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Passive Smoking and Lung Disease Medication

  • Author: Timothy D Murphy, MD; Chief Editor: Girish D Sharma, MD, FCCP, FAAP  more...
Updated: Jun 07, 2016

Medication Summary

Medical therapies for smoking cessation have been used since the early 1900s with poor success. The use of lobeline sulfate to control cravings (later with antacids added) began in 1936 but was seriously challenged in the late 1960s through late 1970s; its use was virtually eliminated by 1980.

Meprobamate, used to minimize withdrawal, and amphetamines, used to counter excess sleepiness, are examples of drugs historically used to assist in smoking cessation. Potential for abuse and demonstration of a complete lack of efficacy led to these drugs falling out of favor. Similarly, other types of drugs have been used and tested (eg, anticholinergics, antidepressants, sedatives, tranquilizers, sympathomimetics, anticonvulsants). None of the drugs tested for smoking cessation worked well. Clonidine has demonstrated promise in helping to reduce symptoms of nicotine withdrawal but is no different than placebo in several well-controlled studies. Of all the medical therapies that have been tried, the only ones that have been shown to be effective are nicotine gum and, more recently, the nicotine patch and the antidepressant bupropion.

The problem with using medical therapy for nicotine addiction lies in nicotine's uniqueness in how it affects the CNS. Nicotine is the only drug that stimulates the CNS, leading to increased mental acuity and alertness, but with a simultaneous soothing of the peripheral nervous system. Drugs that stimulate the CNS to a similar degree, such as amphetamines, are not soothing peripherally; they are associated with tremor, nervousness, agitation, and paranoia. Drugs that are as soothing as nicotine, such as the benzodiazepines, are too depressing to the CNS and are associated with excess sleepiness and decreased mental acuity. For that reason, the best medical therapy for smoking cessation includes treatment with nicotine-replacement products.

The nicotine patch consists of a nicotine-impregnated pad within an acrylate adhesive, covered with a backing film, and attached to the skin with an adhesive layer. Nicotine, an alkaloid that binds to acetylcholine receptors, is thought to work through 2 CNS effects: (1) stimulation in the cortex through the locus ceruleus causing increased alertness and (2) cognitive performance and a reward effect via the pleasure system in the limbic system. Use of the patch is associated with increased quit rates, and the success rate doubles with the addition of some form of concomitant support.

Long-term benefits of the patch or nicotine-containing gum are not well described. In general, efficacy is greatly enhanced by concomitant therapies. Use of the antidepressant bupropion hydrochloride (Zyban, Wellbutrin) has been demonstrated to be of use in smoking cessation. A dose of bupropion of 300 mg/d correlated to nearly doubled quit rates at 2-month, 3-month, and 6-month time points compared to placebo control. Care must be taken to ensure that Wellbutrin (as an antidepressant) is not added inadvertently to Zyban (for smoking cessation) therapy.


Nicotine Replacement

Class Summary

Nicotine is the principal addictive substance in tobacco. Nicotine replacement plays an important role in smoking cessation programs. Nicotine is a pyridine alkaloid and naturally occurring autonomic drug. The drug is commercially available as the base in transdermal systems (Nicoderm CQ, Nicotrol), an oral inhaler, a nasal solution, and the polacrilex in chewing gum or lozenge. Nicotine is a ganglionic (nicotinic) cholinergic-receptor agonist. Pharmacologic actions of nicotine are complex and include various effects mediated by stereospecific binding to receptors in autonomic ganglia, adrenal medulla, neuromuscular junction, and the brain.

The pharmacokinetics of various commercially available dosage forms of nicotine and nicotine polacrilex differ principally in the rate, site, and extent of absorption of the drug; absorption is most rapid with intranasal administration of the spray (peak concentrations achieved within 4-15 min), followed by chewing gum (peaks within 25-30 min) and oral inhalation (peaks within 15-30 min). Absorption is substantially slower with the transdermal systems (peak within 2-10 h).

Buccal (chewing gum) nicotine polacrilex or a transdermal system, intranasal spray, or oral inhaler of nicotine is used for nicotine replacement therapy as a temporary adjunct in the cessation of cigarette smoking. Their use can either be unsupervised or in conjunction with a behavior modification program under medical or dental supervision.

