Smoking/Tobacco Use

In 2015, about 15% of the U.S. population age 18 years and over were currently cigarette smokers. Current smoking increases the risk of stroke 2-4-fold times compared to nonsmokers or former smokers who have quit for >10 years. Specifically, cigarette smoking has been shown to be an independent risk factor for both ischemic stroke and subarachnoid hemorrhage (data on intracerebral hemorrhage are inconsistent). The risk in heavy smokers is somewhat greater than in light smokers. Exposure to secondhand smoke also increases stroke risk about 30%. The health risks of e-cigarettes are not yet fully understood. When an individual quits smoking, stroke risk begins decreasing almost immediately, and after 10 years drops to nearly that of a nonsmoker. 

Populations at special risk

Cigarette smoking increases the stroke risk of individuals with high blood pressure. Smokers using low-estrogen oral contraception also have increased stroke risk. Even nonsmoking, normotensive women have a slightly increased stroke risk associated with these oral contraceptives, but the absolute risk is extremely small – smaller than the stroke risk associated with pregnancy.

Relationship to stroke pathogenesis

Cigarette smoke contains carbon monoxide and nicotine as well as numerous additional toxic compounds. Cigarette smoking has a role in promoting the atherosclerotic process particularly in the carotid arteries. (It is thought that carbon monoxide may play a role in damaging the arterial endothelium). Smoking also causes several changes in the blood. They include increased adhesiveness and clustering of platelets, shortened platelet survival, faster clotting time, and increased viscosity of the blood, which can affect flow velocity. Many of these same changes in the blood can also be caused by short exposures to secondhand smoke; their effects are not known.