During the past years several factors have been established as risk markers for the development of heart disease, including both active and passive smoking. Current evidence has indicated that exposure to passive smoking can lead to a 70-80% increase in the risk of coronary heart disease, nearly as much as light smoking. This disproportionate effect could possibly be explained by a number of different interactions between human physiology of the cardiovascular system and passive smoke exposure. In this review we present the different mechanisms through which passive smoking may induce an inflammatory response that may lead to the development of cardiovascular disease, on a whole and through certain of its toxic constituents. Passive smoke itself, is a volatile mixture of numerous toxins, chemicals and carcinogens, that interact with in vivo mechanisms and induce vascular damage, including endothelium inflammation, atherosclerosis development, lipid peroxidisation, alterations in cytokines and acute phase proteins (such as CRP), as well as platelet aggravation. Acting alone or in synergy, the above mentioned effects suggest a causal relationship between exposure to passive smoking and the development of cardiovascular disease.