Environmental tobacco smoke (ETS), or secondhand smoke, is increasingly recognized as the direct cause of lung disease in adults and children.[1] ETS is responsible for significant mortality in adults, causing approximately 3000 deaths per year from lung cancer. It also causes significant effects on the lung health of adult nonsmokers, including reduced lung function, increased sputum production and cough, and chest discomfort.
In children, ETS is associated with an increased risk of lower respiratory tract infections (LRTIs), such as bronchitis and pneumonia. An estimated 150,000-300,000 cases of LRTIs in children younger than 18 months are attributed to ETS annually. ETS is causally associated with increased prevalence of fluid in the middle ear, upper respiratory tract irritation, and reduced lung function. It is also associated with increased severity of asthma in children;[2] the asthma of an estimated 200,000-1,000,000 children is worsened by ETS. Finally, ETS is a risk factor for the development of asthma in children.
Direct exposure to ETS affects the physiology of the respiratory tract, with symptoms of disease depending on which specific mechanism predominates and which anatomic area is affected most in an individual. The physiologic response to ETS is generally the same as that of the smoker but with a diminished effect. Such changes include increased mucus production (as much as 7-fold); decreased ciliary movement, beat frequency, and transport; increased WBC production and movement to the airway lumen; and increased mucosal permeability to allergens, associated with increased total and specific immunoglobulin E (IgE) levels and increased blood eosinophil counts.
Smoking is associated with acute and long term structural changes in the airways and pulmonary parenchyma, including upper airway mucosal gland hypertrophy and hyperplasia. In 2-week-old children of mothers who smoke, increased lung compliance has been observed. This led the authors to conclude that prenatal exposure to tobacco products negatively affects elastic properties of the fetal lung because 2 weeks of postnatal exposure was not thought to be enough to exert such an effect. Changes have been described in lung compliance and elasticity, including predisposition toward centrilobular emphysema in adults. A fifth-decade follow-up study of the Tasmanian Longitudinal Health Study cohort, which was first studied in 1968, found that heavy maternal smoking during childhood appears to predispose to spirometrically defined COPD in middle-age.[3]
In an animal model, tobacco exposure induced systemic and local responses, including elevation of plasma levels of C5a and brain-derived neurotrophic factor and increases in pulmonary tumor necrosis factor (TNF)-alpha, interleukin (IL)-5, monocyte chemoattractant protein (MCP)-1, and the density of substance P–positive nerves along the bronchial epithelium.[4] Perinatal ETS exposure also significantly increased the numbers of mast cells, eosinophils, monocytes, and lymphocytes in the lungs of infant monkeys. ETS exposure was also associated with decreased phagocytic activity of alveolar macrophages and a significantly decreased level of nerve growth factor in the bronchoalveolar lavage fluid. The effects of ETS on the fetus and infant continue to be studied, and the effects are many and deleterious.
Smokers comprise approximately 26% of the adult population, consuming more than 500 billion cigarettes annually.[5] Urinary cotinine levels, a marker of recent tobacco exposure, are present in 50-75% of adult nonsmokers, confirming that exposure to ETS is nearly ubiquitous. Approximately 9-12 million children younger than 5 years (50-66% of children this age) may be exposed to ETS in the home.
International
Data are lacking regarding the prevalence of international ETS exposure, but trends of increased tobacco consumption in Asia, South America, and Africa will increase the frequency of ETS-related disease.[6, 7] Current estimates are that more than 3 million people die annually from tobacco-related disease worldwide. In 1970-1972, tobacco consumption in developed countries was 3.25 times higher than in the developing world. By 1980-1982, this ratio had decreased to 2.38 and, by 1990-1992, to 1.75.
Mortality/Morbidity
In diseases for which ETS has a known causal link or is a known risk factor, a population-attributable risk factor can be calculated. Approximately 8,000-26,000 new cases of asthma are reported in children of mothers who smoke more than 10 cigarettes a day; if lower levels of exposure are considered, the number of new asthma cases caused by ETS is 13,000-60,000 per year. Exposure to ETS is a major aggravating factor in 10%, or 200,000, of asthma cases in children. Harder to detect, nonthreshold exposure to lower levels of ETS could account for worsening more than 1 million cases of asthma in children. Approximately 150,000-300,000 cases of LRTIs in children younger than 18 months are attributed to ETS, accounting for 7,500-15,000 hospitalizations yearly. Data demonstrate a continued relationship of LRTI to ETS in infants as old as 2 years.
