Saturday, August 30, 2008

Tobacco

TOBACCO

Neal L. Benowitz -

DEFINITION

Harmful Constituents of Tobacco

Tobacco smoke is an aerosol of droplets (particulates) containing water, nicotine and other alkaloids, and tar. Tobacco smoke contains several thousand different chemicals, many of which may contribute to human disease. Major toxic chemicals in the particulate phase of tobacco include nicotine, benzo(a)pyrene and other polycyclic hydrocarbons, N′-nitrosonornicotine, β-naphthylamine, polonium 210, nickel, cadmium, arsenic, and lead. The gaseous phase contains carbon monoxide, acetaldehyde, acetone, methanol, nitrogen oxides, hydrogen cyanide, acrolein, ammonia, benzene, formaldehyde, nitrosamines, and vinyl chloride. Tobacco smoke may produce illness by way of systemic absorption of toxins or cause local pulmonary injury by oxidant gases.

Tobacco Addiction

Tobacco use is motivated primarily by the desire for nicotine. Drug addiction is defined as compulsive use of a psychoactive substance, the consequences of which are detrimental to the individual or society. Understanding addiction is useful in providing effective smoking cessation therapy. Nicotine is absorbed rapidly from tobacco smoke into the pulmonary circulation; it then moves quickly to the brain, where it acts on nicotinic cholinergic receptors to produce its gratifying effects, which occur within 10 to 15 seconds after a puff. Smokeless tobacco is absorbed more slowly and results in less intense pharmacologic effects. With long-term use of tobacco, physical dependence develops in association with an increased number of nicotinic cholinergic receptors in the brain. When tobacco is unavailable, even for only a few hours, withdrawal symptoms often occur, including anxiety, irritability, difficulty concentrating, restlessness, hunger, craving for tobacco, disturbed sleep, and, in some people, depression.

EPIDEMIOLOGY

Currently, about 46 million individuals in the United States are cigarette smokers, including 26% of men and 21% of women. People who are less well educated or have unskilled occupations are more likely to smoke. Smoking is responsible for about 430,000 preventable U.S. deaths annually. A lifelong smoker has about a one in three chance of dying prematurely of a complication of smoking. Smoking is the major preventable cause of death in developed countries.

Other forms of tobacco use include pipes and cigars (used by 8.7% of men and 0.3% of women) and smokeless tobacco (5.5% of men and 1% of women). Smokeless tobacco use in the United States is primarily oral snuff and chewing tobacco, whereas nasal snuff is used to a greater extent in the United Kingdom. Oral snuff (snus) is widely used by men in Sweden.

Addiction to tobacco is multifactorial, including a desire for the direct pharmacologic actions of nicotine, relief of withdrawal symptoms, and learned associations. Smokers report a variety of reasons for smoking, including pleasure, arousal, enhanced vigilance, improved performance, relief of anxiety or depression, reduced hunger, and control of body weight. Environmental cues, such as a meal, a cup of coffee, talking on the phone, an alcoholic beverage, or friends who smoke, often trigger an urge to smoke. Smoking and depression are strongly linked. Smokers are more likely to have a history of major depression than are nonsmokers. Smokers with a history of depression are also likely to be more highly dependent on nicotine and to have a lower likelihood of quitting. When they do quit, depression is more likely to be a prominent withdrawal symptom. Cigarette smoking is also more common in alcoholics and other substance abusers and in people with schizophrenia and attention-deficit disorder.

Most tobacco use begins in childhood or adolescence. Risk factors for youth smoking include peer and parental influences; behavioral problems (e.g., poor school performance); personality characteristics, such as rebelliousness or risk taking, depression, and anxiety; and genetic influences. Adolescent desire to appear older and more sophisticated, such as emulating more mature role models, is another strong motivator. Environmental influences such as advertising also are thought to contribute. Approaches to prevention of tobacco addiction in youth include educational activities in schools, aggressive anti-tobacco media campaigns, taxation, changing the social and environmental norms, and deglamorizing smoking (restricting indoor smoking, educating parents not to smoke around children).

