Tobacco, Cardiopulmonary Vascular Disease, and Aging

Smoking causes disease through oxidative stress, which accelerates aging. Recently, chronic obstructive pulmonary disease (COPD), emblematic of tobacco-related diseases, has come to be viewed as a systemic inflammatory disease. COPD is regarded as contributory to cardiovascular events stemming from vascular inflammation. As an independent risk factor for cardiovascular disease, COPD in combination with smoking also raises cardiovascular risk synergistically. Vascular endotheliopathy caused by tobacco is also closely related to decreases in endothelial progenitor cells (EPC) and elevated cardiovascular risk. α1-antitrypsin-LDL (AT-LDL), an oxidized/modified LDL that contributes to development of arteriosclerosis, is also elevated in smokers. Tobacco-induced cardiopulmonary vascular disease entities are in this way interrelated and deemed to create a vicious circle. The EPC reduced in smokers recovers rapidly after smoking cessation, and increased AT-LDL also decreases after smoking cessation. Smoking cessation is thus essential to breaking this vicious circle. In the interest of arresting and preventing aging and disease, we hope to deepen understanding of smoking cessation among smokers through patient-based awareness.