Authors: Mark S. Gold, MD, Distinguished Professor, Departments of Psychiatry, Neuroscience, Anesthesiology, Community Health and Family Medicine; Chief, Division of Addiction Medicine, Department of Psychiatry, University of Florida, Gainesville; David Q. Wang, University of Florida, Gainesville; and Andrie W. Bruijnzeel, PhD, Assistant Professor, Department of Psychiatry, University of Florida, Gainesville.
Peer Reviewer: Alan Melnick, MD, MPH, Associate Professor, Director of Research, Oregon Health Science University, Department of Family Medicine, Portland.
The role of tobacco in society remains controversial, as the forces of economics and addiction continue to maintain the ubiquity of cigarettes. Despite policy and public sentiment shifts, the tobacco industry remains powerful and maintains a steady supply and demand of their products. In addition to the detrimental health effects to the primary smoker, secondary repercussions of cigarette smoke are found in secondhand smoke exposure. While secondhand smoke differs quantitatively from active tobacco smoke, it remains a health hazard to all exposed. The prevalence of secondhand smoke exposure remains high despite restrictions and public health warnings.
In this paper, health effects of secondhand smoke exposure are examined in both children and adults. A brief overview of methods used to screen for secondhand smoke exposure will be given. Among the complications to be discussed are those of cardiovascular, pulmonary, and neurological systems. The profound implications of secondhand smoke exposure in development and exacerbation of coronary artery disease should be appreciated by the reader. In addition, co-morbid conditions to childhood secondhand smoke exposure are presented. Methods used to curb parental smoking in the presence of children are introduced and examined in efficacy. The role of the physician is to warn smokers of the myriad effects of secondhand smoke exposure to others and to help guide the patient through a smoke cessation program. — The Editor
History
The long history of tobacco is marked with trade, controversy, abuse, and policy shifts. Although tobacco usage has been discouraged and even prohibited throughout much of history, persistence of the drug can be attributed to several factors, including economics, public policy, marketing, and its inherent addictive qualities. Only the past 50 years have seen a marked reduction and restriction in tobacco use. This acceleration of tobacco regulation is credited mostly to public policy changes. While recent advances have been made to curb the usage and proliferation of tobacco, the ultimate fate of tobacco regulation may be determined by the forces of capitalism rather than public health efforts.1
Restriction of tobacco usage is neither a recent policy development nor a novel ideal. Early prohibition of tobacco occurred in the 16th and 17th centuries, though these restrictions mainly were established for religious reasons. While the mechanistic effects of tobacco were not realized until the advent of modern medicine, cancer was suspected to be linked to tobacco as early as the 18th century. Epidemiological studies published in the 1920s confirmed this suspicion. German scientists published further case-control studies in the 1930s and early 1940s, providing considerable evidence for the detrimental health effects of tobacco. These early studies provided strong evidence for a link between lung cancer and tobacco smoke while also suggesting a link to coronary heart disease. The German government strongly shifted policy to reflect these findings, imposing cigarette taxes, advertising restrictions, anti-cigarette advertising, and even a workplace-smoking ban. However, World War II overshadowed these efforts and German medical research was largely ignored.2
United States and United Kingdom publications in the 1950s and 1960s finally brought widespread publicity to the carcinogenicity of tobacco. The 1964 Surgeon General’s Report on Smoking and Health brought tobacco to the forefront of public policy, and an immediate campaign was launched against tobacco use.3 Since then, a wide array of measures have been implemented that include warning labels, consumer education, taxation, marketing regulation, anti-smoking advertising, and restrictions on tobacco sale. Discovery of secondhand smoke effects led to restriction of smoking in public places, restaurants, workplaces, public transportation, elevators, and domestic airline flights.1 Other factors that have led to a recent decrease in tobacco consumption include pharmacological therapies, litigation, and an overall public sentiment shift.3
Definitions
Key Terms. Environmental tobacco smoke (ETS), or secondhand smoke (SHS), is defined as passive smoke exposed to nonsmokers. SHS is composed of smoke given off by smoldering tobacco products and smoke exhaled by active smokers, termed sidestream smoke and mainstream smoke, respectively. It has been estimated that SHS falls behind only active smoking and alcohol abuse for leading causes of preventable poor health and premature death in the United States.4
Composition
Tobacco smoke and SHS share similar chemical compositions, both containing a wide variety of toxic and carcinogenic substances. Sixty of the more than 4000 compounds in tobacco smoke are known or suspected carcinogens, including 4-aminobiphenyl, benzene, nickel, and various polycyclic aromatic hydrocarbons and N-nitrosamines. While mainstream smoke and sidestream smoke are almost identical in chemical compositions, the concentrations of components vary due to differences in temperature of combustion, pH, and dilution in the air. Sidestream smoke contains toxic and carcinogenic substances generated in greater amounts due to lower temperatures and more reducing conditions,5 affecting the chemical composition of SHS and possibly accounting for the carcinogenic effects observed in SHS exposure.
