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Tobacco: Medical Complications



The notion that smoking tobacco is injurious to the body is not of recent origin. King James I of England, in his classic "Counterblaste to Tobacco," written in 1604, outlined a number of beliefs about tobacco's ill effects on health and urged his subjects to avoid it. He called smoking a "filthie noveltie A custome lothsome to the eye, hatefull to the nose, harmefull to the braine, dangerous to the Lungs." Opinions on the possible benefits and health damage caused by use of tobacco varied over the next 300 years. Some nineteenth-century arguments that tobacco use injured health were linked to moral arguments against its use rather than to what today would be considered medical evidence.

In 1926 Sir Humphrey Rolleston of Cambridge University (the same Rolleston who headed the committee on the use of opioids) addressed the Harrogate Medical Society on the subject of medical aspects of tobacco and the possible toxic effects of nicotine. He drew few firm conclusions. Only a few health problems were clearly linked to tobacco. These included some irritation of the throat and upper air passages by furfural, pyridine derivatives, ammonia, and carbon monoxide, which he ascribed to combustion of vegetable material and "not, like Nicotine, in any way special to tobacco." He did mention tobacco amblyopia, a disorder of the optic nerve leading to blindness, now thought to be a rare complication. Among the heart disorders Rolleston mentioned were extrasystoles (irregular heartbeats) and angina (pain caused by insufficient blood reaching the heart). He noted that nicotine constricted coronary arteries but suggested that people who suffered from extrasystoles might consider giving up coffee and tea before tobacco. He observed that cigarette smoking could cause arterial spasms, noting that it was linked to obliterative diseases of the large arteries among young Jews living in London's East End. Rolleston believed that cancers of the lip and oral cavity observed in smokers were probably caused by syphilis and therefore not firmly linked to smoking. He devoted only a few lines to smoking's adverse effects on the respiratory tract, observing that smoking was responsible for "causing cough, hoarseness, bronchial catarrh, and so emphysema of the lungs." In general, Rolleston observed that considering "the large number of heavy smokers, the comparative rarity of undoubted lesions due to smoking is remarkable." He concluded that "to regard tobacco as a drug of addiction may be all very well in a humorous sense, but it is hardly accurate."

But even as Rolleston was lecturing, researchers were looking at the evidence suggesting that smoking was responsible for the increasing number of lung cancer cases, a rare disease in the nineteenth century. Within thirty years there would be a growing consensus among the medical scientific community that tobacco smoking was the principal cause of lung cancer, causally related to other cancers, and a major contributor to cardiovascular diseases, peripheral artery disease, and chronic obstructive lung disease (emphysema and chronic bronchitis). Yet from the 1920s to the 1960s, cigarette smoking gained almost universal social acceptance. Using doctors and nurses and health-related slogans ("not a cough in a carload") in their advertisements, cigarette manufacturers implied that cigarette smoking was without health risk. By the 1960s the majority of adult males were smokers, with more than 70 percent in some age groups.

The turning point in the public's perception of the adverse consequences of tobacco smoking came with the publication of the Report of the Royal College of Physicians in England in 1962 and the Report of the Surgeon General in the United States in 1964. These two reports documented the experimental, epidemiological, and pathological evidence linking tobacco smoking to a variety, of diseases, the most notable of which were lung cancer, illness and death from heart disease, and chronic bronchitis and other lung disorders. Many more reports on the health consequences of smoking followed these two pivotal publications. Since 1969 the Office of Smoking and Health of the U.S. Public Health Service has coordinated the annual publication of a Surgeon General's Report on the health consequences of smoking, with several of the reports focusing on specific topics. In approaching such major reviews of specific health consequences of smoking, the Office of Smoking and Health assigns recognized experts to review and summarize all the existing scientific literature on the topic and then draw some conclusions from it. Some of the special topics that have been considered are health consequences of smoking for women (1980), the changing cigarette (the implications for health of low tar/nicotine cigarettes and filters) (1981), chronic obstructive lung disease (1984), cancer and chronic lung disease in the workplace (1985), and nicotine addiction (1988). The 1972 report was the first to explore the health consequences of involuntary smoking (passive or secondhand smoking).

The 1979 and 1989 reports were overall reviews of the field, marking the fifteenth and twenty-fifth anniversaries of the landmark 1969 report produced when Dr. Luther Terry was Surgeon General. The 1979 report described tobacco smoking as "the largest preventable cause of death in America." It noted that statisticians were able to identify the following as deaths related to smoking: 80,000 each year from lung cancer; 22,000 from other cancers; up to 225,000 from cardiovascular disease; and more than 119,000 from chronic pulmonary disease. As of 2000, cigarette smoking remained the most important cause of preventable disease and premature death in the developed countries of the world. It is estimated that, depending on the age at which a person starts to smoke, 7 to 13 years of life are lost to smoking-related diseases. Nonetheless, nearly 47 million Americans continue to smoke.


