masera, C. Rizzari, L. Bisanti, P. Zambon, A. Greco, S. Cannizzaro, L. Gafa, L. L. Luzzatto, A. Benvenuti, P. Michelozzi, U. Kirchmayer, P. Cocco, C. Galassi, E. Celentano, E. Guarino, G. Assennato, G. de Nichilo, D. F. Merlo, V. Bocchini, P. Mosciatti, L. Minelli, M. Chiavarini, M. Cuttini, V. Casotto, M. V. Torregrossa, R. M. Valenti, R. Haupt, S. Lagorio, S. Risica, A. Polichetti, F. Bochicchio, C. Nuccetelli, P. Biddau, M. Arico, G. L. De Salvo, F. Locatelli, A. Pession, S. Varotto, V. Poggi, P. Massaglia, D. Monetti, R. Targhetta, G. Bernini, F. Pannelli, G. Sampietro, G. Schiliro, and A. Pulsoni
- Subjects
Male ,Pediatrics ,Air pollution ,NO2 ,Land use Regression Model ,Logistic regression ,medicine.disease_cause ,Economica ,Residence Characteristics ,USE REGRESSION-MODELS ,Medicine ,Child ,Children ,Vehicle Emissions ,General Environmental Science ,USE REGRESSION-MODELS, RESIDENTIAL TRAFFIC DENSITY, MAGNETIC-FIELDS, POOLED ANALYSIS, RISK-FACTOR, CANCER, EXPOSURE, CHILDREN, NO2, ASSOCIATION ,Leukemia ,Incidence ,Incidence (epidemiology) ,ASSOCIATION ,CANCER ,Childhood leukaemia ,Italy ,Child, Preschool ,Female ,Case-Control Studie ,Human ,medicine.medical_specialty ,Socio-culturale ,MAGNETIC-FIELDS ,POOLED ANALYSIS ,RISK-FACTOR ,Air Pollution ,Occupational Exposure ,Environmental health ,Traffic Indicator ,Humans ,EXPOSURE ,RESIDENTIAL TRAFFIC DENSITY ,Exposure assessment ,Vehicle Emission ,business.industry ,Public Health, Environmental and Occupational Health ,Case-control study ,Ambientale ,Infant ,Carcinogens, Environmental ,Automobile ,Case-Control Studies ,Residence Characteristic ,Dispersion Model ,Etiology ,General Earth and Planetary Sciences ,Particulate Matter ,Residence ,business ,Automobiles - Abstract
Objectives Leukaemia is the most common cancer in children, but its aetiology is still poorly understood. We tested the hypothesis that traffic-related air pollution is associated with paediatric leukaemia because of chronic exposure to several potential carcinogens. Methods The Italian SETIL study (Study on the aetiology of lymphohematopoietic malignancies in children) was conducted in 14 Italian regions. All incident cases of leukaemia in children aged ≤10 years from these regions (period 1998–2001) were eligible for enrolment. Two controls per case, matched on birth date, gender and region of residence were randomly selected from the local population registries. Exposure assessment at birth residence included traffic indicators (distance to main roads and length of main roads within 100 m) and estimates of pollutants concentrations (particulate matter -PM 2.5 and PM 10 - and gases -NO 2 and O 3 -) from national dispersion model and land use regression models. The association between the exposure variables and leukaemia was assessed by logistic regression analyses. Results Participation rates were 91.4% among cases and 69.2% in controls; 620 cases (544 acute lymphocytic and 76 acute non-lymphocytic leukaemia) and 957 controls were included. Overall, when considering the residence at birth, 35.6% of cases and 42.4% of controls lived along busy roads, and the mean annual PM 10 levels were 33.3 (SD=6.3) and 33.4 µg/m 3 (SD=6.5), respectively. No association was found, and all ORs, independent of the method of assessment and the exposure windows, were close to the null value. Conclusions Using various exposure assessment strategies, air pollution appears not to affect the incidence of childhood leukaemia.