Measuring Secondhand Smoke
Several biomarkers have been developed to detect and quantify uptake of tobacco smoke components in nonsmokers. Among these, human urinary carcinogen metabolites provide an effective method of measuring recent exposure to SHS. Metabolites of the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) have been found to be elevated consistently in the urine of nonsmokers exposed to SHS by active smokers. These metabolites exist mainly in the form of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) and its glucaronides, and typically are found at 1-5% concentrations (as those of active smokers).6 Long-term SHS exposure mainly has been examined by detecting the nicotine metabolite cotinine in hair samples.6 This method also provides the advantage of determining time frame of exposure. Use of biomarkers such as cotinine helps to minimize miscalculation of environmental tobacco exposure in SHS studies. Various studies suffer from confounding variables, such as exposure of "unexposed" groups to SHS from non-parental sources or places outside the home.7 It also is shown that parents tend to underreport SHS exposure for children with respiratory disease.8
Environmental markers serve as a diagnostic measure of SHS exposure in microenvironments. The most common environmental markers include nicotine vapor phase and respirable suspended particulate sampling.9 Nicotine vapor phase determination is used widely to measure SHS levels, due to its specificity for tobacco smoke.10 These diagnostic tests have served as methods to enforce policies against smoking in the workplace.
Pediatric Exposure to SHS
General. Childhood exposure to SHS carries profound repercussions (which will be discussed at length). In addition to postnatal exposure, current literature demonstrates developmental deficits resulting from in utero exposure to maternal smoking, leading to problems such as low birth weight, sudden infant death syndrome (SIDS), childhood attention deficit hyperactivity disorder (ADHD), and behavioral issues.11-14 SHS itself contains adequate levels of nicotine to be taken in by a pregnant mother and passed on to the baby. Unfortunately, extensive discussion of the myriad effects implied by in utero exposure is not within the scope of this paper. Nonetheless, one should assume effects of childhood SHS commonly may overlap with effects of in utero exposure to maternal smoking, as smoking during pregnancy is likely to be associated with postnatal smoking.
The prevalence of smoking in the face of dangerous SHS effects is staggering. A 1996 national survey in China found that 53.6% of nonsmoking children and adults were exposed to passive smoke for at least 15 minutes per day at least twice weekly.15 The World Health Organization estimates that half of the world’s children are exposed to SHS at home. In the United States, an estimated 8.7 to 12.4 million children younger than 5 years of age regularly are exposed to SHS at home. Among American children ranging from 2 months to 11 years of age, approximately 42% live in a home with at least one smoker.1 Clearly, SHS exposure presents a widespread and prevalent health risk in the United States today.
The effects of SHS exposure to children of smoking parents is not limited strictly to physiological factors. Parental smoking exerts genetic, environmental, and social influences, which may contribute to the effects examined in many studies. In addition, smoking parents generally may predispose children to less healthy lifestyles in diet and exercise. These influences provide confounding variables that should be taken into consideration throughout an examination of the literature.
Dependence. As 42% of children in the United States regularly are exposed to SHS, this epidemic level of SHS exposure to children carries profound consequences. Previous studies demonstrate a link between maternal smoking during childhood and increased risk of smoking in young adulthood.16 The significance of adolescent smoking is heightened as approximately three-quarters of adult tobacco users report that their first tobacco use occurred during childhood or adolescence.17 Secondhand exposure to nicotine may mediate an increased risk of smoking by reducing aversive effects during first experimentation with tobacco, as chronic exposure to low levels of nicotine may induce tolerance.17 It has been shown that those who experience less aversive effects during initial tobacco use in childhood or adolescence more likely will become regular tobacco users in adulthood.17 Another suggestion is that early exposure to nicotine potentiates the rewarding effects of the drug during experimentation, which may facilitate the first step in addiction.17 However, more extensive research is required to determine the role of secondhand smoke exposure in the alteration of brain reward pathways to induce higher risk of nicotine dependence.
Complications. Respiratory Disease. The prevalence of respiratory disease in children among smoking households consistently has been shown to be higher than among nonsmoking counterparts. Studies have established increased risk of respiratory symptoms such as wheezing, coughing, phlegm, breathlessness, bronchial reactivity, and asthma among children with at least one smoking parent.18 In addition, childhood exposure to SHS also inhibits lung function.19 The increased risk of respiratory diseases illustrates just one aspect of the damaging effects of SHS in children.