PATHOBIOLOGY

Health Hazards of Tobacco

Tobacco use is a major cause of death from cancer, cardiovascular disease, and pulmonary disease ( Table 1 ). Smoking is also a major risk factor for osteoporosis, reproductive disorders, and fire-related and trauma-related injuries.


TABLE 1 -- HEALTH HAZARDS OF TOBACCO USE (RISKS INCREASED BY SMOKING)

CANCER

See Table 2

CARDIOVASCULAR DISEASE

Sudden death

Acute myocardial infarction

Unstable angina

Stroke

Peripheral arterial occlusive disease (including thromboangiitis obliterans)

Aortic aneurysm

PULMONARY DISEASE

Lung cancer

Chronic bronchitis

Emphysema

Asthma

Increased susceptibility to pneumonia

Increased susceptibility to pulmonary tuberculosis and

desquamative interstitial pneumonitis

Increased morbidity from viral respiratory infection

GASTROINTESTINAL DISEASE

Peptic ulcer

Gastroesophageal reflux

Crohn's disease

REPRODUCTIVE DISTURBANCES

Reduced fertility

Premature birth

Lower birth weight

Spontaneous abortion

Abruptio placentae

Premature rupture of membranes

Increased perinatal mortality

ORAL DISEASE

Oral cancer

Leukoplakia

Gingivitis

Gingival recession

Tooth staining

OTHER

Non–insulin-dependent diabetes mellitus

Earlier menopause

Osteoporosis

Cataract

Tobacco amblyopia

Age-related macular degeneration

Premature skin wrinkling

Graves' disease, including ophthalmopathy

Aggravation of hypothyroidism

Altered drug metabolism or effects

Cancer


Although it is the largest preventable cause of cancer ( Table 2 ), smoking is responsible for about 30% of cancer deaths. Many chemicals in tobacco smoke may contribute to carcinogenesis as tumor initiators, cocarcinogens, tumor promoters, or complete carcinogens. Cigarette smoking induces specific patterns of p53 mutations that are associated with squamous cell carcinomas of the lung, head, and neck. Lung cancer is the leading cause of cancer deaths in the United States and is predominantly attributable to cigarette smoking. The risk of lung and other cancers is proportional to how many cigarettes are smoked per day and the duration of smoking. Exposure in the workplace to asbestos or of uranium miners to α-radiation synergistically increases the risk of lung cancer in cigarette smokers. Alcohol use interacts synergistically with tobacco in causing oral, laryngeal, and esophageal cancer. The mechanism of interaction may involve alcohol-solubilizing tobacco carcinogens or alcohol-related induction of liver or gastrointestinal enzymes that metabolize and activate tobacco carcinogens. The tobacco-related risks of bladder and kidney cancer are enhanced by occupational exposure to aromatic amines, such as in the dye industry. Cervical cancer is more common in women who smoke, presumably the result of exposure to carcinogens in cervical secretions. Smoking seems to be involved in 20 to 30% of leukemia cases in adults, including lymphoid and myeloid leukemia, and in 20% of colorectal cancers.


TABLE 2 -- SMOKING AND CANCER MORTALITY



Relative Risk among Smokers

Mortality Attributable to Smoking

Type of Cancer

Current

Former

Percentage

Number

Lung


Male

22.4

9.4

90

82,800


Female

11.9

4.7

79

40,300

Larynx


Male

10.5

5.2

81

2400


Female

17.8

11.9

87

700

Oral cavity


Male

27.5

8.8

92

4900


Female

5.6

2.9

61

1800

Esophagus


Male

7.6

5.8

78

5700


Female

10.3

3.2

75

1900

Pancreas


Male

2.1

1.1

29

3500


Female

2.3

1.8

34

4500

Bladder


Male

2.9

1.9

47

3000


Female

2.6

1.9

37

1200

Kidney


Male

3.0

2.0

48

3000


Female

1.4

1.2

12

500

Stomach


Male

1.5

?

17

1400


Female

1.5

?

25

1300

Leukemia


Male

2.0

?

20

2000


Female

2.0

?

20

1600

Cervix


Female

2.1

1.9

31

1400

Modified from Newcomb PA, Carbone PP: The health consequences of smoking: Cancer. Med Clin North Am 1992;76:305–331.