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- 2013
48. Air pollution exposure and lung function in children: The ESCAPE Project
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Bert Brunekreef, Rob Beelen, Ulrike Gehring, Barbara Hoffmann, Josef Cyrys, Angela Simpson, Anna Mölter, Erica S. Schultz, Elaine Fuertes, Andrea von Berg, Michal Korek, Claudia Flexeder, Marjan Kerkhof, Olena Gruzieva, Joachim Heinrich, Claudia Klümper, Alet H. Wijga, Johan C. de Jongste, Adnan Custovic, Magnus Svartengren, Göran Pershagen, Raymond Agius, Marloes Eeftens, Dorothea Sugiri, Groningen Research Institute for Asthma and COPD (GRIAC), and Pediatrics
- Subjects
Air pollution exposure ,Health, Toxicology and Mutagenesis ,05 Environmental Sciences ,Air pollution ,010501 environmental sciences ,medicine.disease_cause ,NO2 ,Toxicology ,01 natural sciences ,Pulmonary function testing ,Cohort Studies ,0302 clinical medicine ,USE REGRESSION-MODELS ,Mexico city ,AREAS ,Medicine ,Child ,Nitrogen oxides ,Lung function ,Air Pollutants ,BIRTH COHORT ,SCHOOLCHILDREN ,Environmental exposure ,11 Medical And Health Sciences ,MEXICO-CITY ,respiratory system ,3. Good health ,Respiratory Function Tests ,Europe ,PM2.5 ABSORBENCY ,Respiratory Physiological Phenomena ,Regression Analysis ,Nitrogen Oxides ,Birth cohort ,Environmental Monitoring ,03 medical and health sciences ,Environmental health ,Humans ,ddc:610 ,Particle Size ,METAANALYSIS ,0105 earth and related environmental sciences ,STABILITY ,business.industry ,Research ,Public Health, Environmental and Occupational Health ,PULMONARY-FUNCTION ,Environmental Exposure ,respiratory tract diseases ,030228 respiratory system ,13. Climate action ,business - Abstract
Background: There is evidence for adverse effects of outdoor air pollution on lung function of children. Quantitative summaries of the effects of air pollution on lung function, however, are lacking due to large differences among studies. Objectives: We aimed to study the association between residential exposure to air pollution and lung function in five European birth cohorts with a standardized exposure assessment following a common protocol. Methods: As part of the European Study of Cohorts for Air Pollution Effects (ESCAPE) we analyzed data from birth cohort studies situated in Germany, Sweden, the Netherlands, and the United Kingdom that measured lung function at 6–8 years of age (n = 5,921). Annual average exposure to air pollution [nitrogen oxides (NO2, NOx), mass concentrations of particulate matter with diameters < 2.5, < 10, and 2.5–10 μm (PM2.5, PM10, and PMcoarse), and PM2.5 absorbance] at the birth address and current address was estimated by land-use regression models. Associations of lung function with estimated air pollution levels and traffic indicators were estimated for each cohort using linear regression analysis, and then combined by random effects meta-analysis. Results: Estimated levels of NO2, NOx, PM2.5 absorbance, and PM2.5 at the current address, but not at the birth address, were associated with small decreases in lung function. For example, changes in forced expiratory volume in 1 sec (FEV1) ranged from –0.86% (95% CI: –1.48, –0.24%) for a 20-μg/m3 increase in NOx to –1.77% (95% CI: –3.34, –0.18%) for a 5-μg/m3 increase in PM2.5. Conclusions: Exposure to air pollution may result in reduced lung function in schoolchildren. Citation: Gehring U, Gruzieva O, Agius RM, Beelen R, Custovic A, Cyrys J, Eeftens M, Flexeder C, Fuertes E, Heinrich J, Hoffmann B, de Jongste JC, Kerkhof M, Klümper C, Korek M, Mölter A, Schultz ES, Simpson A, Sugiri D, Svartengren M, von Berg A, Wijga AH, Pershagen G, Brunekreef B. 2013. Air pollution exposure and lung function in children: the ESCAPE project. Environ Health Perspect 121:1357–1364; http://dx.doi.org/10.1289/ehp.1306770
- Published
- 2013