Research into the effects of SHS on asthmatics has yielded inconsistent results. While SHS has been shown to exacerbate pediatric asthma symptoms, it has not been isolated as a single factor for development of the disease itself. Epidemiological evidence indicates that maternal smoking is associated with wheezing illness through age 6, though effects begin to taper off after this age. This increased incidence of wheezing in smoking households is largely attributable to nonatopic "wheezy bronchitis," which is a relatively benign prognosis. However, among children with established asthma, passive smoke is associated with progressively severe disease. Thus, SHS should be considered a co-factor provoking wheezing attacks, rather than a singular cause of the underlying asthmatic disease.20
In addition to wheezing, infants exposed to SHS have a dramatically increased risk of developing lower respiratory tract illnesses, including bronchitis and pneumonia.21 Resulting lower respiratory tract illnesses in infants are higher in both frequency and severity. An early hypothesis for increased incidence of respiratory infection is that smoking parents themselves are more susceptible to infections and may transmit diseases to their children. To account for this confounding variable, studies were performed to examine respiratory symptoms of children adjusted for parental phlegm production.22 However, these results did not explain the higher prevalence rates of respiratory symptoms among children of smoking households. The underlying cause of increased respiratory infection risk requires more extensive examination.
Cardiovascular. While active smoking has been considered a risk factor for developing cardiovascular (CV) disease as early as the 1930s, SHS exposure only recently has come into the spotlight for its role in initiation and progression of CV disease, including underlying problems such as abnormal anatomic development, myocardial abnormalities, dysrhythmias, and derangements in blood pressure and cholesterol metabolism. Though onset of CV symptoms can occur acutely, permanence of these effects is dependent on both developmental stage and length of exposure. Various CV consequences of SHS exposure are demonstrated in the literature and are included in Table 1.23-25
Table 1. Various Consequences
of
Secondhand Smoke Exposure23-25
Cohort studies performed on pubertal children showed that long-term SHS-exposed children exhibited reduced levels of high-density lipoprotein cholesterol (HDL-C). In adults, high levels of low-density lipoprotein cholesterol (LDL-C) and low levels of HDL-C and its major subfractions are associated with myocardial infarction.26 It was concluded that white males with a family history of CV disease, higher weights, and increased diastolic blood pressures might be at special risk for developing coronary artery disease due to SHS exposure.25 As childhood sets the stage for atherosclerotic changes found in middle age, these results may heighten the significance of early SHS exposure.
Neurological. Although the body of literature on neurological alterations due to passive smoking mainly concerns in utero exposure, the development of neural pathways continues through childhood into adolescence. The mechanisms for brain development are becoming increasingly clear, though research in this field still is in its infancy. The role of nicotinic acetylcholine receptors (nAChR) in synaptic signaling has long been established, yet the high concentration of neurotransmitters in early developmental stages hinted toward an additional trophic role. Indeed, the trophic role of nAChRs now is being elucidated and is known to promote neural cell replication, initiate the switch from cell replication to differentiation, enhance or retard axogenesis/synaptogenesis, and enable migration of specific cell populations.26 These effects elicited by acetylcholine and its agonist nicotine are determined by the time period of exposure in neurodevelopment.
Disruption of neural development by nicotine has been attributed to several mechanisms—outright cell loss, specific alterations of neural activity, and misprogramming of receptor signaling mechanisms.26 Such mechanisms can mediate changes in brain development from early embryogenesis through puberty, as neuroproliferation, apoptosis, and synaptic rearrangement continue into adolescence—especially the critical cholinergic pathways that control learning, memory, and psychostimulant responses. A specific mechanism of disruption observed in rats postnatally exposed to SHS involves reduction of cell population and increasing cell size in the hindbrain, a region that undergoes dramatic postnatal developments.27 However, rats exposed exclusively in the prenatal stage did not demonstrate biochemical changes in hindbrain DNA concentration or cell population. This study provided clear evidence of the disruptive effects of SHS specifically in postnatal vs. prenatal development.27
In addition to mechanisms of neurodevelopmental disruption, tobacco exposure has been implicated in a human postnatal condition characterized as more excitable and hypertonic, requiring more handling and displaying more stress and abstinence signs. This physiological condition appears to result from fetal hypoxia due to nicotine-mediated reduction of blood flow to the fetus. Higher concentrations of carboxyhemoglobin due to carbon monoxide also may contribute to hypoxic effects. These consequences are particularly pronounced in the central nervous system (CNS) as well as the gastrointestinal and visual areas.28
Secondhand smoke effects on brain development are compounded in studies that show SHS-exposed infants are more likely to show impaired visual and auditory orientation, increased tremors, and delayed reflex developments.29 In addition, mothers who smoke during pregnancy are significantly more likely to have a child diagnosed with ADHD, while a recent study suggests exposed children are twice as likely to commit a violent crime, even after controlling for other biopsychosocial risk factors.30
Cancer. Due to the different chemical composition and concentrations of agents in SHS, the carcinogenic effects have yet to be clarified. While current literature suggests an increased risk of childhood cancers and leukemia from SHS exposure, conclusive evidence has yet to be gathered. An early study presented a 50% increase in adult-onset cancer for children of smoking fathers. Specific sites with elevated relative risk for cancer included cervix, brain, and hematopoietic tissue.31 The authors noted that this increased risk was not explained by demographic factors, social class, or individual smoking habits, and was not limited to known smoking-related sites. Meta-analysis of maternal pregnancy smoking and childhood cancer found a small increase in risk for all neoplasms [relative risk (RR) 1.10; 95% confidence interval (CI), 1.03-1.19; based on 12 studies], with the exception of the specific neoplasms leukemia (RR 1.05; CI, 0.82-1.34; 8 studies) and CNS tumors (RR 1.04; CI, 0.92-1.18; 12 studies).32 The data presented did not demonstrate a strong association for any single type of tumor. Bias and confounding factors were addressed as weaknesses, and further studies are required to address these issues and provide more convincing results.