Cardiovascular Disease

Cigarette smoking accounts for about 20% of cardiovascular deaths in the United States. Risks are increased for coronary heart disease, sudden death, cerebrovascular disease, and peripheral vascular disease, including aortic aneurysm. Cigarette smoking accelerates atherosclerosis and promotes acute ischemic events. The mechanisms of the effects of smoking are not fully elucidated but are believed to include (1) hemodynamic stress (nicotine increases the heart rate and transiently increases blood pressure), (2) endothelial injury and dysfunction (nitric oxide release and resultant vasodilation are impaired), (3) development of an atherogenic lipid profile (smokers have on average higher low-density lipoprotein, more oxidized low-density lipoprotein, and lower high-density lipoprotein cholesterol than nonsmokers do), (4) enhanced coagulability, (5) arrhythmogenesis, and (6) relative hypoxemia because of the effects of carbon monoxide. Carbon monoxide reduces the capacity of hemoglobin to carry oxygen and impairs the release of oxygen from hemoglobin to body tissues, both of which combine to result in a state of relative hypoxemia. To compensate for this hypoxemic state, polycythemia develops in smokers, with hematocrits often 50% or more. The polycythemia and the increased fibrinogen levels that are found in cigarette smokers also increase blood viscosity, which adds to the risk of thrombotic events. Cigarette smoking also induces a chronic inflammatory state, as evidenced by increased levels of C-reactive protein and other inflammatory markers in the blood of smokers. Chronic inflammation is thought to contribute to atherogenesis.

Cigarette smoking acts synergistically with other cardiac risk factors to increase the risk of ischemic heart disease. Although the risk of cardiovascular disease is roughly proportional to cigarette consumption, the risk persists even at low levels of smoking (e.g., one or two cigarettes per day). Cigarette smoking reduces exercise tolerance in patients with angina pectoris and intermittent claudication. Vasospastic angina is more common, and the response to vasodilator medication is impaired in patients who smoke. The number of episodes and total duration of ischemic episodes as assessed by ambulatory electrocardiographic monitoring in patients with coronary heart disease are substantially increased by cigarette smoking. The increase in relative risk of coronary heart disease because of cigarette smoking is greatest in young adults, who in the absence of cigarette smoking would have a relatively low risk. Women who use oral contraceptives and smoke have a synergistically increased risk of myocardial infarction and stroke.

After acute myocardial infarction, the risk of recurrent myocardial infarction is higher and survival is half during the next 12 years in persistent smokers compared with quitters. Smoking also interferes with revascularization therapy for acute myocardial infarction. After thrombolysis, the reocclusion rate is four-fold higher in smokers who continue than in quitters. The risk of reocclusion of a coronary artery after angioplasty or occlusion of a bypass graft is increased in smokers. Cigarette smoking is not a risk factor for hypertension but does increase the risk of complications, including the development of nephrosclerosis and progression to malignant hypertension. Cigarette smoking has been shown to be a substantial contributor to morbidity and mortality in patients with left ventricular dysfunction. The mortality benefit of stopping smoking in such patients is equal to or greater than the benefit of therapy with angiotensin-converting enzyme inhibitors, β-blockers, or spironolactone.

Pulmonary Disease

More than 80% of chronic obstructive lung disease in the United States is attributable to cigarette smoking. Pulmonary disease from smoking includes the overlapping syndromes of chronic bronchitis (cough and mucus hypersecretion), emphysema, and airway obstruction. The pathologic changes produced in the lung by cigarette smoking include loss of cilia, mucous gland hyperplasia, increased number of goblet cells in the central airways, inflammation, goblet cell metaplasia, squamous metaplasia, mucus plugging of small airways, destruction of alveoli, and reduced number of small arteries. The mechanism of injury is complex and seems to include direct injury by oxidant gases, increased elastase activity (a protein that breaks down elastin and other connective tissue), and decreased antiprotease activity. A genetic deficiency of α1-antiprotease activity produces a similar imbalance between pulmonary protease and antiprotease activity and is a risk factor for early and severe smoking-induced pulmonary disease. Cigarette smoking is associated with an increased risk of desquamative interstitial pneumonitis.

