Nicotine dependence

Nicotine dependence

H. Thomas Milhorn, Jr.

Nicotine Dependence Nicotine is a psychoactive drug with effects that reinforce tobacco use despite known adverse health consequences. Nicotine dependence can be effectively treated. Family physicians are in an excellent position to promote both smoking cessation and smoking prevention. Nicotine is a psychoactive agent whose continued use usually leads to addiction. The pharmacologic and psychologic processes that determine nicotine addiction are similar to those that determine addiction to other drugs, such as heroin and cocaine.(1) The most common form of nicotine dependence is associated with the inhalation of cigarette smoke. Pipe and cigar smoking, tobacco chewing and the use of snuff are less likely to lead to nicotine dependence.(2) This article, therefore, focuses on cigarette smoking as the primary agent of nicotine addiction.

Cigarette smoking may be responsible for as many as 350,000 deaths annually in the United States, representing 18 percent of all deaths.(3) Total costs of smoking-related health care and lost productivity amount to approximately $65 billion each year.(4)

Despite escalating cigarette consumption worldwide, U.S. smoking rates are declining. Consumption reached a peak in the early 1960s, when 42 percent of adults smoked (52 percent of men and 34 percent of women). Per capita consumption began to drop after 1964, when the U.S. Surgeon General reported tobacco use to be a major health hazard. Currently, 26.5 percent of adults smoke (29.5 percent of men and 23.8 percent of women).(3,5,6) Despite the trend toward fewer smokers, the percentage of heavy smokers has risen considerably.(3)

Although cigarette smoking is the largest single preventable cause of death and disability in the United States, most patients report that they have not been counseled by their physicians to stop smoking. This failure occurs, in part, because physicians lack adequate training in the area of smoking cessation.(3)

Pharmacology of Nicotine

The hundreds of substances in cigarette smoke can be divided into cigarette constituents (organic matter, nicotine alkaloids, additives) and pyrolysis products (carbon dioxide, carbon monoxide, coal tar).(7) Carcinogens are found primarily in the particulate phase of smoke.(8)

The smoke itself consists of mainstream smoke, which is inhaled by the smoker directly from the cigarette, and sidestream smoke, which enters the atmosphere from the lighted end of the cigarette and is inhaled by others in the vicinity.(7) About 80 percent of environmental tobacco smoke is sidestream smoke. It contains greater concentrations of toxic and carcinogenic compounds than mainstream smoke.(8)

The average cigarette contains about 10 mg of nicotine. A variable amount, between 1 and 2 mg, is delivered to the lungs when the cigarette is smoked.(9) Absorption of nicotine by the lungs depends on the number of inhalations, the depth and duration of inhalations and pH of the smoke.(7) One puff of smoke results in a measurable nicotine level in the brain within seconds.(5) With regular use, nicotine accumulates in the body during the day and persists overnight. Nicotine readily crosses the blood-brain barrier, where it acts as an agonist on specific cholinergic receptors in the central nervous system.(4) It is metabolized in the liver, and cotinine is its major metabolite.(9)

Medical Complications

The medical complications of smoking may be divided into those resulting from mainstream smoke (active smoking) and those resulting from sidestream smoke (passive smoking). Table 1 lists diseases and conditions associated with active and passive smoking.


Cigarette smoking is associated with elevated rates of cancer of the lung, oral cavity, pharynx, larynx, esophagus, pancreas, bladder and kidney.(3,5) It is a major risk factor for coronary artery disease and other cardiovascular problems.(5) Smoking also increases the potential for serious adverse effects in women using oral contraceptives.(4)

Thromboangiitis obliterans and peptic ulcer disease are exacerbated by smoking.(3,5) The role of smoking in lung infections and chronic obstructive pulmonary disease (COPD) is well documented.(5) Although pulmonary change is progressive with chronic smoking, the severity of the damage depends on individual susceptibility.(6) Abstinence of five to ten years returns the risk of developing most smoking-related diseases to that for the non-smoking population.(5)

Smoking depresses the senses of smell and taste, allowing smokers to avoid the unpleasant taste and odor associated with smoking. Vocal cord irritation causes chronic cough and hoarseness.(6)