Sudden Infant Death Syndrome (SIDS). Sudden death of an otherwise healthy 1-month- to 1-year-old (usually while sleeping), with an idiopathic conclusion after thorough case examination and autopsy is termed SIDS. SIDS accounts for the majority of postneonatal mortalities in developed nations8 and has been linked to particulate air pollution, although the mechanisms that underlie the epidemiological data remain unclear.33 An existing theory is that SHS exposure contributes to reduction of the infant’s ability to respond to hypoxia (such as in sleep apnea).34 An increase in SIDS prevalence was noted for households with maternal smoking after pregnancy, paternal smoking, and smoking by other members of the household.35 Combined data from six studies revealed paternal smoking increased risk of SIDS, while maternal smoking carried a larger relative risk,36 possibly due to a variety of factors such as in utero exposure, breastfeeding, or more extensive exposure to the infant. In a sample of pericardial fluid from SIDS cases, 70% of subjects displayed elevated cotinine levels, underscoring the many studies that consistently link SHS to increased SIDS risk.37 Physicians should discuss the implications of heightened risk of SIDS with potential parents who continue to smoke through pregnancy and birth.
Middle Ear Disease. Otitis media, also known as "glue ear," is a common middle ear disease among children younger than 2 years of age. Data from prospective cohort studies have demonstrated a strong correlation between SHS exposure and otitis media development in the first two years of life. Furthermore, SHS has been linked to chronic otitis media rather than occasional or single occurrences.38 However, case-control studies of older children do not consistently support the correlation between childhood SHS and otitis media development. Despite the conflicting evidence, the Environmental Protection Agency has concluded that an association between childhood SHS exposure and otitis media is present.39
Miscellaneous. SHS exposure has been related to an increased risk of developing dental caries. A recent study found that serum cotinine levels are related to development of dental caries in deciduous but not permanent teeth.40 Additionally, a dose-response, inverse relationship exists between ETS exposure and serum ascorbic acid levels.41 Results from another study demonstrated that plasma ascorbic acid concentrations were lower by an average of 3.2 micromol/L in ETS-exposed children when compared to unexposed children who consumed equivalent amounts of vitamin C (P = 0.002).42 This reduction in plasma ascorbic acid was observed even with very low exposure to ETS. The authors conclude that children exposed to ETS should be encouraged to consume increased amounts of foods rich in vitamin C or should be given the equivalent amount of vitamin C as a supplement, as ascorbic acid is an important blood antioxidant.42
An area of recent research is the correlation between maternal smoking and smoking in adolescents. It has been shown that children of regularly smoking and nicotine-dependent mothers have higher likelihoods of using tobacco and developing nicotine dependence.43 These findings include children whose mothers reported lifetime smoking except during pregnancy. Thus, the results indicate postnatal SHS exposure is a strong predictor of future smoking and nicotine dependence of exposed children.
Pediatric Co-morbid Conditions
Drug Abuse. Although current research has not attributed postnatal childhood SHS exposure to alcohol abuse, in utero exposure has been linked to increased alcohol abuse in adolescence and adulthood. Children of mothers who smoked during pregnancy are more likely to develop alcoholism than non-exposed counterparts.44 Similarly to alcohol abuse, in utero exposure from smoking mothers results in an increased risk for drug abuse. Daughters of mothers who smoked 10 cigarettes a day during pregnancy displayed a 5-fold higher likelihood of adolescent drug abuse. Of the daughters that did abuse drugs, 70% abused more than one, with the most frequent combination being marijuana and cocaine.