Cigarette smoking also increases the risk of respiratory infection, including pneumonia, and results in greater disability from viral respiratory tract infections. Smoking is a substantial risk factor for pneumococcal pneumonia and in particular with invasive pneumococcal disease. Cigarette smoking increases the risk for development of and the severity of viral infections including the common cold, influenza, and varicella. Tuberculosis is perhaps the most important smoking-associated infection. Smoking is a substantial risk factor for tuberculin skin test reactivity, skin test conversion, and development of active tuberculosis. A case-control study from India found a prevalence risk ratio of 2.9 and a mortality risk ratio of 4.2 to 4.5 (for rural and urban residents, respectively) for ever-smokers compared with never-smokers.[1] Thus, smoking contributes substantially to the worldwide disease burden of tuberculosis.

Other Complications Ulcer

Cigarette smoking increases the risk of duodenal and gastric ulcers, delays the rate of ulcer healing, and increases the risk of relapse after ulcer treatment. Smoking also is associated with esophageal reflux symptoms. Smoking produces ulcer disease by increasing acid and pepsinogen secretion, reducing pancreatic bicarbonate secretion, impairing the gastric mucosal barrier (related to decreased gastric mucosal blood flow and inhibition of prostaglandin synthesis), and reducing pyloric sphincter tone.

Diabetes Mellitus

Cigarette smoking is an independent risk factor for the development of non–insulin-dependent diabetes mellitus, which is a consequence of development of resistance to the effects of insulin. The effects of nicotine seem to contribute at least in part to insulin resistance, and insulin resistance has been described in users of smokeless tobacco, who are not exposed to tobacco combustion products.

Osteoporosis

Cigarette smoking is a risk factor for osteoporosis in that it reduces the peak bone mass attained in early adulthood and increases the rate of bone loss in later adulthood. Smoking antagonizes the protective effect of estrogen replacement therapy on the risk of osteoporosis in postmenopausal women.

Reproductive Problems

Cigarette smoking is a major cause of reproductive problems and results in approximately 4600 U.S. infant deaths annually. Growth retardation from cigarette smoking has been termed the fetal tobacco syndrome. Cigarette smoking causes reproductive complications by causing placental ischemia mediated by the vasoconstricting effects of nicotine, the hypoxic effects of chronic carbon monoxide exposure, and the general increase in coagulability produced by smoking.

Other Adverse Effects

Other adverse effects of cigarette smoking include premature facial wrinkling, increased risk of cataracts, olfactory dysfunction, and fire-related injuries; the last-mentioned contribute significantly to the economic costs of tobacco use. Smoking is associated with Graves' disease and especially increases the risk of more severe ophthalmopathy. Smoking also reduces the secretion of thyroid hormone in women with subclinical hypothyroidism and increases the severity of clinical symptoms of hypothyroidism in women with subclinical or overt hypothyroidism, the latter effect reflecting antagonism of thyroid hormone action. Cigarette smoking also potentially interacts with a variety of drugs by accelerating drug metabolism or by the antagonistic pharmacologic actions that nicotine and other constituents of tobacco have with other drugs ( Table 3 ).


TABLE 3 -- INTERACTION BETWEEN CIGARETTE SMOKING AND DRUGS

Drug


Interaction (Effects Compared with Nonsmokers)

Significance

Antipyrine

Imipramine

Accelerated metabolism

May require higher doses in smokers, reduced doses after quitting

Caffeine

Lidocaine



Chlorpromazine

Olanzapine



Clozapine

Oxazepam



Desmethyldiazepam

Pentazocine



Estradiol

Phenacetin



Estrone

Phenylbutazone



Flecainide

Propranolol



Fluvoxamine

Tacrine



Haloperidol

Theophylline



Oral contraceptives

Enhanced thrombosis, increased risk of stroke and myocardial infarction

Do not prescribe to smokers, especially if older than 35 years

Cimetidine and other H2-blockers

Lower rate of ulcer healing, higher ulcer recurrence rates

Consider the use of proton pump inhibitors

Propranolol

Less antihypertensive effect, less antianginal efficacy; more effective in reducing mortality after myocardial infarction

