Cigarette smoking is a well known risk factor for cardiovascular diseases [1]. Commonly accepted pathophysiological mechanisms underlying many cigarette smoking associated adverse health effects are inflammation [2,3], oxidative stress [2,4], platelet activation [5,6] and abnormal lipid metabolism [7,8]. Suitable biomarkers of potential harm (BOPH) have been identified for these four different pathophysiological pathways: white blood cell counts (WBC) for inflammation [3,9,10], urine 8-epi-prostaglandin F2α (EPI8) for oxidative stress [11-13], urine 11-dehydro-thromboxane B2 (DEH11) for platelet activation [11,13,14], and high-density lipoprotein cholesterol (HDL) for abnormal lipid metabolism [15].