Psychiatric Disorders. The association between behavioral problems and maternal smoking during pregnancy has been demonstrated extensively and consistently through many studies.45 Among these behavioral problems are hyperactivity, decreased attention span, conduct disorders, and adulthood criminality.45,46 The association to ADHD has been examined through sibling studies in which the mother smoked in one pregnancy but not the other.45 Maternal smoking during pregnancy has been associated with externalizing (tendency to seek controversy, aggressive, hyperactive) but not internalizing (withdrawn, depressed, anxious) behavioral problems.47 In addition, maternal smoking has been identified as a significant predictor of childhood negativity, independent of demographic, perinatal, relationship, and maternal personality factors.47
Pediatric Intervention
Traditionally, SHS intervention involves smoking cessation of parents or other sources of SHS exposure. These cessation methods may include behavioral, pharmacologic, and alternative methods. Alternative intervention methods to smoking cessation included isolation of ETS from the child by discouraging parents from smoking around children.48 Promotion of smoking cessation or isolation can be accomplished though increasing awareness of childhood vulnerability to SHS while encouraging parents to protect the health of their children. In general, the aims of such approaches are:
1. To increase public awareness of the negative health impacts of SHS;
2. To develop and maintain programs, mass media messages, and integrated communications plans that attract community support and motivate positive behavioral change.
Aggressive programs have been developed to educate physicians about current and effective interventions to help patients stop smoking around their children. It is the role of a pregnant woman’s primary care physician to encourage smoking cessation, educate her on the array of detrimental health effects, and help guide her through a smoke cessation program. A recent meta-analysis indicated that such physician intervention is effective in increasing the likelihood of smoking cessation.49
Increasing the cost of tobacco creates an economic barrier for youth smoking initiation, also motivating adults to quit smoking. Aside from economic intervention, comprehensive inpatient smoking cessation programs have been developed. These programs have been shown to be highly successful in treating those who otherwise would not quit smoking. While such comprehensive inpatient smoking cessation programs have been found to be more effective than minimal treatment programs, less intensive treatment approaches, when combined with high participation rates, are effective in treating large groups. A combination of medicine and cognitive-behavioral group therapy in smoking cessation clinics has demonstrated success in long-term abstinence from smoking.50
Brief Intervention. Less comprehensive methods of intervention are widely available—these include self-help leaflets, videos, and complementary therapies (hypnotherapy, acupuncture). Health educational kits, videos, and fact sheets discussing the benefits of a smoke-free environment comprise the majority of these programs. Examples of these interventions are the Healthy Baby Program, Sure Start Program, and Kids Need Breathing Space Program.
The effectiveness of these programs remains debatable. Most studies have shown a decrease in maternal smoking resulting from intervention, though intervention-control differences are relatively small. Some research has shown that behavioral counseling for mothers is effective in reducing young children’s exposure to tobacco smoke at home.48 Similarly, client-centered intervention aimed at increasing self-efficacy was effective in stemming infant SHS exposure (when applied in a routine clinical setting). However, a recent Cochrane Systematic Review, which identified reduction of SHS exposure to children in both intervention and control groups from 12 of the 18 studies reviewed, questioned the efficacy of such programs. Only four of the 18 studies demonstrated a statistically significant intervention effect. The statistically significant studies employed intensive intervention methods, and it was concluded that brief interventions were not definitively effective for improving child health. More rigorous study designs, interventions of greater intensity and duration, and those based on sound behavior change theory may yield more promising results in the future.
Adult Exposure to SHS
Occupational Exposure. By the early 1990s, the evidence for SHS-related health effects was clear, yet no state legislature had passed legislation banning workplace smoking. While local governments had been successful in enacting such legislation, it was not until 1994 that California passed the first statewide tobacco smoking ban. Due to the success of this ground-breaking legislation, Delaware, New York, Connecticut, and Maine followed enacting similar legislation.51 Florida has enacted a ban on indoor smoking, but it does not apply to bars that generate less than 10% of revenue from food sales. Despite this legislation, it is estimated by the American Cancer Society that each week, 5,573,000 people in Florida are exposed to SHS in the workplace. Nearly 800,000 people in Florida are exposed to SHS on a daily basis. Personal factors affecting SHS exposure are age, occupation, gender, and race, while microenvironmental factors such as the active source and ventilation system also play a role.
Workplace exposure to SHS, while restricted by some smoking policies, continues to affect the health of countless employees worldwide. Airborne nicotine is present, often in excessive concentrations, in various workplaces due to variable public smoking laws.52 Recent regulation of smoking in public places was instituted in response to data published by the American Society of Heating, Refrigerating, and Air Conditioning Engineers (ASHRAE). These regulations prohibit all indoor smoking, regardless of additional ventilation and air-cleaning devices.53 While separation of nonsmokers and smokers (maintaining smoke-free zones, designating smoking zones) reduces SHS exposure to nonsmokers, it does not guarantee SHS-free airspace. The inefficacy of separation methods was illustrated in a study demonstrating that nicotine concentrations in the nonsmoking section of a restaurant were roughly equivalent to that of the smoking sections.54 Due to the overwhelming and continuously mounting evidence of detrimental health effects of SHS, workplace environments have undergone a dramatic shift from smoking to nonsmoking in the past two decades.
