Supporting biological mechanisms Substantial biological evidence shows that components of cigarette smoke lead to endothelial injury, cell dysfunction, atherosclerosis and acute thrombosis, and decreased ability of the blood to carry oxygen.8489 Several such studies were summarised previously with regards to increased platelet aggregation and increased carotid arterial wall thickening at low cigarette consumption, and coronary heart disease and stroke may have common underlying pathways.1284 Harmful effects at low doses are further supported by studies of second-hand smoke that show adverse actions on subclinical vascular disease and thickening of carotid artery walls.89 Barnoya and Glantz describe a wide range of potential mechanisms by using a comprehensive literature review to purport that platelet and endothelial function, arterial stiffness, atherosclerosis, oxidative stress, inflammation, heart rate variability, energy metabolism, and increased infarct size are all sensitive to second-hand smoke.93 They also noted that even brief exposure to second-hand smoke has notable adverse effects on these mechanisms, compared with that in active smokers
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