Gill et al conducted a study to assess the effects of exposure to low levels of environmental tobacco smoke on asthma control, spirometry, and inflammatory biomarkers in school-aged children with asthma whose parents either denied smoking or who only smoked outside the home.[8] Their study cohort consisted of 48 patients (aged 8-18 years) with well-controlled, mild to moderate, persistent asthma that was treated with either inhaled corticosteroids or montelukast. Patients completed an age-appropriate asthma control test and a smoke exposure questionnaire. levels of exhaled nitric oxide, urinary cotinine, and leukotriene E(4) were measured, and spirometry was conducted. Comparisons were then made between findings for patients exposed to environmental tobacco smoke and those who were not exposed. Although only one parent admitted to smoking, 70% of the children had elevated urinary cotinine levels. Urinary leukotriene E(4) was higher in the children exposed to environmental tobacco smoke who were treated with inhaled corticosteroids but not in those treated with montelukast. The investigators concluded that a majority of school-aged children with persistent asthma may be exposed to environmental tobacco smoke, even if their parents insist that they do not smoke in the home.[8]
A population-attributable risk of LRTI for children older than 2 years has not been assessed, but cases of LRTI are expected to decrease. The Centers for Disease Control and Prevention (CDC) has calculated that exposure to maternal smoking accounts for more than 700 deaths from sudden infant death syndrome (SIDS), although the risk attributable to ETS exposure (vs in utero or lactation-related risk factors) is unknown.[9] Data that link ETS to middle ear disease or upper respiratory tract infection (URTI) widely vary, precluding an estimation of the frequency of those problems. Overall, ETS is responsible for hundreds of thousands to millions of episodes of acute illness in children every year. No case-specific determination of deaths attributable to ETS has been calculated other than those related to SIDS.
Sex
Data are limited regarding sex and ETS-related lung disease. In adults, the historical preponderance of male smokers meant that most spousal studies of never-smokers and ETS have examined mostly women. No clear sex-based differences in susceptibility to the effects of ETS are described in the pediatric population. Evidence from many studies demonstrates that the risk of ETS-associated disease is higher in children of smoking mothers than in those of smoking fathers, presumably because of closer contact of children with the mother.
Age
The risk of ETS to children has an inverse relationship to age. The reasons for this are not clear but may relate to a general decrease in illness frequency, physiological development of the lung anatomy or immunologic function, or decreased close contact between mother and child over time.
The specific diagnosis of passive smoke exposure (ie, secondhand smoke) is made by history.
Degree of exposure is best ascertained by questionnaire but can be elicited by simply asking the parents if they smoke or if anyone else smokes around the child.
Determining whether other caregivers, such as grandparents or day care workers, smoke around the child is important.
A history of findings consistent with the different diagnoses associated with ETS exposure should prompt questions related to smoking.[6, 10, 11, 7, 12] A history of the following can suggest environmental tobacco smoke (ETS) exposure:
The physical examination findings depend on the illness associated with ETS exposure.
Findings are consistent with the basic physiologic changes known to occur with smoke exposure, and these changes then predominate.
Increased signs of inflammation in the upper airways (asthma, bronchorrhea, rhinitis/rhinorrhea, bronchiolitis, increased mucus production and/or decreased mucus clearance) can suggest ETS exposure.
Specific findings are associated with specific illnesses (eg, wheezing associated with asthma).
The cause of ETS exposure is straightforward; smokers are in the child's environment.[10, 11, 7, 12]
Sometimes this is difficult to discern, particularly if a primary caregiver is unavailable to provide a history.
The reasons for a caregiver's smoking are myriad but may include a physiologic or psychologic predilection for addiction, the effects of aggressive advertising campaigns by the tobacco industry, and family exposure.
Tobacco use by a parent is a risk factor for initiation of smoking.
The diagnosis of passive smoking exposure (secondhand smoke) is primarily obtained by history.
Urinary cotinine levels have limitations and widely vary between individuals. As many as 50% of nonsmokers may show urinary cotinine, demonstrating the ubiquity of the exposure.
Levels are generally low and are less than 1% of those found in smokers.