High Risk Occupations. Those who remain at high risk of workplace SHS exposure are employed at construction sites, restaurants, cafeterias, bars, casinos, railroads, and other unregulated or under-regulated areas.55,56,57 Various studies have shown that quantitative measures of SHS exposure are directly related to workplace smoking policy. This is particularly true for blue collar occupations, which generally display higher workplace ETS levels.57 In cases where statewide or local legislation has not been enacted, local workplace regulation serves as the best method of maintaining microenvironmental air quality.
Assessment and Detection. As previously mentioned, several biomarkers have been developed for assessment of SHS exposure. Breath analysis recently has gained popularity as an assessment tool for smoking. This analysis technique measures organic compound values, which are predominantly blood borne and therefore enable monitoring of different processes in the body. A recent study employing this technique detected the presence of volatile organic compounds in nonsmokers after SHS exposure.58 While improvements are being made to ensure accuracy of this technique, current studies employing this method suffer sampling and normalization issues.
Currently, a combination of urine cotinine levels, hair cotinine tests, and a questionnaire appears to be the optimal method for determining SHS exposure. Empirical studies show general concordance of reported and environmental/biological measures of SHS exposure.59 In addition, urinary cotinine often is used for evaluating impact of smoking cessation programs, monitoring high-risk groups such as pregnant women, and assessing occupational SHS exposure.60
Complications. Pulmonary. In adults, SHS exposure has been associated with pulmonary complications such as asthma, lung function impairment, and increased "bronchial responsiveness."61 The consequences associated with workplace SHS exposure are considered to be worse than household exposure. This is due to several factors that may augment the effects of ETS in the workplace, including synergistic effects with occupational toxins, cigarette surface contamination, and higher levels of ETS.57 While current findings are not comprehensive, it generally is accepted that there is a relationship between SHS exposure and reduction of lung function in adults. In addition, several studies suggest passive smoking may cause respiratory illnesses and symptoms. Unfortunately, few studies have been conducted comparing respiratory symptoms in exposed nonsmokers and unexposed nonsmokers, and reliable evidence of an association is not yet available. However, a Swiss study on air pollution and lung diseases in adults sampling 4197 nonsmoking adults demonstrated an SHS-associated increase in risk of asthma, wheezing, bronchitis, and dyspnea.62
The link between SHS exposure and aggravation of adult asthma has been suggested in several studies. Passive smoking is believed to aggravate and intensify the symptoms of asthma in adults, as studies have shown asthmatics express dramatic exacerbation upon SHS exposure.63 However, physiological response due to suggestibility may be considered a confounding variable as the subjects cannot be blinded.
Cardiovascular. It is estimated that heart disease accounts for 37,000 of 53,000 SHS-related deaths each year in the United States.64 Through this epidemiological data, it becomes clear that heart disease is the main consequence of passive smoking. The consequences of passive smoking are almost immediate, as it was demonstrated that 30 minutes of SHS exposure resulted in a decrease of endothelial function identical to levels of routine smokers.61 A recent study was conducted to determine the association of SHS and risk of myocardial infarction. It was determined that smoking bans at public workplaces correlated with reduced morbidity from heart disease.65 This corroborated the CDC’s earlier assertion that people at risk for heart disease should avoid SHS, as it raises risk for acute myocardial infarction. Possible mechanisms for this relationship involve platelet activation, endothelial dysfunction, and broad inflammation.65 Additionally, exposure to SHS may promote vasoconstriction, facilitating blood clotting. This combination of factors raises the risk for myocardial infarction.
While the association between active smoking and coronary heart disease (CHD) has long been established, passive smoking also has been implicated in CHD. A recent study found a 50-60% increase in risk for CHD development among SHS-exposed nonsmokers.66 Both active and passive smoking are known to:
- Increase incidence and frequency of cardiac arrhythmias;
- Decrease oxygen-carrying capacity of blood;
- Increase incidence of coronary artery spasm;
- Promote atherosclerosis; and
- Increase incidence and tendency for thrombosis (Table 2).