Nicotine easily crosses the placenta. An increase in fetal heart rate can be seen for 90 minutes after a pregnant woman smokes a cigarette. Heavy smokers have an increased risk of spontaneous abortion, are more likely to deliver babies small for gestational age and have an increased risk of giving birth to children with congenital abnormalities, including patent ductus arteriosus, tetralogy of Fallot, and cleft palate and lip. Children of mothers who smoked heavily during pregnancy may exhibit symptoms of hyperactivity in childhood and adolescence and may be at higher risk of cancer in later life.(5)

Cigarette smoking has a harmful effect on fertility: the fertility rate decreases as the number of cigarettes smoked per day increases.(10) Smoking is also associated with abnormal sperm forms and evidence of chromosomal damage.(5)

Nicotine can alter the activity of many drugs, usually by induction of liver microsomal enzymes. Smokers may have reduced blood levels of theophylline, pentazocine (Talwin), propranolol (Inderal), propoxyphene (Darvon), phenothiazines, benzodiazepines, insulin and some antidepressants.(9) The rate of metabolism of warfarin may be increased.(5)

Compared with nonsmokers, smokers are more likely to drive after drinking, to fail to use automobile seat belts and to have accidents at work.(6)


Urinary cotinine and carboxyhemoglobin levels in nonsmokers have been shown to increase directly with the number of cigarettes smoked in the local environment.(3,8) Passive smoking leads to significant morbidity and mortality: it may be a causative factor in as many as 5,000 deaths per year.(3)

Passive exposure causes increased heart rate, elevated blood pressure and increased carboxyhemoglobin levels. As a result, passive exposure can further compromise the cardiovascular systems of persons with heart disease, producing premature ventricular contractions and earlier onset of angina with activity.(8)

Adult nonsmokers who are exposed to tobacco smoke in the workplace demonstrate impaired pulmonary function consistent with that of smokers who consume a half-pack of cigarettes per day.(6) Acute asthma attacks can be provoked by passive smoke exposure.(3) Lung cancer risk increases directly with the level of passive smoke exposure.(8)

Children exposed to passive smoke in the home face a variety of consequences. The risk of middle ear effusions and sinusitis rises in direct proportion to the amount of smoke exposure.(8) Children of smoking parents have increased rates of pulmonary infection.(6) Passive smoking may decrease the forced expiratory volume in one second (FEV1) of children by 7 percent in five years.(3,8) Low birth weight is a well-known effect of maternal smoking, and birth weight has now been shown to be adversely affected by paternal smoking as well.(11) The rate of hospital admissions for infants in the first year of life increases directly with the level of maternal smoking, primarily because of lower respiratory tract infections.(8)

Nicotine Addiction

A recent report of the Surgeon General(1) stated that cigarettes and other forms of tobacco are addicting, that nicotine is the drug causing the addiction and that the pharmacologic and psychologic processes that determine nicotine addiction are similar to those that determine addiction to drugs such as heroin and cocaine. Many cigarette smokers have known these facts for years. In research protocols where nicotine has been given intravenously, it has proved to be more addicting than cocaine.(3) The view that smoking is merely a “habit,” rather than a true drug addiction, may impede successful treatment.

The central element of all forms of drug addiction is that the user’s behavior is largely controlled by a psychoactive substance. Compulsive use of the drug often occurs despite damage to the individual or society. It frequently takes precedence over other important matters. The drug use may persist despite a desire to quit or even after repeated attempts to quit.(1) This is certainly true of cigarette smoking. Most smokers who have a myocardial infarction, for example, resume smoking after leaving the hospital.(5)

Addicting drugs are reinforcing; that is, the pharmacologic action of the drug is sufficiently rewarding to maintain self-administration.(1) This is true of nicotine.

Addictive behavior often involves regular and temporal patterns of use. Environmental factors, including drug-associated stimuli and social pressures, are important influences on initiation and patterns of use.(1) Deprivation increases desire for the drug. This is commonly observed during theater intermissions, for example, when smokers have been deprived of cigarettes for an extended period.(1) Paired stimuli are known to increase drug use. In the case of nicotine, the sight, smell or taste of tobacco or smoke increases the desire to smoke.

