Analysis of inflammatory markers in adult Japanese smokers and non-smokers
Presented at II World Asthma & COPD Forum
The most important risk factor for chronic obstructive pulmonary disease (COPD) is cigarette smoking, and it has been estimated that smoking accounts for up to 95% of COPD in the developed world. However, the precise mechanisms by which smoking causes COPD are unknown. An observational study has been performed to measure biomarkers of exposure (BoExp) to cigarette smoke and biomarkers of effect (BoEff) in adult Japanese smokers and non-smokers. The main purpose of this study was to determine the levels and variability of BoEff and to understand the effect of smoking on these biomarkers. For exploratory purposes, multiplex analysis of inflammatory biomarkers was performed in plasma of study participants. These results constitute the principal focus of this abstract. This study was conducted in 9 study centres in Japan, and was performed according to the principles of good clinical practice. The site locations were selected to cover a broad geographical range. This study included adult smokers and non-smokers 30 years of age and above in a ratio of 2:1 (smokers to non-smokers). Altogether, 1098 subjects (731 smokers and 367 non-smokers) were enrolled; data from 1077 of the subjects (716 smokers and 361 non-smokers) were analysed as part of the full analysis set. Plasma samples from two visits were analysed using multiplex technology (rules based medicine). The human map™ was used to simultaneously analyse 52 analytes in each sample. Statistical analysis indicated differences between adult smokers and non-smokers in the following biomarkers: α-1 antitrypsin, intracellular adhesion molecule-1 (ICAM-1), immunoglobulin A (IgA), macrophage-derived chemokine (MDC), matrix metalloproteinases 2 and 9 (MMP-2 and MMP-9), tumour necrosis factor rii (TNF R2), and vascular cell adhesion molecule-1 (VCAM 1). This analysis provides semi-quantitative information about biomarkers affected by cigarette smoking, some of which may be involved in the pathogenesis of COPD.