eMedicine Specialties > Pediatrics: General Medicine > Pulmonology
Passive Smoking and Lung Disease: Treatment & Medication
Updated: Mar 3, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Treatment
Medical Care
Treatment for environmental tobacco smoke (ETS) exposure (secondhand smoke) consists of avoidance of ETS. This single step, although difficult for many families, can be facilitated with education about ETS effects and assistance with smoking cessation.6,7
- As a first, and often more manageable, step for families, a recommendation is made to stop smoking in the home or car.
- This simple step can reduce clinical symptoms of asthma and lead to reductions in maintenance therapy.
- In clinical practice, this recommendation must convey the importance of avoidance of these behaviors at all times, not simply while the child is in the home.
- Similarly, smoking in a distant area of the home is unacceptable; parents can be told, "Having a smoking area in your home is like having a urinating area in the bathtub."
- The effect of residual smoke or the odor of smoke in the home or on the clothing of the parents on the health of children is unknown, as is the value of cleaning up the environment after smoking cessation. Air filtration is insufficient to prevent the effects of ongoing exposure (without concomitant cessation), suggesting that the single best step is for the smoking to stop.
- Initiation of smoking cessation helps the health of the child exposed to ETS as well as that of the caregivers who smoke.
- A multitude of methods are available to help smokers quit; however, most people quit on their own and not through organized programs or with the help of others, such as a therapist, group, physician, or acupuncturist. Methods to quit smoking include the following:
- Self-care (without professional or medical assistance)
- Group programs
- Hypnosis or self-hypnosis
- Acupuncture
- Physician counseling
- Commercial smoking cessation programs
- Mass media or community programs
- Behavioral programs (including aversive therapy, rapid smoking, or gradual withdrawal)
- Work site smoking programs or policies
- The impetus to quit for many people comes from the advice or warnings of a physician, reinforcing the importance of the role played by the doctor and of ascertaining smoking behaviors.
- Although the percentage of people who succeed in quitting after a brief warning by a physician is small,8 the yield is large because so many people smoke.
- If all doctors counseled all smokers who came to them to quit and only 4% of those smokers succeeded in quitting, approximately 1.5 million smokers would become ex-smokers.
- The training of physicians in smoking cessation techniques and in the use of transdermal delivery of nicotine ("the patch") increases the success rates as much as 7-fold.
- All methods of quitting are enhanced by the addition of medical therapy to treat nicotine addiction.
- The use of the patch or of nicotine chewing gum enhances quit rates in smokers regardless of the quitting method used.
- The requirement of a physician to prescribe the nicotine patch may increase quit rates due to physician intervention.
- The odds of successfully quitting are enhanced by subsequent attempts to quit, reinforcing the importance of education to help motivate the smoker to attempt or reattempt to quit.
Diet
- Although nicotine can be found in small amounts in some dietary sources (see Laboratory Studies), data suggesting a dietary role in smoking cessation are sparse.
- Dietary counseling may be important because weight gain while quitting smoking is an important cause of recidivism.
- Sometimes, incorporation of smoking cessation within a general health maintenance program focuses on the role of dietary changes in helping to reduce overall cardiovascular risk factors, and incorporation of such a program is associated with improved success in quitting.
Activity
- The role of exercise in reduction of relapse in smoking cessation is not well proven.
- Successful cessation attempts are known to be associated with efforts to increase exercise in both men and women, though the role of counseling in eliciting this behavior (as opposed to self-motivation) is less certain.
Medication
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
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.
