Cigarette smoking increases the risk of stroke about 1.5 times, after controlling for other risk factors. The risk in heavy smokers is greater than in light smokers, and is somewhat greater for women than for men. Passive exposure to cigarette smoke may also increase stroke risk, but this has not been documented. When an individual quits smoking, their stroke risk begins to decrease almost immediately. After 5 years, ex-smokers have the same stroke risk as non-smokers.

Populations at special risk
In the US, currently 27.1% of men and 22.2% of women age 18 and over smoke. Smoking prevalence is even higher among African American men and American Indians (men and women). The early forms of oral contraceptives, with higher doses (>50 micrograms) of estrogen and progestin, increased a woman's risk of stroke, especially in those who smoked heavily. However, the lower-dose oral contraceptives now being prescribed carry a much lower risk of stroke except for women who smoke or have hypertension.

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. Smokers have an increased risk of both ischemic and hemorrhagic stroke.