Nicotine intake appears to remain remarkably stable from day to day. Smokers tend to adjust their intake to maintain stable plasma nicotine levels.(7) Tolerance develops to nicotine, as it does to most addicting drugs.(1) The amount that a person smokes builds up over a period of time, usually years (Table 2).(12)


Physical dependence may develop with the use of an addicting drug. If so, removal of the drug is characterized by a withdrawal syndrome. This is also true of nicotine. Withdrawal from nicotine, however, is not as dramatic as that from alcohol.(5) It more closely resembles withdrawal from central nervous system stimulants, such as cocaine and amphetamines. Following abrupt smoking cessation or attempts to reduce consumption, withdrawal symptoms (Table 3) occur within hours. They tend to be disturbing, although their intensity varies greatly from person to person.(5) The symptoms are greatest during the first week. During the second week, they tend to decline gradually, although they may increase slightly in some patients. Symptoms continue to decline during the third week. Few subjects have withdrawal symptoms, other than occasional cravings, after 21 days of abstinence.

Heavy smokers generally have more severe withdrawal symptoms than light smokers do, probably because of greater physical dependence on nicotine. Tapering may result in more intense cravings than sudden cessation.(13)

Relapse is common in nicotine-dependent persons who attempt to stop smoking. Less than two in ten succeed in their first effort at smoking cessation. Even after seven or more attempts, less than half succeed.


The critical factor for developing nicotine dependence is exposure. Numerous factors contribute to this, including social acceptance of smoking, the relatively low cost and ready availability of tobacco, and promotion by the tobacco industry, a $20 billion business providing annual tax revenues in excess of $10 billion to state and federal governments.(7) Tobacco companies make a considerable effort to promote smoking as not only an acceptable habit but also a desirable one. Advertising and marketing expenditures for tobacco products equal approximately $2.5 billion per year in the United States alone.(7)

Leading national and international organizations, including the World Health Organization,(1) have recognized chronic tobacco use as a drug addiction. The U.S. Public Health Service now considers cigarette smoking a form of drug abuse, in which nicotine is the abuse-producing drug, and the term “tobacco dependence” has been changed to “nicotine dependence” in the 1987 revised edition of the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders (DSM-III-R).(2)

Treatment of Nicotine Addiction

Patients make a conscious decision to stop smoking when three factors are present: (1) a perceived risk from continued smoking, (2) a net value in stopping and (3) a belief that smoking cessation can be achieved (Table 4).(3) The family physician can make an extremely important contribution by helping the patient arrive at this point and by taking advantage of it.

Stages of Quitting

Investigators have identified five stages in smoking cessation:

1. Precontemplation. In this stage, patients are unlikely to be responsive to direct intervention. They have little concern about the negative aspects of smoking, and heavy-handed messages may increase their resistance to quitting. If pushed hard, these patients will simply find another physician. A calm, factual presentation of the risks, delivered in a low-key manner, is the best approach.

2. Contemplation. In this stage, patients are much more receptive to information about the dangers of smoking. They will often ask for help.

3. Action. This is the stage of quitting tobacco use.

4. Maintenance. This is the most difficult stage of all. It involves remaining abstinent from tobacco use.

5. Relapse. A return to smoking occurs so frequently in patients attempting to give up cigarettes that it has to be considered part of the quitting process.(12)

Methods of Treatment

Various social, psychologic and pharmacologic factors encourage the continued use of tobacco. To be effective, treatment must address all these factors,(1) ideally by alleviating withdrawal symptoms and teaching new behaviors. It is not enough to advise patients to switch from cigarettes to pipes or cigars, because they will probably continue to inhale. Tapering has been shown to be less effective than sudden cessation as a method of quitting.(5) However, patients who are unwilling to set a definite date and quit may benefit from tapering. If they are successful at this, they may gain the confidence to stop smoking. Approaches with several components have been shown to be more effective than those with a single component.(3)


Many resources are available to persons who wish to stop smoking.(4) Self-help material, smoking cessation kits for health professionals and videotape cessation programs are available from a number of local and national health agencies (Table 5).