The Pharmacological Actions of Nicotine.

Nicotine, the addictive component in tobacco, is a colorless liquid alkaloid that turns brown and begins to smell like tobacco when it is exposed to air. In addition to the psychological and social dimensions of tobacco dependence, nicotine by itself produces reinforcement. It has both stimulant and depressant effects on the body, and stimulates the release of endogenous opioids. Nicotine has negative as well as positive reinforcement effects. Negative reinforcement refers to the fact that smoking for some persons is related as much to avoidance of the discomfort of nicotine withdrawal as to seeking the pleasurable effects of nicotine.

Nicotine is quickly absorbed through the skin, mucous membranes, and lungs. Absorption through the lungs produces measurable effects on the central nervous system in as little as 7 seconds. This rapid rate of absorption means that each puff on a cigarette produces some reinforcement of the smoking habit.

Pure nicotine is a poison that can kill within minutes by causing respiratory failure. Nicotine poisoning most commonly results from accidental ingestion of insecticides containing nicotine. A fatal dose of nicotine for an adult is 40 to 60 mg.


Tobacco smoking has been shown to be the major cause of lung cancer in both men and women. The increased risk for lung cancer is directly related to the amount smoked. The risk of death from lung cancer is about twenty times greater for men who smoke two packs a day than for those who have never smoked. It is about ten times higher for those who smoke one-half to one pack a day. Depth of inhalation also influences risk of disease. Tobacco smoking is synergistic (produces a multiplier effect) with the effects of other carcinogenic risks, such as exposure to radon or asbestos. Smoking is also synergistic with alcohol in causing cancers of the oral cavity, larynx, pharynx, and esophagus.

Cardiovascular Disease.

Smoking is one of three major causes of coronary heart disease (CHD); risk of death from CHD is 70 percent higher for men who smoke, with a similar effect for women. The risk due to smoking increases if there are risk factors present such as hypertension and elevated cholesterol levels. Smoking increases risk for stroke. For example, women who smoke twenty-five cigarettes or more per day have a risk for stroke almost four times higher than nonsmokers. Smoking also increases the risk of atherosclerosis (formation of plaques) in the peripheral arteries and the aorta. In peripheral arteries this condition can lead to insufficient oxygen reaching the muscles; in the aorta it can lead to a rupture that is usually fatal.

Lung Disease.

The link between tobacco smoking and chronic obstructive pulmonary disease (COPD) was noted in the 1964 Surgeon General's Report. COPD includes three related disorders: chronic mucous hypersecretion that causes cough and phlegm production; airway thickening and obstruction of expiratory airflow; and emphysemaabnormal dilation of air sacs and destruction of walls of the alveoli. Compared to nonsmokers, male smokers are three times more likely and female smokers are twice as likely to have a persistent cough.

Other Medical Disorders.

These include peptic ulcers, upper respiratory infections, osteoporosis, and cancers of the pancreas, bladder, and esophagus.

The toxic properties and carcinogenic effects of tobacco smoke and its constituents have been studied in the laboratory using animals. The evidence linking tobacco use to death and disease in humans, however, relies heavily on epidemiological studies comparing the rates of various diseases as they occur in smokers versus nonsmokers, in light versus heavy smokers, and in continuing versus former smokers. The level of certainty that links tobacco use to a particular disease varies. Shopland and Burns (1993) have grouped diseases according to their established epidemiological association with cigarette smoking in five categories. These are outlined below.

Category A.

Diseases for which a direct causal association has been firmly established and smoking is considered the major single contributor to excess mortality from the disease: cancers of the lung, larynx, pharynx (oral cavity), and esophagus; chronic obstructive pulmonary disease, including emphysema; peripheral vascular disease

Category B.

Diseases for which a direct causal association has been firmly established but for which smoking is only one of several causes: stroke; coronary heart disease; cancers of the bladder and pancreas; aortic aneurysm; perinatal mortality

Category C.

Diseases for which an increased risk (association) has been demonstrated but a risk whose exact nature has not been firmly established: cancers of the cervix, uterus, stomach, and liver; gastric and duodenal ulcers; pneumonia; sudden infant death syndrome

Category D.

Diseases for which excess mortality in smokers has been observed but for which this observation is attributed to confounding variables (other factors that are commonly found among smokers): alcoholism; cirrhosis of the liver; poisoning; suicide

Category E.

Diseases for which smokers have lower death rates than nonsmokers: endometrial cancer; Parkinson's disease; ulcerative colitis

The effects of tobacco use are not limited to specific diseases that lead to death. Tobacco use can stimulate enzymes in the liver, and this stimulation can result in alterations in the way various medications are metabolized. This alteration in metabolism can mean that the levels of medications in the body will not be high enough to be optimally therapeutic.