Adult
Gum: Chew 1 piece per h prn to abstain from smoking; not to exceed 24 pieces per d
Begin decreasing frequency after 6 wk; use 2 mg if <25 cigarettes per d and 4 mg for >25 cigarettes per d
Chew gum slowly until mouth tingles, then park the gum between the cheek and gum; when tingle is gone, begin chewing again until tingle returns; repeat process until most of tingle is gone (approximately 30 min)
Lozenge: Dissolve 1 lozenge PO q1-2h while awake for 6 wk, then reduce dose to 1 lozenge q2-4h during weeks 7-9, then reduce dose to 1 lozenge q4-8h during weeks 10-12; not to exceed 5 lozenges within 6 h and no more than 20 lozenges/d
Note: Initiate with 4 mg lozenge if first cigarette smoked within 30 min of waking, if first smoked is >30 min after waking, initiate with 2 mg lozenge
Pediatric
Not established
May decrease diuretic effects of furosemide and decrease cardiac output; may decrease absorption of glutethimide; may increase circulating cortisol and catecholamines; do not use if patient continues to smoke, use snuff, chew tobacco, or use other nicotine products because may increase toxicity of nicotine
Documented hypersensitivity
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Do not smoke cigarettes in addition to nicotine replacement; caution in peptic ulcer, coronary artery disease, angina, hypertension, peripheral arterial disease, diabetes mellitus, severe renal dysfunction, and hepatic dysfunction
Chew gum 4-6 times or until tingling sensation or peppery taste appears, then place between cheek and teeth until tingling dissipates, repeat this chewing process for about 30 min; do not eat or drink 15 min before or while chewing gum
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.
Adult
Nicoderm CQ initial dosage: 21 mg/d or 14 mg/d, depending on degree of addiction; apply patch qd for 6 wk, then decrease to next dosage per instructions
Nicotrol: Apply 15 mg every am for 6 wk; remove patch hs; then 10 mg qam for 2 wk, then 5 mg for 2 more wk, then discontinue
Apply new transdermal patch at same time each day and rotate application sites to avoid irritation; initiate with lower dose (ie, step 2 for each type of patch) if person smokes 10 or fewer cigarettes daily
Pediatric
Not established
May decrease diuretic effects of furosemide and decrease cardiac output; may decrease absorption of glutethimide; may increase circulating cortisol and catecholamines; do not use if patient continues to smoke, use snuff, chew tobacco, or use other nicotine products because may increase toxicity of nicotine
Documented hypersensitivity
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Do not smoke cigarettes in addition to nicotine replacement; caution in peptic ulcer, coronary artery disease, angina, hypertension, peripheral arterial disease, diabetes mellitus, severe renal dysfunction, and hepatic dysfunction; may cause skin irritation; if persistent insomnia occurs, remove 24-h patch at bedtime
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.
Adult
1-2 sprays per h intranasally; each spray contains 0.5 mg of nicotine; use at least 8 sprays per d but not to exceed >5 sprays per h or 40 sprays per d
Pediatric
Not established
May decrease diuretic effects of furosemide and decrease cardiac output; may decrease absorption of glutethimide; may increase circulating cortisol and catecholamines; do not use if patient continues to smoke, use snuff, chew tobacco, or use other nicotine products because may increase toxicity of nicotine
Documented hypersensitivity
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Do not smoke cigarettes in addition to nicotine replacement; caution in peptic ulcer, coronary artery disease, angina, hypertension, peripheral arterial disease, diabetes mellitus, severe renal dysfunction, and hepatic dysfunction; causes moderate-to-severe irritation in 94% of patients during the first 2 d of treatment, then declines to 81% and less severity (eg, runny nose. throat irritation, watering eyes, sneezing, cough, nasal congestion) after 3 wk of treatment; may cause coughing or exacerbation of asthma; may also cause burning or irritation upon administration
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).
Adult
Each inhaler cartridge delivers 4 mg of nicotine; once activated, may be used over several min to simulate smoking, although drug is generally absorbed from PO mucosa; instruct patients to use at least 6 cartridges daily for the initial 3-6 wk; not to exceed 16 cartridges per d
Pediatric
Not established
May decrease diuretic effects of furosemide and decrease cardiac output; may decrease absorption of glutethimide; may increase circulating cortisol and catecholamines; do not use if patient continues to smoke, use snuff, chew tobacco, or use other nicotine products because may increase toxicity of nicotine
Documented hypersensitivity
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Do not smoke cigarettes in addition to nicotine replacement; caution in peptic ulcer, coronary artery disease, angina, hypertension, peripheral arterial disease, diabetes mellitus, severe renal dysfunction, and hepatic dysfunction; may cause rhinitis and irritate the throat and mouth
Antidepressants
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.