Group smoking-cessation programs are sponsored locally by many health agencies, universities and hospitals. Local private practitioners, such as health psychologists, also can be helpful.


Behavioral techniques that may be useful to the family physician include self-control strategies, stimulus-control strategies, coping skills and contingency management.

Self-control strategies consist of continuously reminding oneself of reasons to stop smoking and of smoking in the least pleasurable way possible (for example, not smoking after meals, always smoking alone and using the least preferred brand of cigarettes).(5)

Stimulus-control strategies involve limiting the number of cues for smoking and reducing the ability of cues to evoke the desire for a cigarette (cue extinction). The first step is identifying the cues which may include a specific time, place, emotion or social setting. Environmental cues (cigarette lighters, ashtrays, pipes and other smoking paraphernalia) should be removed from the home and work environments. Stimuli that trigger smoking (for example, completing a meal, drinking a cocktail or talking on the telephone) must continually be guarded against. Situations that may provoke relapse (for example, social pressures, stress, anger, frustration or depression) should be acknowledged and dealt with in a healthy manner.(3)

The following approach is helpful in cue extinction: Seven to ten days before quitting, the smoker selects three cues he or she has identified as being the most difficult to endure without a cigarette. During this time, the smoker continues to smoke, but not in response to the selected cues. This usually involves waiting at least ten minutes after the cue has passed before lighting a cigarette.(12)

Coping skills include using stress reduction and stress relaxation techniques, as well as seeking out nonsmoking environments and social support. Useful techniques involve thinking of the negative aspects of smoking and the positive aspects of not smoking, using self-encouragement, avoiding situations in which the temptation to smoke will be particularly strong, and substituting low-calorie food or beverages for cigarettes.(4) Social support from family members, friends and co-workers is needed to help the ex-smoker maintain the altered behavior. Quitters who have few smokers among their friends and relatives are more likely to succeed in their cessation efforts.(3)

Contingency management involves arranging for a reward contingent on not smoking during a specified period following cessation. This is best accomplished through a written contract with friends, the family or the physician. Reward for abstaining is usually more effective than punishment for smoking. The reward does not have to be large, but it should be frequent (for example, having the kids agree to clear the table each night that the mother or father does not smoke).(12)


Pharmacologic approaches to smoking cessation that have been studied include nicotine fading, nicotine-containing gum, clonidine (Catapres), mecamylamine (Inversine) and various anticholinergic agents.

Nicotine Fading. This approach involves a gradual reduction of nicotine consumption by changing to brands with less tar and nicotine and by progressively smoking fewer and fewer cigarettes. Smokers tend to compensate for the reduced nicotine in these cigarettes by taking more puffs, inhaling more deeply and prolonging the smoking of each cigarette. For obvious reasons, this approach, when used by itself, has a limited impact on smoking cessation. A similar approach makes use of a series of dilution filters that progressively mix more air with the smoke in hopes that the smoker can gradually decrease nicotine intake to zero. This system also has shortcomings.(3)

Nicotine Gum. Each piece of nicotine gum (Nicorette) contains 2 mg of nicotine and a polacrilex exchange resin. This product should be used only after smoking has stopped. The rapid nicotine blood levels obtained from smoking are not achieved from chewing the gum. The average daily dose is eight to ten pieces, but more can (and probably should) be used. Smokers tend to underutilize the gum, thus limiting its effectiveness. Heavy smokers who have signs of physical dependence are the best candidates for the gum.(14)

About 10 percent of the gum users may become dependent on the product. To minimize dependence, prescriptions should be given on a restricted basis.(3) The gum should not be prescribed for more than three months. Tapering should extend over three to four weeks. The gum does reduce the desire to smoke, although it does not eliminate it, and withdrawal symptoms are lessened.(15) The gum is most effective when combined with a clear-cut treatment plan.(11,16) It is the only medication approved by the Food and Drug Administration for smoking cessation.