Consider the use of cardioselective β-blockers

Nifedipine (and probably other calcium blockers)

Less antianginal effect

May require higher doses or multiple-drug antianginal therapy

Diazepam, chlordiazepoxide (and possibly other sedative-hypnotics)

Less sedation

Smokers may need higher doses

Chlorpromazine (and possibly other neuroleptics)

Less sedation, possibly reduced efficacy

Smokers may need higher doses

Propoxyphene

Reduced analgesia

Smokers may need higher doses

Health Hazards of Smokeless Tobacco

Smokeless tobacco refers to snuff and chewing tobacco. Oral snuff is placed (as a “pinch”) between the lip and gum or under the tongue; chewing tobacco is actively chewed and generates saliva that is spit out (“spit tobacco”). Smokeless tobacco products are usually flavored, many with licorice, and also contain sodium bicarbonate to keep the local pH alkaline to facilitate buccal absorption of nicotine. Nicotine absorption from smokeless tobacco is similar in magnitude to that from cigarette smoking. Other chemicals, including sodium, glycyrrhizinic acid (from licorice), and potentially carcinogenic chemicals such as nitrosamines also are absorbed systemically.

Smokeless tobacco is addictive and is associated with an increased risk of oral cancer at the site where the tobacco is usually placed (inside the lip, under the cheek or tongue) or nasal cancer in nasal snuff users. Other oral diseases also associated with smokeless tobacco include leukoplakia, gingivitis, gingival recession, and staining of the teeth. Cardiovascular effects of smokeless tobacco include acute aggravation of hypertension or angina pectoris as a result of the sympathomimetic effects of nicotine, hypokalemia and hypertension secondary to the effects of glycyrrhizinic acid (a potent mineralocorticoid, and excessive sodium absorption resulting in aggravated hypertension or sodium-retaining disorders.

Health Hazards of Secondhand Smoke

Considerable evidence indicates that exposure to secondhand smoke is harmful to the health of nonsmokers ( Table 4 ). The U.S. Environmental Protection Agency classifies secondhand smoke as a class A carcinogen, which means that it has been shown to cause cancer in humans.

TABLE 4 -- HEALTH HAZARDS OF ENVIRONMENTAL TOBACCO SMOKE IN NONSMOKERS

Children

Adults


Hospitalization for respiratory tract infection in first year of life



Wheezing



Middle ear effusion



Asthma



Sudden infant death syndrome



Lung cancer



Myocardial infarction



Reduced pulmonary function



Aggravation of asthma and chronic obstructive pulmonary disease



Irritation of eyes, nasal congestion, headache



Cough

Secondhand smoke consists of smoke that is generated while the cigarette is smoldering and mainstream smoke that has been exhaled by the smoker. Of the total combustion product from a cigarette, 75% or more enters the air. The constituents of environmental tobacco smoke are qualitatively similar to those of mainstream smoke. However, some toxins, such as ammonia, formaldehyde, and nitrosamines, are present in much higher concentrations in secondhand smoke than in mainstream smoke. The Environmental Protection Agency has estimated that secondhand smoke is responsible for approximately 3000 lung cancer deaths annually in nonsmokers in the United States, is causally associated with 150,000 to 300,000 cases of lower respiratory tract infection in infants and young children up to 18 months of age, and is causally associated with the aggravation of asthma in 200,000 to 1 million children. Secondhand smoke exposure is also responsible for about 40,000 cardiovascular deaths per year. An appreciation of the hazards of secondhand smoke is important to the physician because it provides a basis for advising parents not to smoke when children are in the home, for insisting that child care facilities be smoke free, and for recommending smoking restrictions in work sites and other public places