Adult
150 mg/d PO for 3 d, then increase to 150 mg PO bid with at least 8 h between each dose for 7-12 wk
Pediatric
Not established
Carbamazepine, cimetidine, phenytoin, and phenobarbital may decrease effects; toxicity increases with concurrent administration of levodopa and MAOIs; concurrent use with other bupropion products may result in toxicity and seizures (eg, bupropion hydrochloride [Wellbutrin])
Documented hypersensitivity; seizure disorder; anorexia nervosa; concurrent use with MAOIs
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Caution in renal or hepatic insufficiency (decrease dose); doses >450 mg/d significantly decrease seizure threshold; initiate 1 wk before smoking quit date to obtain adequate serum levels; may cause hypertension; may increase risk of suicidal ideation or worsening depression
Nicotinic acetylcholine receptor partial agonists
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.
Adult
Initiate 1 wk before date chosen to stop smoking
Days 1-3: 0.5 mg PO qd pc
Days 4-7: 0.5 mg PO bid pc
Day 8 to end of treatment: 1 mg PO bid pc
Continue treatment for 12 wk; if successfully stopped smoking at end of 12 wk, an additional 12-wk course is recommended; take pc with full glass of water
Severe renal impairment (ie, CrCl <30 mL/min): Not to exceed 0.5 mg PO bid
End-stage renal disease (ESRD) with hemodialysis: Not to exceed 0.5 mg PO qd
Pediatric
<18 years: Not established
Data limited; coadministration with nicotine replacement therapy (NRT) may increase incidence of nausea, headache, vomiting, dizziness, and dyspepsia compared with NRT alone
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Common adverse effects include nausea, headache, vomiting, flatulence, insomnia, abnormal dreams, and dysgeusia; decrease dose with severe renal impairment (ie, CrCl <30 mL/min) or ESRD undergoing hemodialysis
Serious neuropsychiatric symptoms have been reported during postmarketing surveillance and may include changes in behavior, agitation, depressed mood, suicidal ideation, and attempted and completed suicide; these adverse events have been exhibited in patients without pre-existing psychiatric illness, and patients with pre-existing psychiatric illness have reported worsening symptoms during varenicline treatment (patients with serious psychiatric illness were not included in premarketing studies and safety and efficacy in these patients is not established); for more information, see the FDA MedWatch Safety Information
The FDA has published recommendations and considerations for health care professionals that include monitoring all patient taking varenicline for symptoms of serious neuropsychiatric behavior that may emerge during or following withdrawal of varenicline; to explain risks to patients, please see the Chantix Medication Guide
More on Passive Smoking and Lung Disease |
| Overview: Passive Smoking and Lung Disease |
| Differential Diagnoses & Workup: Passive Smoking and Lung Disease |
 Treatment & Medication: Passive Smoking and Lung Disease |
| Follow-up: Passive Smoking and Lung Disease |
| References |
| « Previous Page | Next Page » |
References
Gajewska E, Malak R, Mojs E, Samborski W. [Cigarette smoking--threat from first days of life]. Przegl Lek. 2008;65(10):709-11. [Medline].
Halterman JS, Borrelli B, Tremblay P, et al. Screening for environmental tobacco smoke exposure among inner-city children with asthma. Pediatrics. Dec 2008;122(6):1277-83. [Medline].
Yu M, Zheng X, Peake J, Joad JP, Pinkerton KE. Perinatal environmental tobacco smoke exposure alters the immune response and airway innervation in infant primates. J Allergy Clin Immunol. 2008;122:640-7. [Medline].
USDHHS. US Department of Health and Human Services. The health consequences of smoking: a report of the surgeon general. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health; 2004.
Centers for Disease Control and Prevention. Disparities in Secondhand Smoke Exposure–United States, 1988–1994 and 1999–2004. MMWR Morb Mortal Wkly Rep. 2008;57:744–7. [Medline].
Schwartz JL. Review and Evaluation of Smoking Cessation Methods: The United States and Canada, 1978-1985. US DHHS, National Cancer Institute, Division of Cancer Prevention; 1987.
US DHHS. The Health Benefits of Smoking Cessation: A Report of the Surgeon General. US DHHS Public Health Service, Office of the Surgeon General, Office on Smoking; 1990.
