دورية أكاديمية

Interaction between air pollution exposure and genes in relation to levels of inflammatory markers and risk of myocardial infarction

التفاصيل البيبلوغرافية
العنوان: Interaction between air pollution exposure and genes in relation to levels of inflammatory markers and risk of myocardial infarction
المؤلفون: Panasevich, Sviatlana, Leander, Karin, Ljungman, Petter, Bellander, Tom, de Faire, Ulf, Pershagen, Göran, Nyberg, Fredrik
المصدر: BMJ Open ; volume 3, issue 9, page e003058 ; ISSN 2044-6055 2044-6055
بيانات النشر: BMJ
سنة النشر: 2013
الوصف: Objectives Air pollution exposure induces cardiovascular effects, possibly via systemic inflammation and coagulation misbalance. Genetic variation may determine individual susceptibility. Our aim was to investigate effect modification by inflammation ( Interleukin6 (IL6) , tumour necrosis factor-α (TNF-α) ) and coagulation ( fibrinogen Bβ , plasminogen activator inhibitor-1 ( PAI-1) ) gene variants on the effect of long-term or short-term air pollution exposure on both blood marker levels and non-fatal myocardial infarction (MI) risk. Design Population-based case–control study with a nested case-crossover study. Gene-environment interactions for short-term and long-term air pollution on blood marker levels were studied in population controls, for long-term exposure on MI risk using case–control design, and for short-term exposure on MI onset using case-crossover design. Setting The Stockholm Heart Epidemiology Programme (SHEEP) conducted in 1992–1994 in Stockholm, Sweden. Spatial modelling was used to assess long-term (up to 30 years retrospectively) air pollution exposure to traffic-NO 2 and heating-SO 2 emissions at home addresses. Urban background NO 2 , SO 2 , PM 10 and O 3 measurements were used to estimate short-term (up to 5 days) air pollution exposure. Participants 1192 MI cases and 1506 population controls aged 45–70 years. Outcomes The levels of blood markers of inflammation (IL-6, TNF-α) and coagulation (fibrinogen, PAI-1) and MI risk. Results We observed gene–environment interaction for several IL6 and TNF SNPs in relation to inflammation blood marker levels. One-year traffic-NO 2 exposure was associated with higher IL-6 levels with each additional IL6 -174C allele, and 1-year heating-SO 2 exposure with higher levels of TNF-α in TNF -308AA homozygotes versus −308G carriers. Short-term air pollution exposure also interacted with IL6 and TNF in relation to marker levels. The risk of MI followed the effect on blood markers in each genotype group. Conclusions Genetic variants in IL6 and TNF may modify ...
نوع الوثيقة: article in journal/newspaper
اللغة: English
DOI: 10.1136/bmjopen-2013-003058
الإتاحة: https://doi.org/10.1136/bmjopen-2013-003058Test
رقم الانضمام: edsbas.3BA1C271
قاعدة البيانات: BASE