Cotinine is a biomarker of environmental tobacco smoke (ETS) exposure but may not be related to the adverse effect under study.
Cotinine may not be specific for ETS exposure because dietary nicotine (eg, eggplant, green pepper, tea, tomato) may elevate cotinine levels.
Salivary or serum levels may also be measured.
Outside of a clinical history, questionnaires are the most common method to attempt to quantitate ETS exposure, but these can be limited by a lack of understanding of the questionnaire, bias, faulty memory, or intentional alteration of answers.
Kim et al investigated the relationship between exposure to secondhand smoke and lung cancer by histologic type on the basis of pooled data from 18 case-control studies in the International Lung Cancer Consortium.[13] Their data included those for 2,504 never-smoker case patients and 7,276 never-smoker control individuals; and 10,184 ever-smoker case patients and 7,176 ever-smoker control individuals. The researchers used multivariable logistic regression, adjusted for age, sex, race/ethnicity, smoking status, and pack-years of smoking. Among never-smokers, the odds ratios (ORs) comparing those ever exposed to secondhand smoke with those never exposed were 1.31 for all histologic types combined, 1.26 for adenocarcinoma, 1.41 for squamous cell carcinoma, 1.48 for large-cell lung cancer, and 3.09 for small-cell lung cancer. The estimated association with secondhand smoke exposure was greater for small-cell lung cancer than for non–small-cell lung cancers (OR, 2.11). The investigators concluded that the association with secondhand smoke is stronger for small-cell lung cancer than for cancers of other histologic types.[13]
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.[14, 15]
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[16, 17]
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,[18] 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.
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 relapse.
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.
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.
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 polacrilex gum or lozenge (Nicorette Gum, Commit Lozenge)
Clinical Context:
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.
Clinical Context:
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.
Clinical Context:
Intranasal nicotine may closely approximate time course of plasma nicotine levels observed after cigarette smoking. Peak plasma levels occur within 15 min.
Clinical Context:
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).
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).
Clinical Context:
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.
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).
Clinical Context:
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.
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.
The principal requirement of the care provider is to continue to assess for smoking in parents and to provide support and treatment for parents. Reiteration of the importance of not smoking in the home and provision of either smoking cessation information or referrals to the proper care providers are important.
The requirements for inpatient care depend on the illness associated with passive smoke exposure (secondhand smoke).
For further details, please refer to Medscape Reference articles on the specific illnesses (ie, bronchiolitis, bronchitis, upper respiratory tract infection, otitis media).
Prevention of the effects of environmental tobacco smoke (ETS) occurs through prevention of smoking; however, the effects of education regarding reducing ETS exposure to children in the family milieu are not well known.
A common clinical practice in pediatric and pediatric pulmonology offices is to counsel parents against smoking and, in particular, to focus on cessation of smoking in the home and in the car. Emphasis is placed on the importance of maintaining this rule at all times, not merely when the child is present; however, the efficacy of this approach has not been well studied.
Clearly, parental concerns for a child's health are motivating factors to change parental behavior, both during pregnancy and after birth.
Enactment of laws regarding ETS exposure in public spaces has significantly reduced exposures in many communities, but these laws vary in how aggressively they are enacted or enforced.[19]
Ordinances against smoking in public places first started to appear in the 1970s. In 1977, the first modern ordinance limiting smoking in restaurants and other public places was enacted in Berkeley, California.
Following the 1986 Surgeon General's report on the health consequences of involuntary smoking, the number of ordinances rapidly grew to nearly 400 by 1988.
Ordinances usually limit ETS in confined public spaces, workplaces, and restaurants.
Restrictions in restaurants are usually limited; a proportion of space or seating availability is usually required to be set aside for nonsmokers.
Special regulations regarding ventilation usually are not enacted.
After the release of the Environmental Protection Agency (EPA) draft report on Risk Assessment of ETS in 1990, more aggressive regulation started to appear, including ordinances banning any smoking in restaurants.
By 1992, the number of smoke-free ordinances passed into law began to significantly accelerate.
The tobacco industry has responded by attempting to push for enactment of state laws that are less restrictive and that limit the ability of local government to enact more aggressive ordinances.
The tobacco industry has legally challenged some ordinances on constitutional grounds, but state and federal courts have consistently upheld the constitutionality of local ordinances.