The manufacturers currently do not recommend use of these preparations in children; however, because of the potential benefits of smoking cessation and the established efficacy of nicotine replacement therapy in adults, some clinicians recommend that such therapy be considered for adolescents who are nicotine dependent (ie, those who experience nicotine withdrawal manifestations with smoking cessation).

Nicotine polacrilex gum or lozenge (Nicorette Gum, Commit Lozenge)


Nicotine is quickly absorbed through the PO mucosa. Levels peak within 15-30 min, which closely approximates the time course of plasma nicotine levels observed after cigarette smoking. The gum or lozenge should not be swallowed.

Nicotine transdermal system (Nicotrol, Nicoderm CQ)


Designed to provide systemic nicotine delivery over 16 h. Apply daily after awakening and remove before retiring; instruct patients not to use the same Nicotrol transdermal system for >16 h.

Duration of daily use for Nicoderm CQ is longer (16-24 h) than Nicotrol. Patients who crave a cigarette upon awakening should wear Nicoderm CQ system for 24 h; patients who experience vivid dreams or other sleep disturbances with application of Nicoderm CQ for 24 h should remove the transdermal system after approximately 16 h of application, before retiring. Instruct patients not to use the same Nicoderm CQ transdermal system for >24 h.

Nicotine nasal spray (Nicotrol NS)


Intranasal nicotine may closely approximate time course of plasma nicotine levels observed after cigarette smoking. Peak plasma levels occur within 15 min.

Nicotine inhaler (Nicotrol Inhaler)


Quickly absorbed and closely approximates time course of plasma nicotine levels observed after cigarette smoking (within 15 min).

Amount of nicotine released depends on method of inhalation; unlike asthma medications in metered dose inhalers, nicotine can be administered effectively with either slow deep inhalations (pulmonary administration) or rapid shallow inhalations (buccal administration).



Class Summary

The mechanism of how bupropion helps in smoking cessation is unclear, although noradrenergic and/or dopaminergic effects presumably are involved. The 2 primary clinical uses for bupropion are in treatment of major depression and, as extended-release tablets, as an adjunct in the cessation of smoking.

Therapy may be combined with transdermal nicotine therapy if necessary; however, labeling for both bupropion and transdermal nicotine recommends that patients who receive bupropion and transdermal nicotine concurrently be monitored for the development of hypertension related to such therapy. Patients should begin receiving bupropion while they are still smoking because steady-state plasma concentrations of the drug are not achieved until after approximately 1 wk. A cessation date should be scheduled within the first 2 weeks of therapy with bupropion and generally should be set for the second week (eg, day 8).

Bupropion hydrochloride (Zyban)


Used in conjunction with a support group and/or behavioral counseling. Inhibits neuronal dopamine reuptake and is a weak blocker of serotonin and norepinephrine reuptake.


Nicotinic acetylcholine receptor partial agonists

Class Summary

These agents bind to nicotine receptors and elicit mild nicotine central effects to ease withdrawal symptoms. They also decrease the stimulatory effect of consuming nicotine products by blocking nicotine receptors.

Varenicline (Chantix)


Partial agonist selective for alpha4, beta2 nicotinic acetylcholine receptors. Action is thought to be result of activity at a nicotinic receptor subtype, where its binding produces agonist activity while simultaneously preventing nicotine binding. Agonistic activity is significantly lower than nicotine. Also elicits moderate affinity for 5-HT3 receptors. Maximum plasma concentrations occur within 3-4 h after oral administration. Following regular dosing, steady state reached within 4 d.

Contributor Information and Disclosures

Timothy D Murphy, MD Consulting and Attending Staff, Pediatric Pulmonary and Sleep Medicine, Mary Bridge Children's Hospital

Timothy D Murphy, MD is a member of the following medical societies: American Thoracic Society, American Academy of Sleep Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Chief Editor

Girish D Sharma, MD, FCCP, FAAP Professor of Pediatrics, Rush Medical College; Director, Section of Pediatric Pulmonology and Rush Cystic Fibrosis Center, Rush Children's Hospital, Rush University Medical Center

Girish D Sharma, MD, FCCP, FAAP is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, Royal College of Physicians of Ireland

Disclosure: Nothing to disclose.


Heidi Connolly, MD Associate Professor of Pediatrics and Psychiatry, University of Rochester School of Medicine and Dentistry; Director, Pediatric Sleep Medicine Services, Strong Sleep Disorders Center

Heidi Connolly, MD is a member of the following medical societies: American Academy of Pediatrics, American Thoracic Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

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