Table 2. Cardiovascular Effects
of Active and Passive Smoking
A recent study was performed to characterize the relationship between SHS and inflammatory markers. It was demonstrated that SHS exposure resulted in elevated levels of white blood cells, C-reactive protein, homocysteine, fibrinogen, and oxidized LDL cholesterol. Additionally, the concentration of inflammatory markers was proportional to length of SHS exposure. Subjects undergoing only occasional SHS exposure also exhibited elevated levels of inflammatory markers, suggesting even mild SHS exposure is a risk factor for CHD.67 This risk is mediated by increased platelet aggregation, lipid peroxidation, and endothelial damage by ETS.68 ETS may cause arteriosclerosis by altering cholesterol concentrations or by accelerating lipid peroxidation via suppression of serum antioxidant defense.69
While nicotine plays a major role in mediating the undesirable effects of SHS, other elements of SHS such as carbon monoxide and polycyclic aromatic hydrocarbons also contribute to the damaging effects. When abstinent smokers with nicotine patches were compared to active smokers, platelet activity differed significantly despite similar nicotine levels. Studies examining platelet sensitivity suggest nicotine is not the sole cause of increased aggregation.70 The cardiovascular consequences of SHS are clear and have been declared by the American Heart Association, the Scientific Committee on Tobacco and Health in the United Kingdom, and the California Environmental Protection Agency.
Cancer. SHS exposure has been implicated in the cause of several types of cancer, though lung cancer remains the predominant resulting neoplasm. Hair, urine, and blood analysis of SHS-exposed subjects display increased concentration of tobacco-related carcinogens.71 Many of the components of SHS have shown genotoxic activity. After extensive studies were performed, the United Kingdom’s Scientific Committee on Tobacco and Health concluded that ETS is a cause of lung cancer.72 Furthermore, SHS is classified as a Group A carcinogen by the United States Environmental Protection Agency. This designation falls under the category, "there is sufficient evidence that the substance causes cancer in humans."
Many studies examining couples of smoking and nonsmoking spouses have shown a profound relationship between passive smoking and lung cancer development. These studies exhibit a positive correlation and a dose-dependent relationship between SHS and tumor development.73,74,75,76
In addition to such carcinogenic compounds found in ETS such as 4-aminobiphenyl, benzene, nickel, polycyclic aromatic hydrocarbons, and N-nitrosamines, recent research also shows that nicotine may function as a carcinogen by accelerating tumor angiogenesis. Neoangiogenesis (the formation of new blood vessels) is a crucial step in tumor development. Through its interaction with nicotinic acetylcholine receptors in vascular endothelium and bronchial epithelium, indirect mechanisms may account for progression of tumorogenesis.77 Murine models implanted with Lewis lung cancer cells demonstrated that SHS-exposed specimens developed tumors with increased size, weight, and vascularity when compared with non-exposed controls. However, administration of nicotine antagonists partially reversed these effects. The author concludes that nicotine may exert carcinogenic effects through several mechanisms: raising vascular endothelial growth factor (VEGF) and monocyte chemoattractant protein-1 (MCP-1) levels while increasing circulating endothelial progenitor cells.77 Thus, nicotine also may play a role in cancer development in addition to the many other clearly carcinogenic compounds found in ETS.
Neurological Changes. The neurological complications that may result from tobacco exposure are complex and are being scrutinized by ongoing research. Tobacco smoke confers addictive qualities that have been recognized by the CDC.3 Nicotine serves as the dominant addictive ingredient in tobacco smoke and is one of the most addictive compounds known. The neural effects of nicotine administration have been strongly correlated with dopaminergic pathways in the ventral striatum. Nicotine-stimulated dopamine release in the nucleus accumbens is a common feature shared by other addictive drugs, such as amphetamines and cocaine. The mechanistic properties that underlie nicotine addiction are similar to those that underlie addiction to other drugs of abuse—positive reinforcing effects and negative withdrawal effects. The specific properties of nicotine’s reinforcing effects (alertness, calming, improved concentration) and withdrawal effects (irritability, restlessness, impaired concentration, increased appetite, craving) are reported almost invariably by those addicted to nicotine.
Recent advances in positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) technology have led to a better understanding of the neurological processes that are altered by environmental tobacco smoke. Due to the previous association of depression and tobacco consumption, the monoamine oxidase (MAO) activity of smokers has been examined. MAO A is responsible for the oxidation of serotonin and norepinephrine, whereas MAO B oxidizes benzylamine and phenethylamine. Both classes oxidize dopamine and primarily function to modulate restriction of neurotransmitter concentration. The MAO inhibitor class of antidepressants mediates their effects mainly through inhibition of MAO A. Fowler et al confirmed with PET examination that tobacco smoke exposure reduces MAO A levels in the brain, effectively providing an antidepressant therapeutic effect.78 While the 28% reduction in MAO A activity is not overwhelmingly drastic, it is within the range of the 20-80% reduction required for clinical efficacy. MAO B also was shown to be reduced in smoking subjects by as much as 45%.
