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Ljungman, P.* ; Bellander, T.* ; Schneider, A.E. ; Breitner-Busch, S. ; Forastiere, F.* ; Hampel, R. ; Illig, T. ; Jacquemin, B.* ; Katsouyanni, K.* ; von Klot, S. ; Koenig, W.* ; Lanki, T.* ; Nyberg, F.* ; Pekkanen, J.* ; Pistelli, R.* ; Pitsavos, C.* ; Rosenqvist, M.* ; Sunyer, J.* ; Peters, A.

Modification of the interleukin-6 response to air pollution by interleukin-6 and fibrinogen polymorphisms.

Environ. Health Perspect. 117, 1373-1379 (2009)
Verlagsversion Volltext DOI PMC
Open Access Gold
BACKGROUND: Evidence suggests that cardiovascular effects of air pollution are mediated by inflammation and that air pollution can induce genetic expression of the interleukin-6 gene (IL6). OBJECTIVES: We investigated whether IL6 and fibrinogen gene variants can affect plasma IL-6 responses to air pollution in patients with cardiovascular disease. METHODS: We repeatedly determined plasma IL-6 in 955 myocardial infarction survivors from six European cities (n = 5,539). We conducted city-specific analyses using additive mixed models adjusting for patient characteristics, time trend, and weather to assess the impact of air pollutants on plasma IL-6. We pooled city-specific estimates using meta-analysis methodology. We selected three IL6 single-nucleotide polymorphisms (SNPs) and one SNP each from the fibrinogen alpha-chain gene (FGA) and beta-chain gene (FGB) for gene-environment analyses. RESULTS: We found the most consistent modifications for variants in IL6 rs2069832 and FBG rs1800790 after exposure to carbon monoxide (CO; 24-hr average; p-values for interaction, 0.034 and 0.019, respectively). Nitrogen dioxide effects were consistently modified, but p-values for interaction were larger (0.09 and 0.19, respectively). The strongest effects were seen 6-11 hr after exposure, when, for example, the overall effect of a 2.2% increase in IL-6 per 0.64 mg/m(3) CO was modified to a 10% (95% confidence interval, 4.6-16%) increase in IL-6 (p-value for interaction 0.002) for minor homozygotes of FGB rs1800790. CONCLUSIONS: The effect of gaseous traffic-related air pollution on inflammation may be stronger in genetic subpopulations with ischemic heart disease. This information could offer an opportunity to identify postinfarction patients who would benefit more than others from a cleaner environment and antiinflammatory treatment.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter air pollution; fibrinogen; gene-environment interaction; interleukin-6; myocardial infarction survivors; polymorphisms; myocardial-infarction survivors; coronary-artery-disease; c-reactive protein; inflammatory response; particulate matter; carbon-monoxide; heart-disease; gene; particles; health; MYOCARDIAL-INFARCTION SURVIVORS; CORONARY-ARTERY-DISEASE; C-REACTIVE PROTEIN; INFLAMMATORY RESPONSE; PARTICULATE MATTER; CARBON-MONOXIDE; HEART-DISEASE; GENE; PARTICLES; HEALTH
Sprache
Veröffentlichungsjahr 2009
HGF-Berichtsjahr 2009
ISSN (print) / ISBN 0091-6765
e-ISSN 1552-9924
Zeitschrift Environmental Health Perspectives
Quellenangaben Band: 117, Heft: 9, Seiten: 1373-1379 Artikelnummer: , Supplement: ,
Verlag Research Triangle Park
Verlagsort NC [u.a.]
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Epidemiology (EPI)
POF Topic(s)
30503 - Chronic Diseases of the Lung and Allergies
Forschungsfeld(er)
Genetics and Epidemiology
PSP-Element(e) G-503900-005
G-503900-003
DOI 10.1289/ehp.0800370
WOS ID 000269479900024
Scopus ID 69949085873
PubMed ID 19750100
Erfassungsdatum 2009-10-09
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