The overall increased mortality from smoking varies with the amount smoked. For those who smoke two or more packs of cigarettes per day, it is about double that of nonsmokers; for those who smoke less, it is about 1.7 times higher than for nonsmokers. The risk for various diseases can be powerfully affected by cessation, but not all risks decline at the same rate. Cardiovascular disease risk decreases markedly within a year of quitting smoking; risks of cancer decline more slowly, with some elevated risk still evident ten years after cessation. By ten to fifteen years after quitting, overall mortality of former smokers is not much higher than that of nonsmokers. Increased mortality rates are not as marked for pipe and cigar smokers, but they are still substantially elevated. The mortality risk for users of smokeless tobacco comes primarily from cancers of the oral cavity and throat.

The adverse effects of passive inhalation (second-hand smoke) are not considered here except in connection with the higher incidence of respiratory illness among the infants of mothers who smoke. But there is no question that there are differences in composition of mainstream smoke (the smoke inhaled by the smoker), sidestream smoke (produced by tobacco burning between puffs), and environmental smoke (the mixture of exhaled mainstream and sidestream smoke). Sidestream smoke is produced at lower combustion temperatures and has higher concentrations of carbon monoxide and organic constituents believed to be carcinogenic.

Psychiatric Disorders.

Dependence on tobacco is associated with dysthymic disorder and other forms of depression. It is not yet known, however, whether depression prompts people to begin smoking or whether it develops in the course of dependence on tobacco. Mood disorders increase significantly during withdrawal from nicotine, and are common reasons for relapse.


Women who smoke tobacco have the same risks for adverse effects as men. The early impression that women suffered fewer adverse effects from smoking was really due to lower levels of exposure (fewer women smokers and a tendency of women smokers to smoke less heavily.) As has been written more than once, women who smoke like men die like men. In 1986 deaths due to lung cancer among women exceeded deaths from breast cancer, becoming the leading cause of cancer death for women. Some women are at special risk. It has been documented that while the use of oral contraceptives alone does not constitute a serious health risk, the combination of oral contraceptives and cigarette smoking raises substantially the risk of cardiovascular disease, including subarachnoid hemorrhage (bleeding inside the skull).

Women who smoke have higher infertility rates than those who do not and are also more likely to have menstrual irregularities. Nicotine crosses the placenta, and because it constricts blood vessels, a decreased amount of oxygen is delivered to the fetus. In addition, smoking elevates the amount of carbon monoxide in the mother's blood so that it carries less oxygen to the fetus. Women who smoke during pregnancy have higher rates of premature detachment of the placenta (abruptio placentae), premature rupture of membranes, and preterm delivery. The greater the amount of tobacco smoked during the pregnancy, the higher the frequency of spontaneous abortion and fetal death. In the United States smoking has been associated with a 20 percent increase in preterm births among women who smoked a pack a day or more compared with those who did not smoke.

There is no consensus on whether smoking increases the probability of congenital malformations. However, it is well established that babies born to women who smoke during pregnancy weigh on average about seven ounces less than those born to nonsmokers. Apgar scores, a composite of measurements of the breathing, skin color, and reflexes of infants taken at one and five minutes after delivery, are lower for babies of women who smoked during pregnancy. Women who stop smoking early in pregnancy increase their likelihood of having normal deliveries and normal-birth-weight babies. Interestingly, epidemiological data suggest that passive smoke exposure during pregnancy (e.g., living with a smoker) can adversely affect birth weight of the baby. Infants born to mothers who smoke are far more likely to die before their first birthday, primarily as a result of respiratory complications and sudden infant death syndrome. Children of mothers who smoke seem in general more likely to suffer from colds, asthma, bronchitis, pneumonia, and other respiratory problems.

Efforts to educate the public about the health consequences of smoking, including smoking-prevention programs directed at young people and encouragement of smokers to quit, have led to a reduction in the prevalence of smoking in the United States and in several European countries since the mid-1960s. In general, white males in higher socioeconomic groups have lowered their smoking rate more than women and members of ethnic and racial minorities and lower socioeconomic groups. By the early 1960s lung cancer deaths among African-American men exceeded those among white men; by 1990 it was 30 percent higher. The lung cancer rate among both African-American and white women was virtually the same, reflecting similar smoking patterns. On the other hand, smoking rates are increasing in younger age groups in the United States. The rates of smoking have increased from 34.6 percent of the young adult population (aged 18-25) in 1994 to 40.6 percent in 1997 and 41.6 percent in 1998. An estimated 18.2 percent of young people in the 12-17 age bracket were smokers in 1998.

In contrast to the general decline of smoking in the West, the prevalence of smoking may actually be increasing in developing and newly industrialized countries where, even among medical students, cigarette smoking retains a cachet of sophistication and affluence.

(See also: Advertising and Tobacco Use ; Complications ; Nicotine ; Treatment: Tobacco )


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Jerome H. Jaffe

Donald R. Shopland

Revised by Rebecca J. Frey

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