[Best Evidence] Priest N, Roseby R, Waters E, et al. Family and carer smoking control programmes for reducing children's exposure to environmental tobacco smoke. [update of Cochrane Database Syst Rev. 2003; (3): CD001746; PMID: 12917911]. Cochrane Database of Systematic Reviews. 2008;4:CD001746. [Medline].
US DHHS. Preventing Tobacco Use Among Young People: A Report of the Surgeon General. Atlanta, Ga: USDHH, Public Health Service, CDC, National Center for. Chronic Disease Prevention and Health Promotion, Office on Smoking and Health;1994. [Full Text].
Al-Delaimy WK, Crane J, Woodward A. Questionnaire and hair measurement of exposure to tobacco smoke. J Expo Anal Environ Epidemiol. Jul-Aug 2000;10(4):378-84. [Medline].
American Academy of Pediatrics, Committee on Environmental Hazards. American Academy of Pediatrics. Involuntary smoking--a hazard to children. Committee on Environmental Hazards. Pediatrics. May 1986;77(5):755-7. [Medline].
Cloutier MM, Wakefield DB, Hall CB, Bailit HL. Childhood asthma in an urban community: prevalence, care system, and treatment. Chest. Nov 2002;122(5):1571-9. [Medline].
Fiore MC, Novotny TE, Pierce JP, et al. Trends in cigarette smoking in the United States. The changing influence of gender and race. JAMA. Jan 6 1989;261(1):49-55. [Medline].
Fuji Y, Shima M, Ando M, et al. Effect of air pollution and environmental tobacco smoke on serum hyaluronate concentrations in school children. Occup Environ Med. Feb 2002;59(2):124-8. [Medline].
Groner J, Wadwa P, Hoshaw-Woodard S, et al. Active and passive tobacco smoke exposure: a comparison of maternal and child hair cotinine levels. Nicotine Tob Res. Oct 2004;6(5):789-95. [Medline].
Host A. The role of passive smoking and indoor pollution. Pediatr Pulmonol. Feb 2004;37 Suppl 26:218-9. [Medline].
Jaakkola MS, Piipari R, Jaakkola N, Jaakkola JJ. Environmental tobacco smoke and adult-onset asthma: a population-based incident case-control study. Am J Public Health. Dec 2003;93(12):2055-60. [Medline].
Lee YL, Hsiue TR, Lee CH, et al. Home exposures, parental atopy, and occurrence of asthma symptoms in adulthood in southern Taiwan. Chest. Feb 2006;129(2):300-8. [Medline].
National Institutes of Health, National Cancer Institute. Changes in cigarette-related disease risks and their implication for prevention and control. In: Smoking and Tobacco. 1997.
National Research Council. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: National Academy Press; 1986.
Overpeck MD, Moss AJ. Children's exposure to environmental cigarette smoke before and after birth. Health of our nation's children, United States, 1988. Adv Data. Jun 18 1991;1-11. [Medline].
Rushton L, Courage C, Green E. Estimation of the impact on children's health of environmental tobacco smoke in England and Wales. J R Soc Health. Sep 2003;123(3):175-80. [Medline].
Shiva F, Nasiri M, Sadeghi B, Padyab M. Effects of passive smoking on common respiratory symptoms in young children. Acta Paediatr. Dec 2003;92(12):1394-7. [Medline].
US DHHS. Major Local Tobacco Control Ordinances in the United States. 1993:1993.
US DHHS. Respiratory Health Effects of Passive smoking: Lung Cancer and Other Disorders. The Report of the U.S. Environmental Protection Agency. US DHHS, Public Health Service, National Institutes of Health;. US Environmental Protection Agency;1993.
Further Reading
Keywords
environmental tobacco smoke, ETS, second hand smoke, second hand smoking, smoke exposure, secondhand smoke, secondhand smoking, second-hand smoke, second-hand smoking, ETS-related lung disease, ETS-associated lung disease, recurrent pneumonia, asthma, bronchiolitis, upper respiratory infection, otitis media, bronchitis, sudden infant death syndrome, SIDS, lower respiratory tract infections, LRTIs, bronchiolitis, otitis media, sinusitis, upper respiratory tract infections, URTIs