TREATMENT

Cessation Intervention

Of cigarette smokers, 70% would like to quit, and 46% try to quit each year. Spontaneous quit rates are about 1% per year. Simple advice from the physician to quit increases the quit rate to 3%. Minimal-intervention programs increase quit rates to 5 to 10%, whereas more intensive treatments, including smoking cessation clinics, can yield quit rates of 25 to 30%. A practical office smoking cessation program developed by the U.S. Public Health Service consists of 5 As: (1) ask about smoking at every opportunity, (2) advise all smokers to stop, (3) assess willingness to make a quit attempt, (4) assist the patient in stopping and maintaining abstinence, and (5) arrange follow-up to reinforce nonsmoking. Assistance in quitting should include providing self-help material or quit kits, which are widely available from governmental health agencies, professional societies, and local organizations such as cancer, heart, and lung associations. The physician may offer additional education and counseling through the office (most efficiently provided by office staff and by teaching aids such as videotapes) or through referral to community smoking cessation programs. Telephone counseling is effective in promoting smoking cessation.[2] Telephone quitlines are available at no cost in most states in the United States. Thus, the busiest physician can easily refer patients to telephone quitlines for counseling if personal counseling time is not available. Smokers who are interested should be offered nicotine replacement or other pharmacologic therapy.

Medical Therapy

Currently, three medications have been approved for smoking cessation: nicotine, bupropion, and varenicline. All types of smoking cessation medications, if used properly, double smoking cessation rates compared with placebo treatments.

Nicotine Replacement

Nicotine replacement medications include 2- and 4-mg nicotine polacrilex gum, 2- and 4-mg nicotine buccal lozenges, transdermal nicotine patches, nicotine nasal spray, and nicotine inhalers. All seem to have comparable efficacy, but in a randomized study, compliance was greatest for the patch, lower for gum, and very low for the spray and the inhaler. A smoker should be instructed to quit smoking entirely before beginning nicotine replacement therapies. Optimal use of nicotine gum includes instructions not to chew too rapidly, to chew 8 to 10 pieces per day for 20 to 30 minutes each, and to use it for an adequate period for the smoker to learn a lifestyle without cigarettes, usually 3 months or longer. Side effects of nicotine gum are primarily local and include jaw fatigue, sore mouth and throat, upset stomach, and hiccups. Nicotine lozenges have recently been marketed over-the-counter. The lozenges are placed in the buccal cavity where they are slowly absorbed for 30 minutes. Smokers are instructed to choose their dose according to how long after awakening in the morning they smoke their first cigarette (a measure of the level of nicotine dependence). Those who smoke within 30 minutes are advised to use the 4-mg lozenge, whereas those who smoke their first cigarette at 30 minutes or more are advised to use 2-mg lozenges. Use is recommended every 1 to 2 hours.

Several different transdermal nicotine preparations are marketed; three deliver 21 or 22 mg during a 24-hour period, and one delivers 15 mg during 16 hours. Most have lower dose patches for tapering. Patches are applied in the morning and removed either the next morning or at bedtime, depending on the patch. Full-dose patches are recommended for most smokers for the first 1 to 3 months, followed by one or two tapering doses for 2 to 4 weeks each. Nicotine nasal spray, one spray into each nostril, delivers about 0.5 mg of nicotine systemically and can be used every 30 to 60 minutes. Local irritation of the nose commonly produces burning, sneezing, and watery eyes during initial treatment, but tolerance develops to these effects in 1 or 2 days. The nicotine inhaler delivers nicotine to the throat and upper airway, from where it is absorbed similarly to nicotine from gum. It is marketed as a cigarette-like plastic device and can be used ad libitum.

Nicotine medications seem to be safe in patients with cardiovascular disease and should be offered to cardiovascular patients. Although smoking cessation medications are recommended by the manufacturer for relatively short-term use (generally 3 to 6 months), the use of these medications for 6 months or longer is safe and may be helpful in smokers who fear relapse without medications. Combination therapy—combining bupropion and nicotine or combining slow-release nicotine patches with preparations with more rapid release, such as gum, inhaler, or nasal spray—increases the likelihood of cessation compared with single-drug therapy.

Buproprion

Bupropion, also marketed as an antidepressant drug, is dosed at 150 to 300 mg/day (150 mg BID) for 7 days before stopping smoking, then at 300 mg/day (150 mg BID) for the next 6 to 12 weeks; the sustained-release preparation should be used. Bupropion also can be used in combination with a nicotine patch.[3] Bupropion in excessive doses can cause seizures and should not be used in individuals with a history of seizures or with eating disorders (bulimia or anorexia). On average, nicotine medications or bupropion treatment doubles the cessation rates found with placebo treatment, and absolute rates of smoking cessation have increased from 12% (placebo) to 24% (active medication) in clinical trials.