Other Agents. Pharmacologic agents currently under study for use in smoking cessation include clonidine (an alpha2-adrenergic agonist), mecamylamine (a centrally acting, nicotine-blocking agent) and several anticholinergic drugs (atropine, scopolamine, chlorpromazine [Promapar, Thorazine, Thor-Prom]) that are thought to attentuate withdrawal symptoms by preventing the acetylcholine rebound that follows smoking cessation. At present, there is not enough information on these agents to justify their routine use for smoking cessation.(17-20)


Relapse is so frequent among persons attempting to quit smoking that it must be anticipated. Circumstances leading to relapse generally vary over time. The most common reason given for relapse in the first week is withdrawal symptoms. After the first week, coping with crisis situations and exposure to smoking triggers (for example, the presence of other smokers or the consumption of alcohol or coffee) are prominent reasons. Most smoking crises occur at work or involve family situations such as an argument with the spouse or the serious illness of a family member. Inactivity and boredom are also dangerous. Relapses during the first week are more apt to occur in the home and in the evening. After the second week, they are more likely to occur outside the home.(21,22)

The patient should not view relapse as a failure but should learn from the reason for the relapse. Another quit date should be set, and the reason for relapse should be included in the revised maintenance program. Continued support and encouragement are important. The best predictor of relapse may be the quality of support from family members, friends and co-workers.(12)

Role of the Family Physician

About 75 percent of adult Americans make at least one visit to a physician each year; the mean number is five visits per year. Thus, for most family physicians, opportunities for instructing patients about smoking prevention and smoking cessation arise in the office.(3)


Because most cigarette smokers begin the practice in their early teenage years (12 to 16), and because people who do not become regular smokers in adolescence rarely begin later in life, preventive efforts should start in childhood. Multiple environmental factors influence the onset of smoking. Among there, peer pressure and parental smoking are the greatest predictors of adolescent smoking, with peer influence as the more potent factor.(23)

A social environment that is tolerant of smoking facilitates the adoption of smoking. As the total number of smokers in the child’s environment increases, the risk of the child’s becoming a smoker escalates. Advertisements contribute to the acceptance of smoking by portraying smokers as attractive, outgoing, popular and sexy.

The success of tobacco advertising is evident. According to a 1987 report,(23) adolescents believe that 83 percent of people their age are smokers, whereas only 15 to 30 percent actually are. They also believe that 70 percent of teachers smoke, when only 20 percent do. Thus, adolescents tend to exaggerate the prevalence of smoking and believe that smoking is the norm. Teenagers from low socioeconomic backgrounds, those who are female and those from single-parent households are most likely to smoke. Intervention with these high-risk adolescents should be a priority.(23)

It is important for physicians to counter-balance factors that encourage tobacco use. A physician’s statement is generally accepted as fact by children. Six strategies(8,23) are useful in this regard:

1. Provide information about the harmful health consequences of smoking, including those from passive smoking, but avoid dwelling on the long-term adverse effects of smoking. Adolescents are considerably more motivated by concern for the earlier consequences of smoking, such as greater skin wrinkling, tobacco-stained teeth and fingers, and stale odor on breath and clothes.

2. Discuss societal changes in attitude toward smoking.

3. Correct mistaken notions about the percentage of adults who smoke.

4. Emphasize that smoking is addicting and that not starting to smoke is the best way to avoid becoming a regular smoker.

5. Teach children to see the falsity of smoking advertisements aimed at young people.

6. Provide a nonsmoking environment in the patients’ waiting room.


The smoking history should be part of every medical history. It should cover the following questions: Does the patient smoke? How much? How long? How early is the first cigarette of the day taken? What type of cigarettes are used? Has the patient ever tried to quit? What were the reasons for success or failure of smoking cessation? Does the patient smoke in public or in restricted places? Does the patient smoke when ill? Why does the patient smoke? These questions are aimed at determining the degree of nicotine addiction, as well as obtaining information on past successes and failures in smoking cessation.(3)

During the physical examination, abnormalities related to smoking should be emphasized as they are found. These might include tobacco-stained fingers, smoker’s lines and crow’s-feet on the face, pulmonary rales or rhonchi, and increased resonance on percussion.(3)