49. Traffic-related air pollution and hyperactivity/inattention, dyslexia and dyscalculia in adolescents of the German GINIplus and LISAplus birth cohorts
- Author
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Tamara Schikowski, Joan Forns, Marie Standl, Joachim Heinrich, Dietrich Berdel, Gerd Schulte-Koerne, Dorothea Sugiri, Iana Markevych, Carla M. T. Tiesler, Judith Garcia-Aymerich, and Elaine Fuertes
- Subjects
Male ,Pediatrics ,Neurodevelopment ,010501 environmental sciences ,BEHAVIORAL-PROBLEMS ,Adolescents ,01 natural sciences ,German ,Dyslexia ,0302 clinical medicine ,DIFFICULTIES QUESTIONNAIRE ,Interquartile range ,USE REGRESSION-MODELS ,AREAS ,Germany ,030212 general & internal medicine ,Child ,lcsh:Environmental sciences ,General Environmental Science ,Vehicle Emissions ,Air pollution ,Hyperactivity ,Inattention ,lcsh:GE1-350 ,education.field_of_study ,Air Pollutants ,ESCAPE PROJECT ,Strengths and Difficulties Questionnaire ,LUNG-FUNCTION ,Motor Vehicles ,PM2.5 ABSORBENCY ,Dyscalculia ,language ,STRENGTHS ,Female ,Life Sciences & Biomedicine ,medicine.medical_specialty ,Adolescent ,NORMATIVE DATA ,Population ,Nitrogen Dioxide ,Environmental Sciences & Ecology ,03 medical and health sciences ,MD Multidisciplinary ,medicine ,Humans ,EXPOSURE ,education ,0105 earth and related environmental sciences ,Science & Technology ,Odds ratio ,medicine.disease ,language.human_language ,Confidence interval ,Attention Deficit Disorder with Hyperactivity ,Particulate Matter ,Nervous System Diseases ,Environmental Sciences - Abstract
Background: Few studies have examined the link between air pollution exposure and behavioural problems and learning disorders during late childhood and adolescence. Objectives: To determine whether traffic-related air pollution exposure is associated with hyperactivity/inattention, dyslexia and dyscalculia up to age 15 years using the German GINIplus and LISAplus birth cohorts (recruitment 1995–1999). Methods: Hyperactivity/inattention was assessed using the German parent-completed (10 years) and self-completed (15 years) Strengths and Difficulties Questionnaire. Responses were categorized into normal versus borderline/abnormal. Parent-reported dyslexia and dyscalculia (yes/no) at age 10 and 15 years were defined using parent-completed questionnaires. Individual-level annual average estimates of nitrogen dioxide (NO2), particulate matter (PM)10 mass, PM2.5 mass and PM2.5 absorbance concentrations were assigned to each participant's birth, 10 year and 15 year home address. Longitudinal associations between the air pollutants and the neurodevelopmental outcomes were assessed using generalized estimation equations, separately for both study areas, and combined in a random-effects meta-analysis. Odds ratios and 95% confidence intervals are given per interquartile range increase in pollutant concentration. Results: The prevalence of abnormal/borderline hyperactivity/inattention scores and parental-reported dyslexia and dyscalculia at 15 years of age was 12.9%, 10.5% and 3.4%, respectively, in the combined population (N = 4745). In the meta- analysis, hyperactivity/inattention was associated with PM2.5 mass estimated to the 10 and 15 year addresses (1.12 [1.01, 1.23] and 1.11 [1.01, 1.22]) and PM2.5 absorbance estimated to the 10 and 15 year addresses (1.14 [1.05, 1.25] and 1.13 [1.04, 1.23], respectively). Conclusions: We report associations suggesting a potential link between air pollution exposure and hyperactivity/inattention scores, although these findings require replication. Keywords: Adolescents, Air pollution, Hyperactivity, Inattention, Neurodevelopment
- Published
- 2016
50. Particulate matter air pollution components and risk for lung cancer
- Author