While it is unclear whether the concentrations of nicotine found in SHS exposure are sufficient to elicit the neurological effects seen in firsthand exposure, improved models are required to provide definitive evidence. There is clear evidence that nicotine is taken up by nonsmokers when exposed to SHS, as elevated cotinine levels have been detected in urine screening. In addition, nicotine uptake is highly variable—exposure to flight attendants has resulted in serum cotinine levels seven times that of the average nonsmoking SHS-exposed employee.79 Currently, it should be assumed that no amount of nicotine is a safe amount of nicotine. This falls in line with the CDC’s assertion that there is no safe level of SHS exposure.
Adult SHS Intervention
Intervention methods for adults overlap with many of those employed in pediatric intervention, including the cognitive-behavioral therapies mentioned previously. However, the lack of motivation to quit for a child must be replaced with other motivational factors. Several methods traditionally have been employed. These include work site health promotion, legal strategies, and pharmacological treatments. Due to the higher prevalence of smoking in blue collar occupations, work site intervention in these occupations is at greater need. However, studies examining efficacy of work site programs for blue-collar workers are not encouraging, noting that such workers are both less likely to participate in programs and less likely to maintain successful abstinence.80,81
Legal intervention is another method commonly employed, and includes legislation that has been passed by Congress in the past years. Pertinent regulations include health warnings on all cigarette packaging, prohibition of advertising through electronic media regulated by the Federal Trade Commission, and an age limit of 18 for the purchase of cigarettes. Litigation also has played a role in intervention, with the first recorded SHS lawsuit in 1976 serving as a springboard. Since then, more than 420 such cases have been filed, with increasing success. Litigation efforts to curb SHS exposure recently have been reviewed by Sweda.82 A recent high profile case involved 60,000 flight attendants who filed and won a suit alleging that they had endured smoking-related illnesses from being exposed to high concentrations of environmental smoke.83 There is hope that increasing success of such litigation will encourage business owners and others to voluntarily make their facilities smoke-free.
Pharmacological therapies can assist greatly with smoking cessation, with several approved by the U.S. Food and Drug Administration (FDA) to treat nicotine dependence. These include bupropion (an antidepressant) and several nicotine-replacement products (gum, transdermal patch, nasal spray, vapor inhaler). These methods have not only been consistently demonstrated to be the most cost-effective method of treating smoking-related diseases,84 but display great efficacy, doubling long-term abstinence rates in comparison to placebo.85 However, health insurance coverage for treatment of tobacco use and dependence is uncommon.86 Thus, the physician should consider such factors when guiding the patient through a cessation regimen.
Conclusion
Secondhand smoke remains a ubiquitous and preventable health threat today. Exposure to nicotine, carcinogens, and other compounds contained in SHS can mediate a host of disease processes. Pediatric exposure to SHS is highly prevalent, as smoking parents chronically expose their children and pollute the household environment. The result of such chronic exposure is found in respiratory, cardiovascular, neurological, and neoplastic complications, as well as increasing the likelihood of SIDS. These risks are particularly important if the child has a pre-existing disease, such as asthma or heart conditions. Co-morbid conditions also exist with pediatric SHS exposure, stressing the importance of interventional methods.
Adult SHS exposure is compounded by exposure at the workplace, which tends to be worse than household exposure. Despite state legislation restricting smoking in certain places, national legislation has yet to be passed against indoor smoking. Thus, many occupations remain at high risk for SHS exposure, especially those in blue collar fields. Exposure can lead to serious cardiovascular consequences, including exacerbation of coronary heart disease and myocardial infarction. Physicians should warn patients with underlying heart disease of the immediate danger posed by SHS exposure. In addition to cardiovascular complications, SHS exposure has been implicated in development of several types of cancers. Patients with cancer or in remission should avoid exposure, and physicians should introduce interventional methods. Other consequences of SHS exposure are undergoing continuous research and soon may be added to the list of health complications due to exposure.
Several methods exist for intervention in pediatric and adult SHS exposure. The highest standard of intervention is smoking cessation, though this is also the most difficult to accomplish. The most effective method of achieving long-term abstinence is through intensive inpatient treatments. However, such methods can be prohibitively expensive or time-consuming. Less intensive methods of group therapy combined with pharmacological treatment also have shown success in long-term smoking abstinence. The efficacy of brief intervention methods is debatable, while pharmacological therapies have been shown to be the most cost-effective method of treatment. If smoking cessation cannot be achieved, physicians should educate parents and patients on the risks of secondhand smoke exposure and urge isolation of smoke from others. Workplace intervention includes litigation, which is becoming increasingly successful in curbing SHS exposure. The role of the physician is to educate the patient on consequences, suggest therapies, and guide the patient through the regimen suggested. Such physician intervention has been shown to be effective in increasing likelihood of successful smoking cessation and remains an important factor in reducing SHS exposure to nonsmokers.
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In this paper, health effects of secondhand smoke exposure are examined in both children and adults. A brief overview of methods used to screen for secondhand smoke exposure is given. Among the complications discussed are those of cardiovascular, pulmonary, and neurological systems.
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