A smoking cessation contract (either handwritten or a printed form) can be signed with patients who are ready to quit. The benefits of a contract are additive to other cessation strategies. The patient who is unwilling to sign is probably not ready to quit.(3)

A major obstacle to abstinence, and a problem that must be addressed, is weight gain, either anticipated or actual. Increased exercise and good nutrition are essential for weight maintenance.(24)

Some of the immediate consequences of smoking cessation include improved ability to breathe, less coughing, regained sense of taste and smell, fresher breath, improved exercise tolerance, no more burn holes in clothing, no more tobacco stains on teeth and fingers, no ashtrays to empty, better insurance status, decreased risk of passive smoking damage to family members and others, and financial savings. The physician can use these benefits as early positive reinforcement.

Patients should be encouraged to call the physician if they relapse, so that the reason can be identified and used in a revised maintenance program after a new quit date has been set.(3)

Even if the physician chooses not to counsel patients on smoking cessation, the minimum intervention should be to explain the health risks and advise the patient to quit. From 5 to 10 percent of smoking patients quit simply on the advice of a physician.(8)

A recommended smoking cessation program consists of the following five steps, which are summarized in Table 6.

Step 1: Review the patient’s smoking status and take a brief smoking history. Providing health-risk information about continued smoking is an integral part of this step. Medical findings should be personalized whenever possible. The effects of passive smoking on the health of the patient’s spouse, children and co-workers should be included in this discussion.(8,25)

Step 2: Assess the patient’s interest in quitting. The patient’s readiness to stop smoking, level of motivation and confidence in success should be determined. If the patient is in the “precontemplation” stage and is not ready to make an attempt to stop smoking, recommendations and materials can be supplied that may influence the patient later. The patient should be encouraged to reduce the number of cigarettes smoked. If the patient seems to be in the “contemplation” stage, the physician should determine the main reason the patient is considering quitting. This reason can be used to reinforce the quitting effort.

Step 3: Set a target quit date. The patient may be asked to sign a contract acknowledging that a date has been set and promising to stop smoking entirely on that date.(8)

The physician may wish to prescribe nicotine gum for use once smoking has ceased. If the patient will be referred to a community program, be sure that gum use is compatible with that program. The gum should be prescribed in a tapering dose over three to four weeks and should not be continued for more than three months. Nicotine gum is not a “magic bullet,” and the risk of addiction is significant.(8,25-27) The physician should refer to the package insert for information on the use, contraindications and side effects of the gum.

Step 4: Suggest smoking cessation strategies. This step is usually the most difficult for the physician, because there are so many options. The physician may choose to provide the patient with self-help material, work personally with the patient using material from several organizations, or refer the patient to a community smoking-cessation program.

Cessation strategies include preparatory steps for quitting; discussions of withdrawal symptoms and their time course; strategies for dealing with situations of high risk for relapse, and follow-up appointments or telephone calls. Preparatory techniques that can be used by the patient before the quit date include listing reasons for wanting to quit; becoming more aware of the situations in which cigarettes seem necessary; obtaining social support; reducing tobacco intake to ten to 15 cigarettes per day; substituting sugar-free chewing gum or low-calorie food for cigarettes developing a plan to deal with weight gain, and eliminating sight cues for smoking, such as ashtrays and matches.(8,25)

Step 5. Schedule follow-up visits or telephone calls on a weekly basis initially. Follow-up serves two purposes: to provide support and to observe patient adherence. The visits may also be used to taper nicotine gum. Successful abstinence involves continued effort, not instant mastery. At least six months must elapse before the ex-smoker is at a relatively low risk of resuming smoking. During this period, occasional brief slips may occur, or the patient may totally relapse. These setbacks should be viewed by patient and physician as part of the cessation process. The patient should be urged to examine the reason for the slip and use it to prevent recurrence in a continuing smoking cessation effort.(8,25)


