Over 400,000 individuals die prematurely each year in the United States from cigarette use; this represents approximately one out of every five deaths in the United States. Approximately 40% of cigarette smokers will die prematurely due to cigarette smoking unless they are able to quit.
The major diseases caused by cigarette smoking are listed in Table 375-1. The incidence of smoking-related diseases is proportionately greater in younger than in older smokers, particularly for coronary artery disease and stroke. At older ages, the background rate of disease in nonsmokers increases, diminishing the fractional contribution of smoking and the relative risk; however, absolute excess rates of disease mortality found in smokers compared to nonsmokers increase with increasing age. The organ damage caused by smoking and the number of smokers who die from smoking are both greater among the elderly, as one would expect from a process of cumulative injury.
Cigarette smokers are more likely than nonsmokers to develop large-vessel atherosclerosis as well as small-vessel disease. Approximately 90% of peripheral vascular disease in the nondiabetic population can be attributed to cigarette smoking, as can 50% of aortic aneurysms. In contrast, 20 to 30% of coronary artery disease and 10% of occlusive cerebrovascular disease are caused by cigarette smoking. There is a multiplicative interaction between cigarette smoking and other cardiac risk factors such that the increment in risk produced by smoking among individuals with hypertension or elevated serum lipids is substantially greater than the increment in risk produced by smoking for individuals without these risk factors.
In addition to its role in promoting atherosclerosis, cigarette smoking also increases the likelihood of myocardial infarction and sudden cardiac death by promoting platelet aggregation and vascular occlusion. Reversal of these effects may explain the rapid benefit of smoking cessation for a new coronary event demonstrable among those who have survived a first myocardial infarction. This effect may also explain the substantially higher rates of graft occlusion among continuing smokers following vascular bypass surgery for cardiac or peripheral vascular disease, as well as the high failure rate of angioplasty procedures among continuing smokers.
Cessation of cigarette smoking reduces the risk of a second coronary event within 6 to 12 months; rates of first myocardial infarction or death from coronary heart disease also decline within the first few years following cessation. After 15 years of cessation, the risk of a new myocardial infarction or death from coronary heart disease in former smokers is similar to that for those who have never smoked.
Tobacco smoking causes cancer of the lung, oral cavity, naso-, oro-, and hypopharynx, nasal cavity and paranasal sinuses, larynx, esophagus, stomach, pancreas, liver, kidney (body and pelvis), ureter, urinary bladder, and uterine cervix and also causes myeloid leukemia. There is evidence suggesting that cigarette smoking may play a role in increasing the risk of colorectal and possibly breast cancer. There does not appear to be a causal link between cigarette smoking and cancer of the endometrium, and there is a lower risk of uterine cancer among postmenopausal women who smoke. The risks of cancer increase with the increasing number of cigarettes smoked per day and with increasing duration of smoking, and there are synergistic interactions between cigarette smoking and alcohol use for cancer of the oral cavity, esophagus, and possibly lung. Several occupational exposures also synergistically increase lung cancer risk among cigarette smokers, most notably occupational asbestos and radon exposure.
Cessation of cigarette smoking reduces the risk of developing cancer relative to continuing smoking, but even 20 years after cessation there is a modest persistent increased risk of developing lung cancer.
Cigarette smoking is responsible for 90% of chronic obstructive pulmonary disease. Within 1 to 2 years of beginning to smoke regularly, many young smokers will develop inflammatory changes in their small airways, although lung function measures of these changes do not predict development of chronic airflow obstruction. After 20 years of smoking, pathophysiologic changes in the lungs develop and progress proportional to smoking intensity and duration. Chronic mucous hyperplasia of the larger airways results in a chronic productive cough in as many as 80% of smokers over age 60. Chronic inflammation and narrowing of the small airways and/or enzymatic digestion of alveolar walls resulting in pulmonary emphysema can result in reduced expiratory airflow sufficient to produce clinical symptoms of respiratory limitation in 15% of smokers.
Changes in the small airways of young smokers will reverse after 1 to 2 years of cessation. There may also be a small increase in measures of expiratory airflow among individuals who have developed chronic airflow obstruction, but the major change following cessation is a slowing of the rate of decline in lung function with advancing age rather than a return of lung function toward normal.
Cigarette smoking is associated with several maternal complications of pregnancy: premature rupture of membranes, abruptio placentae, and placenta previa; there is also a small increase in the risk of spontaneous abortion among smokers. Infants of smoking mothers are more likely to experience preterm delivery, have a higher perinatal mortality, are small for their gestational age, have higher rates of infant respiratory distress syndrome, are more likely to die of sudden infant death syndrome, and appear to have a developmental lag for at least the first several years of life.
Smoking delays healing of peptic ulcers; increases the risk of osteoporosis, senile cataracts, and macular degeneration; and results in premature menopause, wrinkling of the skin, gallstones and cholecystitis in women, and male impotence.
Environmental Tobacco Smoke
Long-term exposure to environmental tobacco smoke increases the risk of lung cancer and coronary artery disease among nonsmokers. It also increases the incidence of respiratory infections, chronic otitis media, and asthma in children as well as causing exacerbation of asthma in children.
Revision date: June 20, 2011
Last revised: by Janet A. Staessen, MD, PhD