Vanessa J Soppa1, Samir Shinnawi2, Frauke Hennig3, Birgitta Sasse4, Bryan Hellack5, Heinz Kaminski6, Ulrich Quass7, Roel P F Schins8, Thomas A J Kuhlbusch9, Barbara Hoffmann10. 1. Institute for Occupational, Social and Environmental Medicine, Center for Health and Society, Heinrich Heine University of Düsseldorf, 40225, Düsseldorf, Germany. Electronic address: vanessa.soppa@uni-duesseldorf.de. 2. Institute for Occupational, Social and Environmental Medicine, Center for Health and Society, Heinrich Heine University of Düsseldorf, 40225, Düsseldorf, Germany. Electronic address: samir.shinnawi@uni-duesseldorf.de. 3. Institute for Occupational, Social and Environmental Medicine, Center for Health and Society, Heinrich Heine University of Düsseldorf, 40225, Düsseldorf, Germany. Electronic address: frauke.hennig@uni-duesseldorf.de. 4. Institute for Occupational, Social and Environmental Medicine, Center for Health and Society, Heinrich Heine University of Düsseldorf, 40225, Düsseldorf, Germany. Electronic address: birgitta.sasse@uni-duesseldorf.de. 5. Federal Environment Agency of Germany, Paul-Ehrlich-Str. 29, 63225, Langen, Germany; Institute of Energy and Environmental Technology (IUTA) e.V., 47229, Duisburg, Germany. Electronic address: bryan.hellack@uba.de. 6. Institute of Energy and Environmental Technology (IUTA) e.V., 47229, Duisburg, Germany. Electronic address: kaminski@iuta.de. 7. LANUV - Landesamt für Natur, Umwelt und Verbraucherschutz Nordrhein-Westfalen Fachbereich 44, 45133, Essen, Germany. Electronic address: Ulrich.Quass@lanuv.nrw.de. 8. IUF-Leibniz Research Institute for Environmental Medicine, 40225, Düsseldorf, Germany. Electronic address: roel.schins@IUF-Duesseldorf.de. 9. Federal Institute for Occupational Safety and Health (BAuA), 44149, Dortmund, Germany; CENIDE - Center for Nanointegration, 47057, Duisburg, Germany. Electronic address: Kuhlbusch.Thomas@baua.bund.de. 10. Institute for Occupational, Social and Environmental Medicine, Center for Health and Society, Heinrich Heine University of Düsseldorf, 40225, Düsseldorf, Germany. Electronic address: b.hoffmann@uni-duesseldorf.de.
Abstract
OBJECTIVES: Particulate air pollution is linked to adverse cardiovascular effects, including arterial stiffness. The aim of the study was to investigate the effect of short-term exposure to indoor fine and ultrafine particles on augmentation index (AIx), augmentation pressure (AP), and pulse wave velocity (PWV), early signs of vascular damage. METHODS: We analyzed the association of particle emissions from typical indoor sources (candle burning - CB, toasting bread - TB, and frying sausages - FS) with changes in pulse wave analysis indices in 55 healthy adults in a randomized cross-over controlled exposure study. Particle mass concentration (PMC), size-specific particle number concentration (PNC) and lung-deposited particle surface area concentration (PSC) were measured during the 2 h exposure. AIx and AP were measured before, directly, 2, 4 and 24 h after exposure. PWV was measured directly and 24 h after exposure. We performed multiple mixed linear regression analyses of different particle metrics and AIx, AP and PWV. RESULTS: The highest mean PMC was observed during FS reaching a maximum of 210 μg/m3 PM10. The maximal PNC for UFP <100 nm was reached during CB with 2.3 million particles/cm3. PSC was similar across all three exposures (about 3000 μm2/cm³). Strongest associations between different particles metrics and arterial stiffness indices could be observed for UFP from CB and FS and for PMC from TB. The highest mean increase could be observed for the UFP fraction <10 nm, measured during CB, and AIx with an increase of 9.5%-points (95%-CI: 3.1; 15.9). PSC seemed to follow the pattern of PNC. PM10 and PM2.5 from TB led to clear changes in AIx with biggest increases for PM10 of 5.8%-points (95%-CI: 3.2; 8.4) 2 h after exposure and for PM2.5 of 8.1%-points (95%-CI: 2.5; 13.7) directly after exposure. CONCLUSIONS: Our study indicates effects of indoor exposure to fine and ultrafine particles on systemic arterial stiffness indices that depend on the indoor source as well as on particle metric. Differences in size-specific physical characteristics of source-specific particles might account for these differential effects. We did not observe clear and stable associations of indoor particle exposure and PWV.
RCT Entities:
OBJECTIVES: Particulate air pollution is linked to adverse cardiovascular effects, including arterial stiffness. The aim of the study was to investigate the effect of short-term exposure to indoor fine and ultrafine particles on augmentation index (AIx), augmentation pressure (AP), and pulse wave velocity (PWV), early signs of vascular damage. METHODS: We analyzed the association of particle emissions from typical indoor sources (candle burning - CB, toasting bread - TB, and frying sausages - FS) with changes in pulse wave analysis indices in 55 healthy adults in a randomized cross-over controlled exposure study. Particle mass concentration (PMC), size-specific particle number concentration (PNC) and lung-deposited particle surface area concentration (PSC) were measured during the 2 h exposure. AIx and AP were measured before, directly, 2, 4 and 24 h after exposure. PWV was measured directly and 24 h after exposure. We performed multiple mixed linear regression analyses of different particle metrics and AIx, AP and PWV. RESULTS: The highest mean PMC was observed during FS reaching a maximum of 210 μg/m3 PM10. The maximal PNC for UFP <100 nm was reached during CB with 2.3 million particles/cm3. PSC was similar across all three exposures (about 3000 μm2/cm³). Strongest associations between different particles metrics and arterial stiffness indices could be observed for UFP from CB and FS and for PMC from TB. The highest mean increase could be observed for the UFP fraction <10 nm, measured during CB, and AIx with an increase of 9.5%-points (95%-CI: 3.1; 15.9). PSC seemed to follow the pattern of PNC. PM10 and PM2.5 from TB led to clear changes in AIx with biggest increases for PM10 of 5.8%-points (95%-CI: 3.2; 8.4) 2 h after exposure and for PM2.5 of 8.1%-points (95%-CI: 2.5; 13.7) directly after exposure. CONCLUSIONS: Our study indicates effects of indoor exposure to fine and ultrafine particles on systemic arterial stiffness indices that depend on the indoor source as well as on particle metric. Differences in size-specific physical characteristics of source-specific particles might account for these differential effects. We did not observe clear and stable associations of indoor particle exposure and PWV.