Diseases and Conditions Associated with Smoking Active smoking Cancer Oral cavity, pharynx, larynx, esophagus, lung, pancreas, kidney, bladder Cardiovascular Aggravation of exercise-induced angina, coronary artery disease, myocardial infarction, cardiac arrhythmias, sudden cardiac death, stroke, aortic aneurysm, arteriosclerotic peripheral vascular disease, thromboangiitis obliterans (Buerger’s disease) Pulmonary Imparied pulmonary function, emphysema, acute and chronic bronchitis, chronic cough, hoarseness due to vocal cord irritation Perinatal effects of maternal smoking Increase in fetal mortality, low birth weight, spontaneous abortion, sudden infant death syndrome, congenital abnormalities, hyperactivity in childhood, risk of cancer in later life Miscellaneous peptic ulcer disease, erythrocytosis, peripheral blood leukocytosis, smoker’s skin, decreased ability to taste and smell, abnormal sperm counts and evidence of chromosomal damage, decreased fertility, increased accident rate, altered drug metabolism, adverse health consequences in women taking oral contraceptives Passive smoking Cancer Lung Cardiovascular Aggravation of exercise-induced angina, premature ventricular contractions Pulmonary Impaired pulmonary function in adults and children, asthma attacks, pulmonary infections, bronchiolitis, decreased growth rate of lungs Perinatal effects Low birth weight Miscellaneous Increased hospital admissions of infants, middle ear effusions and sinusitis in children, decreased growth rate


Addictive Characteristics of Nicotine 1. Drug produces psychoactive effects (euphoria,

stimulation, relaxation). 2. Compulsive use occurs. 3. Use continues despite known harmful effects. 4. Effects reinforce use. 5. Regular and temporal patterns of use exist. 6. Deprivation increases desire to use drug. 7. Paired stimuli increase use. 8. Tolerance develops. 9. Physical dependence occurs. 10. Withdrawal syndrome occurs. 11. Relapse is common after smoking cessation.


Signs and Symptoms of Nicotine Withdrawal Decreased heart rate Restlessness Dullness or sleepiness Inability to concentrate Irritability Feelings of hostility Sleep disturbances Altered rapid eye movement (REM) during sleep Slowing of electroencephalogram with decreased

arousal pattern Constipation or diarrhea Weight gain Nicotine craving


Patients’ Reasons for Attempting to Stop Smoking General health awareness; decision to lead healthier life Specific health reason (e.g., genetic, occupational or metabolic risk factor,

development of smoking-related disease) Parental desire to provide positive role model for children Awareness of health risks to family due to passive smoking Awareness of health risks to fetus High cost of habit Desire to gain better control of life Awareness that smoking no longer fills the need it once did Increasing social pressure not to smoke


Sources of Smoking Cessation Material American Academy of Family Physicians, Health Education Department B,

8880 Ward Parkway, Kansas City, MO 64114-2797 American Heart Association, 7320 Greenville Ave., Dallas, TX 75231 Health Promotion Group, Inc., P.O. Box 59687, Homewood, AL 35259 Warner Brothers, Attention Lorimar Home Video, 4000 Warner Blvd.,

Burbank, CA 91522; or phone (800) 323-5275 National Cancer Institute, Office of Cancer Communications, National

Institutes of Health, Bldg. 31, Room 4B43, Bethesda, MD 20892 National Audio Visual Center, Customer Services Section, 8700 Edgeworth

Dr., Capital Heights, MD 20743-3701 National Heart, Lung, and Blood Institute, Smoking Education Program,