Varenicline

Varenicline is an α4 β2 nicotinic acetylcholine receptor partial agonist. Thus, varenicline both stimulates the receptor and blocks actions of nicotine on the receptor. The α4 β2 receptor subtype is believed to mediate the rewarding properties of nicotine. Varenicline appears both to reduce craving and other withdrawal symptoms after stopping smoking and to block the nicotine satisfaction if a person lapses to smoking. Clinical trials find cessation rates for varenicline treatment to be greater than either placebo (odds ratio 2.82) or bupropion (odds ratio 1.56).[4] The main side effects are nausea and abnormal dreams. Treatment is started 1 week before the target quit date. Dose escalation is recommended to reduce the risk of nausea: 0.5 mg per day for 3 days; 0.5 mg twice daily for 4 days; then 1 mg twice daily for 12 weeks. For those who have quit successfully at 12 weeks but would like futher pharmacologic support, treatment for an additional 12 weeks has been shown to sustain higher quit rates.

Follow-up

Follow-up office visits or telephone calls during and after active treatment increase long-term smoking cessation rates. Even in the best treatment circumstances, 70% or more of smokers relapse. Most smokers go through a quitting process three or four times before they finally succeed. When a quit attempt fails, the health care provider should encourage patients to try again as soon as they are ready. Cost-effectiveness studies find average costs per year of life saved of $400 to $900 for brief counseling by a physician alone and an incremental cost for adding a course of nicotine patch therapy of $2000 to $4000, depending on the individual's gender and age, to aid cessation. Smoking cessation treatment is much less costly per year of life saved than are other widely accepted preventive therapies, including treatment of mild to moderate hypertension or hypercholesterolemia.

Benefits of Quitting Smoking

The benefits of quitting smoking are substantial for smokers of any age. A person who quits smoking before the age of 50 years has half the risk of dying in the next 15 years compared with a continuing smoker. Smoking cessation reduces the risks for development of lung cancer, with the risk falling to half that of a continuing smoker by 10 years and one sixth that of a smoker after 15 years' cessation. Quitting smoking in middle age substantially reduces lung cancer risk, with a 50% reduction in risk if a lifelong smoker quits at 55 years of age compared with 75 years. The risk of acute myocardial infarction falls rapidly after quitting smoking and approaches nonsmoking levels within a few years of abstinence. Cigarette smoking produces a progressive loss of airway function over time that is characterized by an accelerated loss of forced expiratory volume in 1 second (FEV1) with increasing age. FEV1 loss to cigarette smoking cannot be regained by cessation, but the rate of decline slows after smoking cessation and returns to that of nonsmokers. Women who stop smoking during the first 3 to 4 months of pregnancy reduce the risk of having a low-birth-weight infant to that of a woman who has never smoked.

After quitting, smokers gain an average of 5 to 7 pounds, which is perceived as undesirable and a reason not to quit by some smokers. Smokers tend to be thinner because of the effects of nicotine to increase energy expenditure and reduce compensatory increases in food consumption. After they quit smoking, ex-smokers tend to reach the weight expected had they never smoked. On balance, the benefits of quitting far outweigh the risks associated with weight gain, and patients should be counseled accordingly.

2 comments:

VJ Sleight, Queen of Quitting said...

Great information but most smokers have an optomistic bias that they can smoke without any harmful effects. Unfortunately the doctors of smokers listen to their lungs say-"Your lungs sound fine." What the smoker hears is, "I can smoke without consequences, smoking is not hurting me." But the reality is that no one who smokes is healthy. The first step though, is developing a discrepancy between values that are important to the smoker and how that conflicts with their image of smoking. For free quitting tips visit: www.StopSmokingStayQuit.blogspot.com
VJ Sleight, Queen of Quitting, a former smoker, cancer thrivor and Tobacco Treatment Specialist.

pammi said...

Heart disease is one of the most dangerous disease which takes thousands of life every years all over the world. If we know its symptoms and Treatment for heart disease. We can prevent is to large extent.