As of 1993, 543 city and county smoking ordinances were in effect.
The most rapidly growing population exposed to ETS (and the source of a significantly large proportion of ETS exposure in children) is children of young mothers of lower socioeconomic status. For this reason, prevention of smoking in the adolescent population should have a direct impact on ETS exposure in infants.
In the Surgeon General's report of 1994, entitled Preventing Tobacco Use Among Young People, the following major conclusions were reached:[20]
Almost all adult tobacco users began using during adolescence; this suggests that if adolescents were kept tobacco free, most would never start using tobacco.
Most young people who smoke are addicted to nicotine and report that they want to quit but are unable to do so. They experience relapse rates and withdrawal symptoms similar to those reported by adults.
Tobacco is often the first drug used by young people who use alcohol, marijuana, and other drugs.
Among young people, those with lower levels of school achievement, fewer skills to resist pervasive influences to use tobacco, friends who use tobacco, and lower self-images are more likely than their peers to use tobacco.
Cigarette advertising appears to increase young people's risks of smoking by affecting their perceptions of the pervasiveness, image, and function of smoking.
Community-wide efforts that include tobacco tax increases, enforcement of minor's access laws, youth-oriented mass media campaigns, and school-based tobacco-use prevention programs are most successful in reducing adolescent use of tobacco.
Currently, research is focused on determining which method of education will prove to be most effective in preventing tobacco use in adolescents and, increasingly, preadolescents.
Attention to the social status, educational level, race, and sex of the adolescent, with regard to which approach is best, is increasingly recognized as an important determinant of success.
Focusing on more than the health effects of smoking can lead to alterations in behavior. Looking instead at social issues such as the way in which the tobacco industry has attempted to addict children, or the role of the use of additives in enhancing addiction can serve to motivate adolescents to avoid tobacco, in some cases more effectively than information on negative health consequences alone.
The principal task of the care provider is to provide information to allow the parent to stop exposing the child to ETS. Because understanding the effects of passive smoke exposure on children is one of the most powerful motivating factors in smoking cessation, such information should be available in all primary care physician offices. Validation and comparison of different interventions remains an area of research, but separate studies have demonstrated the efficacy of an "intensive counseling" strategy. The time required to optimally educate the parent regarding ETS is unknown, but this education is commonly performed during a routine office visit.
Ortega Cuelva et al conducted a multicenter, open, cluster-randomized clinical trial to determine the effectiveness of a brief primary care intervention directed at parents who smoke.[21] The purpose of the intervention is to reduce exposure to tobacco smoke in babies. The study included 83 primary health pediatric teams of the Catalan Health Service and 1,101 babies whose parents were smokers. The intervention group received a brief tobacco smoke pollution intervention; the control group received the usual care. Outcomes were measured by parents' reported strategies to avoid exposing their babies to tobacco smoke. Baseline clinical data and characteristics of each baby's tobacco smoke exposure were collected, along with infant hair samples and parents' tobacco use and related attitudes/behaviors. At 3-month and 6-month follow-up, behavioral changes to avoid infant tobacco smoke exposure were recorded. During follow-up, tobacco smoke avoidance strategies improved more in the intervention groupthan in the control group. Reduced nicotine concentration was associated with improved implementation of effective strategies reported by parents at home and in cars. The researchers concluded that the intervention produced behavioral changes to avoid babies' exposure to tobacco smoke.[21]
For excellent patient education resources, visit eMedicineHealth's Healthy Living Center, Lung Disease and Respiratory Health Center, and Children's Health Center. Also, see eMedicineHealth's patient education articles Cigarette Smoking and Sudden Infant Death Syndrome (SIDS).
For more information on the pharmacology of nicotine and smoking cessation, go to Medscape Reference article Nicotine Addiction: Treatment & Medication.
Timothy D Murphy, MD, Consulting and Attending Staff, Pediatric Pulmonary and Sleep Medicine, Mary Bridge Children's Hospital
Disclosure: Nothing to disclose.
Specialty Editors
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
Disclosure: Nothing to disclose.
Acknowledgements
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
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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.
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.
National Institutes of Health, National Cancer Institute. Changes in cigarette-related disease risks and their implication for prevention and control. Smoking and Tobacco. 1997.
National Research Council. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: National Academy Press; 1986.
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