National Institutes of Health, Bldg. 31, Room 4A-18, Dept. A-1, Bethesda,

MD 20892 Office on Smoking and Health, 5600 Fishers Lane, Park Bldg., Room 110,

Rockville, MD 20857 Local offices/divisions American Cancer Society (see local telephone directory) American Heart Association (see local telephone directory) American Lung Association (see local telephone directory) REFERENCES (1)U.S. Public Health Service. The health consequences of smoking: nicotine addiction. A report of the Surgeon General Rockville, Md.: U.S. Department of Health and Human Services, 1988. (2)American Psychiatric Association Task Force on Nomenclature and Statistics. Diagnostic and statistical manual of mental disorders. 3d ed rev. Washington, D.C.: American Psychiatric Association, 1987:181-2. (3)Greene HL, Goldberg RJ, Ockene JK. Cigarette smoking: the physician’s role in cessation and maintenance. J Gen Intern Med 1988;3:75-87. (4)Gritz ER. Cigarette smoking: the need for action by health professionals. CA 1988;38:194-212. (5)Shuckit MA. Drug and alcohol abuse: a clinical guide to diagnosis and treatment. 2d ed. New York: Plenum, 1984:189-97. (6)Brown R, Pinkerton R, Tuttle M. Respiratory infections in smokers. Am Fam Physician 1987;36(5):133-40. (7)Henningfield JE, Nemeth-Coslett R. Nicotine dependence. Interface between tobacco and tobacco-related disease. Chest 1988;93(2 Suppl):37S-55S. (8)Chesebro MJ. Passive smoking. Am Fam Physician 1988;37(5):212-8. (9)American Medical Association. Drug evaluations. Philadelphia: Saunders, 1986;157-60. (10)Howe G, Westhoff C, Vessey M, Yeates D. Effects of age, cigarette smoking, and other factors on fertility: findings in a large prospective study. Br Med J [Clin Res] 1985;290(6483):1697-700. (11)Rubin DH, Krasilnikoff PA, Leventhal JM, Weile B, Berget A. Effect of passive smoking on birth-weight. Lancet 1986;2(8504):415-7. (12)Fisher EB Jr, Bishop DB, Goldmuntz J, Jacobs A. Implications for the practicing physician of the psychosocial dimensions of smoking. Chest 1988;93(2 Suppl):69S-78S. (13)Hughes JR, Hatsukami DK, Pickens RW, Svikis DS. Consistency of the tobacco withdrawal syndrome. Addict Behav 1984;9:409-12. (14)Jarvik ME, Schneider NG. Degree of addiction and effectiveness of nicotine gum therapy for smoking. Am J Psychiatry 1984;141:790-1. (15)West RJ, Russell MA. Effects of withdrawal from long-term nicotine gum use. Psychol Med 1985;15: 891-3. (16)Schneider NG, Jarvik ME. Nicotine gum versus placebo gum: comparison of withdrawal symptoms and success rates. Natl Inst Drug Abuse Res Monogr Ser 1988;53:83-101. (17)Henningfield JE. Pharmacologic basis and treatment of cigarette smoking. J Clin Psychiatry 1984;45(12 Pt 2):24-34. (18)Glassman AH, Jackson WK, Walsh BT, Roose SP, Rosenfeld B. Cigarette craving, smoking withdrawal, and clonidine. Science 1984;226(4676):864-6. (19)Tennant FS Jr, Tarver AL. Withdrawal from nicotine dependence using mecamylamine: comparison of three-week and six-week dosage schedules. Natl Inst Drug Abuse Res Monogr Ser 1984;55:291-7. (20)Bachynsky N. The use of anticholinergic drugs for smoking cessation: a pilot study. Int J Addict 1986;21:789-805. (21)Shiffman S, Read L, Jarvik ME. Smoking relapse situations: a preliminary typology. Int J Addict 1985;20:311-8. (22)Cummings KM, Jaen CR, Giovino G. Circumstances surrounding relapse in a group of recent exsmokers. Prev Med 1985;14:195-202. (23)Silvis GL, Perry CL. Understanding and deterring tobacco use among adolescents. Pediatr Clin North Am 1987;34:363-79. (24)Fagerstrom KO. Reducing the weight gain after stopping smoking. Addict Behav 1987;12:91-3. (25)McCusker K. Notes from a smoking cessation clinic. Chest 1988;93(2 Suppl):66S-8S. (26)Hughes JR, Hatsukami DK, Skoog KP. Physical dependence on nicotine in gum. A placebo substitution trial. JAMA 1986;255:3277-9. (27)Hjalmarson AI. Effect of nicotine chewing gum on smoking cessation. A randomized, placebo-controlled, double-blind study. JAMA 1984;252:2835-8.

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