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Raaschou-Nielsen, O, Beelen, R, Wang, M, Hoek, G, Andersen, Z J, Hoffmann, B, Stafoggia, M, Samoli, E, Weinmayr, G, Dimakopoulou, K, Nieuwenhuijsen, M, Xun, W W, Fischer, P, Eriksen, K T, Sørensen, M, Tjønneland, A, Ricceri, F, de Hoogh, K, Key, T, Eeftens, M, Peeters, P H, Bueno-de-Mesquita, H B, Meliefste, K, Oftedal, B, Schwarze, P E, Nafstad, P, Galassi, C, Migliore, E, Ranzi, A, Cesaroni, G, Badaloni, C, Forastiere, F, Penell, J, De Faire, U, Korek, M, Pedersen, N, Östenson, C-G, Pershagen, G, Fratiglioni, L, Concin, H, Nagel, G, Jaensch, A, Ineichen, A, Naccarati, A, Katsoulis, M, Trichpoulou, A, Keuken, M, Jedynska, A, Kooter, I M, Kukkonen, J, Brunekreef, B, Sokhi, R S, Katsouyanni, K, Vineis, P, LS IRAS EEPI ME (Milieu epidemiologie), Dep IRAS, dIRAS RA-2, LS IRAS EEPI ME (Milieu epidemiologie), Dep IRAS, dIRAS RA-2, and Commission of the European Communities
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Male ,Pathology ,Lung Neoplasms ,010504 meteorology & atmospheric sciences ,air pollution ,010501 environmental sciences ,01 natural sciences ,Cohort Studies ,Environmental Science(all) ,Nickel ,USE REGRESSION-MODELS ,AREAS ,Prospective Studies ,SPATIAL VARIATION ,Non-U.S. Gov't ,Prospective cohort study ,lcsh:Environmental sciences ,General Environmental Science ,Inhalation exposure ,lcsh:GE1-350 ,Air Pollutants ,Inhalation Exposure ,Research Support, Non-U.S. Gov't ,Incidence ,Hazard ratio ,ELEMENTAL COMPOSITION ,Air pollution ,Cohort study ,Lung cancer ,Particulate matter ,Sulfur ,Adult ,Aged ,Environmental Exposure ,Europe ,Female ,Humans ,Middle Aged ,Particle Size ,Particulate Matter ,Proportional Hazards Models ,Risk ,ESCAPE PROJECT ,Environmental exposure ,ASSOCIATION ,Particulates ,LONG-TERM EXPOSURE ,Multicenter Study ,PM2.5 ABSORBENCY ,Cohort ,TRUCKING INDUSTRY ,Life Sciences & Biomedicine ,medicine.medical_specialty ,Environmental Sciences & Ecology ,Research Support ,complex mixtures ,nickel ,Animal science ,MD Multidisciplinary ,Journal Article ,medicine ,cohort study ,0105 earth and related environmental sciences ,particulate matter ,Science & Technology ,Proportional hazards model ,MORTALITY ,medicine.disease ,lung cancer ,sulfur ,Environmental Sciences - Abstract
Background: Particulate matter (PM) air pollution is a human lung carcinogen; however, the components responsible have not been identified. We assessed the associations between PM components and lung cancer incidence. Methods: We used data from 14 cohort studies in eight European countries. We geocoded baseline addresses and assessed air pollution with land-use regression models for eight elements (Cu, Fe, K, Ni, S, Si, V and Zn) in size fractions of PM2.5 and PM10. We used Cox regression models with adjustment for potential confounders for cohort-specific analyses and random effect models for meta-analysis. Results: The 245,782 cohort members contributed 3,229,220 person–years at risk. During follow-up (mean, 13.1 years), 1878 incident cases of lung cancer were diagnosed. In the meta-analyses, elevated hazard ratios (HRs) for lung cancer were associated with all elements except V; none was statistically significant. In analyses restricted to participants who did not change residence during follow-up, statistically significant associations were found for PM2.5 Cu (HR, 1.25; 95% CI, 1.01–1.53 per 5 ng/m3), PM10 Zn (1.28; 1.02–1.59 per 20 ng/m3), PM10 S (1.58; 1.03–2.44 per 200 ng/m3), PM10 Ni (1.59; 1.12–2.26 per 2 ng/m3) and PM10 K (1.17; 1.02–1.33 per 100 ng/m3). In two-pollutant models, associations between PM10 and PM2.5 and lung cancer were largely explained by PM2.5 S. Conclusions: This study indicates that the association between PM in air pollution and lung cancer can be attributed to various PM components and sources. PM containing S and Ni might be particularly important. Keywords: Air pollution, Particulate matter, Sulfur, Nickel, Cohort study, Lung cancer
- Published
- 2016
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