Regina Hampel1, Annette Peters2, Rob Beelen3, Bert Brunekreef4, Josef Cyrys5, Ulf de Faire6, Kees de Hoogh7, Kateryna Fuks8, Barbara Hoffmann9, Anke Hüls8, Medea Imboden10, Aleksandra Jedynska11, Ingeborg Kooter11, Wolfgang Koenig12, Nino Künzli10, Karin Leander6, Patrik Magnusson13, Satu Männistö14, Johanna Penell6, Göran Pershagen6, Harish Phuleria15, Nicole Probst-Hensch10, Noreen Pundt16, Emmanuel Schaffner10, Tamara Schikowski17, Dorothea Sugiri8, Pekka Tiittanen18, Ming-Yi Tsai10, Meng Wang3, Kathrin Wolf2, Timo Lanki18. 1. Institute of Epidemiology II, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany. Electronic address: regina.hampel@helmholtz-muenchen.de. 2. Institute of Epidemiology II, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany. 3. Institute for Risk Assessment Sciences, Division Environmental Epidemiology, Utrecht University, Utrecht, The Netherlands. 4. Institute for Risk Assessment Sciences, Division Environmental Epidemiology, Utrecht University, Utrecht, The Netherlands; Department of Epidemiology, Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, The Netherlands. 5. Institute of Epidemiology II, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany; ESC-Environmental Science Center, University of Augsburg, Augsburg, Germany. 6. Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden. 7. MRC-PHE Centre for Environment and Health, Department of Epidemiology and Biostatistics, Imperial College London, London, UK. 8. IUF Leibniz Research Institute for Environmental Medicine, Düsseldorf, Germany. 9. Medical School, The Heinrich Heine University of Düsseldorf, Düsseldorf, Germany. 10. Swiss Tropical and Public Health Institute, Basel, Switzerland; University of Basel, Basel, Switzerland. 11. The Netherlands Organisation for Applied Scientific Research, Utrecht, The Netherlands. 12. Department of Internal Medicine II - Cardiology, University of Ulm Medical Center, Ulm, Germany; Deutsches Herzzentrum München, Technische Universität München, Munich, Germany; DZHK (German Centre for Cardiovascular Research), Partner Site Munich Heart Alliance, Munich, Germany. 13. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. 14. Department of Chronic Disease Prevention, National Institute for Health and Welfare (THL), Helsinki, Finland. 15. Swiss Tropical and Public Health Institute, Basel, Switzerland. 16. Institute for Medical Informatics, Biometry and Epidemiology, University Hospital Essen, Essen, Germany. 17. IUF Leibniz Research Institute for Environmental Medicine, Düsseldorf, Germany; Swiss Tropical and Public Health Institute, Basel, Switzerland; University of Basel, Basel, Switzerland. 18. Department of Health Protection, National Institute for Health and Welfare (THL), Kuopio, Finland.
Abstract
BACKGROUND: Epidemiological studies have associated long-term exposure to ambient particulate matter with increased mortality from cardiovascular and respiratory disorders. Systemic inflammation is a plausible biological mechanism behind this association. However, it is unclear how the chemical composition of PM affects inflammatory responses. OBJECTIVES: To investigate the association between long-term exposure to elemental components of PM and the inflammatory blood markers high-sensitivity C-reactive protein (hsCRP) and fibrinogen as part of the European ESCAPE and TRANSPHORM multi-center projects. METHODS: In total, 21,558 hsCRP measurements and 17,428 fibrinogen measurements from cross-sections of five and four cohort studies were available, respectively. Residential long-term concentrations of particulate matter <10μm (PM10) and <2.5μm (PM2.5) in diameter and selected elemental components (copper, iron, potassium, nickel, sulfur, silicon, vanadium, zinc) were estimated based on land-use regression models. Associations between components and inflammatory markers were estimated using linear regression models for each cohort separately. Cohort-specific results were combined using random effects meta-analysis. As a sensitivity analysis the models were additionally adjusted for PM mass. RESULTS: A 5ng/m(3) increase in PM2.5 copper and a 500ng/m(3) increase in PM10 iron were associated with a 6.3% [0.7; 12.3%] and 3.6% [0.3; 7.1%] increase in hsCRP, respectively. These associations between components and fibrinogen were slightly weaker. A 10ng/m(3) increase in PM2.5 zinc was associated with a 1.2% [0.1; 2.4%] increase in fibrinogen; confidence intervals widened when additionally adjusting for PM2.5. CONCLUSIONS: Long-term exposure to transition metals within ambient particulate matter, originating from traffic and industry, may be related to chronic systemic inflammation providing a link to long-term health effects of particulate matter.
BACKGROUND: Epidemiological studies have associated long-term exposure to ambient particulate matter with increased mortality from cardiovascular and respiratory disorders. Systemic inflammation is a plausible biological mechanism behind this association. However, it is unclear how the chemical composition of PM affects inflammatory responses. OBJECTIVES: To investigate the association between long-term exposure to elemental components of PM and the inflammatory blood markers high-sensitivity C-reactive protein (hsCRP) and fibrinogen as part of the European ESCAPE and TRANSPHORM multi-center projects. METHODS: In total, 21,558 hsCRP measurements and 17,428 fibrinogen measurements from cross-sections of five and four cohort studies were available, respectively. Residential long-term concentrations of particulate matter <10μm (PM10) and <2.5μm (PM2.5) in diameter and selected elemental components (copper, iron, potassium, nickel, sulfur, silicon, vanadium, zinc) were estimated based on land-use regression models. Associations between components and inflammatory markers were estimated using linear regression models for each cohort separately. Cohort-specific results were combined using random effects meta-analysis. As a sensitivity analysis the models were additionally adjusted for PM mass. RESULTS: A 5ng/m(3) increase in PM2.5 copper and a 500ng/m(3) increase in PM10 iron were associated with a 6.3% [0.7; 12.3%] and 3.6% [0.3; 7.1%] increase in hsCRP, respectively. These associations between components and fibrinogen were slightly weaker. A 10ng/m(3) increase in PM2.5 zinc was associated with a 1.2% [0.1; 2.4%] increase in fibrinogen; confidence intervals widened when additionally adjusting for PM2.5. CONCLUSIONS: Long-term exposure to transition metals within ambient particulate matter, originating from traffic and industry, may be related to chronic systemic inflammation providing a link to long-term health effects of particulate matter.
Authors: Mohammad Nayeb Yazdi; Mohammad Arhami; Maryam Delavarrafiee; Mehdi Ketabchy Journal: Environ Sci Pollut Res Int Date: 2018-11-07 Impact factor: 4.223
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Authors: Aurore Lavigne; Anna Freni-Sterrantino; Daniela Fecht; Silvia Liverani; Marta Blangiardo; Kees de Hoogh; John Molitor; Anna L Hansell Journal: Environ Epidemiol Date: 2020-07-16