AIRGENE - AIR POLLUTION AND INFLAMMATORY RESPONSE IN MYOCARDIAL INFARCTION SURVIVORS: GENE-ENVIRONMENT INTERACTION IN A HIGH RISK GROUP

Abstract

ISEE-165 Introduction: Epidemiological research during the last decade has indicated that exposure to air pollution at the levels presently measured in Europe is associated with an increase in respiratory and cardiovascular morbidity and mortality. However, susceptibility to ambient air pollution may vary between individuals. Methods: The AIRGENE study, a longitudinal study of myocardial infarction survivors was conducted in 6 European cities to study the association between ambient air pollution concentrations and inflammatory markers as indicators of early biological responses. In addition, it aims to assess the potential role of candidate gene polymorphisms. DNA will be analysed for polymorphisms of candidate genes involved in the regulation of inflammatory response, which may potentially modify the susceptibility of individuals to environmental exposures. Outcomes of interest will be plasma concentrations of inflammatory biomarkers such as interleukin 6 as well as acute phase proteins such as C-reactive protein and fibrinogen. Results: 1105 myocardial infarction survivors aged 35 to 80 were recruited in Athens, Greece, Augsburg, Germany, Barcelona, Spain, Helsinki, Finland, Rome, Italy and Stockholm, Sweden. Baseline examinations characterised the patients with respect to classical cardiovascular disease risk factors, disease history and medication intake. In total, 6321 repeated blood samples were collected in order to assess the variability of inflammatory markers in association with ambient particle mass and particle number concentrations as well as gaseous pollutants. The data collecting period spans the time from May 2003 to July 2004. Each subject has data for a minimum of 2 repeated blood samples, and a maximum of 8 samples. Data processing and sample analyses are ongoing. Conclusion: A large database on myocardial infarction survivors has been compiled and quality assurance measures proved to be successful. We foresee we will be able to evaluate the role of air pollution in inducing inflammatory responses, and to determine the role of genetic variability in inflammatory pathways as a potential effect modifier.