Secondhand smoke exposure: Effects in children

INTRODUCTION — Tobacco consumption is a worldwide epidemic with devastating consequences due to smoking-related disease including lung and other cancers, heart disease, and chronic lung disease. Smoking patterns reflect powerful social determinants of health and are a critical source of health disparities [1]. There has been notable success with tobacco control in resource-abundant countries; however, tobacco smoking remains prevalent in resource-limited countries.

The risks of secondhand smoke (SHS) exposure have been recognized since the late 1960s [2-4]. SHS exposure has been associated with a variety of adverse health effects among infants and children [5,6] and with increased risk for lung cancer and cardiovascular disease in nonsmoking adults [5,7-10]. The comprehensive 2014 report of the Surgeon General, The Health Consequences of Smoking—50 Years of Progress, leaves no doubt that involuntary exposure to tobacco smoke is harmful to nonsmokers, both children and adults [11]. The findings on SHS and disease have been the foundation of promoting smoke-free indoor environments and educating parents concerning the effects of their smoking on their children's health.

The effects of SHS on the health of children will be reviewed here. The health effects of SHS in adults and approaches to limit exposure to SHS are discussed separately. (See "Secondhand smoke exposure: Effects in adults" and "Control of secondhand smoke exposure".)

WHAT IS SECONDHAND SMOKE?

Secondhand smoke — Secondhand smoke (SHS) is one of several terms used for the involuntary exposure of nonsmokers to tobacco smoke from the smoking of others. The smoke inhaled by nonsmokers is sometimes described as environmental tobacco smoke, a term generally eschewed because of its origins with the tobacco industry. More than one billion adults worldwide are smokers [12], implying that some SHS exposure is almost unavoidable for children and for the two-thirds of adults who do not smoke.

SHS is a mixture of sidestream smoke given off by the smoldering cigarette (or pipe or cigar) and of mainstream smoke that is exhaled back into the air by active smokers. Sidestream smoke, generated under the lower temperature conditions in the smoldering cigarette, has higher concentrations of many of the toxic compounds found in mainstream smoke, including nicotine and carbon monoxide [13]. However, it is quickly diluted as it moves away from the cigarette to contaminate the immediate environment.

Exposure to SHS can be estimated by measuring concentrations of smoke components in the air (eg, small particles or nicotine) or by measuring biomarkers in exposed people (eg, cotinine, nicotine, and tobacco-specific carcinogens) [14-16]. Cotinine is a primary metabolite of nicotine and is specific for exposure to tobacco smoke [16,17]. Cotinine can be measured in blood, urine, saliva, and other tissues [18]. Hair nicotine level has proved to be a useful biomarker in children [19]. Biomarkers in blood samples provide the most accurate quantitative measure of SHS exposure and reflect nicotine exposure from SHS and thirdhand smoke (THS) over approximately three days preceding the test. However, the clinical use of cotinine levels to provide feedback to parents is limited by lack of a rapid commercially available assay and substantial within-subject variability. (See "Secondhand smoke exposure: Effects in adults", section on 'Measurement of secondhand smoke'.)

Thirdhand smoke — The term "thirdhand smoke" (THS) has been used to refer to smoke components deposited on surfaces, along with metabolites of these components generated through oxidation [20]. Laboratory research has documented that carcinogens may be formed by these chemical reactions. These toxins may be absorbed through the skin, by ingestion, or by inhalation of gaseous components and resuspended dust, and the potential risks to health are under investigation. (See "Control of secondhand smoke exposure", section on 'Thirdhand smoke exposure'.)

HEALTH CONSEQUENCES OF SECONDHAND SMOKE — Despite quantitative differences between SHS and the mainstream smoke inhaled by the active smoker, sufficient qualitative similarity exists to warrant concern that the health of nonsmokers may be injured by SHS, just as active smokers are harmed by mainstream smoke [21]. There is now ample scientific evidence to justify these concerns about adverse health effects in nonsmokers. Indeed, the Institute for Health Metrics and Evaluation estimated that exposure to SHS is responsible for more than 1.3 million premature deaths and loss of 37 million disability-adjusted life years (DALYs) worldwide in 2019 [22]. Of the total global DALYs attributed to SHS exposure, 11.2 percent result from the impact of SHS on children under the age of five. Another study estimated that for every 52 individuals who smoke, there is one associated death in a nonsmoker attributable to SHS exposure, with children under the age of five making up 6.1 percent of the deaths linked to SHS exposure in 2016 [23]. A retrospective analysis of 2004 data from the Global Burden of Disease study found that mortality and morbidity from SHS in children was mostly due to lower respiratory infections and asthma [24]. (See 'Respiratory symptoms and illness' below.)

Effects in childhood — Evidence of the health risks of SHS comes from epidemiologic studies, which have directly assessed the associations of measures of SHS exposure with disease outcomes, and also from animal studies and in vitro testing. Judgments about the causality of associations between SHS exposure and health outcomes are based not only upon this epidemiologic evidence but also upon the extensive evidence derived from epidemiologic and toxicologic investigation of the health consequences of active smoking [11]. (See "Benefits and consequences of smoking cessation", section on 'Benefits of smoking cessation'.)

The literature on SHS and health is reviewed in the 50^th anniversary Report of the Surgeon General published in 2014 [11]. Evidence of a causal association between SHS exposure and lung cancer in nonsmokers was found as early as 1986 [5,9,10], leading to classification of SHS as a group A carcinogen by the United States Environmental Protection Agency (see "Cigarette smoking and other possible risk factors for lung cancer"). Cardiac and cerebrovascular disease also has been causally associated with SHS exposure. These and other consequences of SHS that manifest during adulthood are reviewed separately. (See "Secondhand smoke exposure: Effects in adults".)

Evidence of adverse respiratory effects of SHS exposure for children was included in the 1986 reports of the United States Surgeon General and the National Research Council [5,10]. Subsequent public health reports from the United States and elsewhere have identified additional health risks associated with SHS exposure in children [11,25-27]. These reports describe the following specific risks for children, each discussed in detail below:

●Quality of life and costs

●Prematurity and perinatal mortality [28]

●Fetal growth and development

●Sudden infant death syndrome (SIDS)

●Respiratory symptoms and illness

•Lower respiratory illnesses

•Chronic respiratory symptoms

•Asthma

•Reduced lung function

●Atherogenesis

●Middle ear disease

In addition, there is suggestive but not definitive evidence for an association between SHS exposure and dental caries, renal function, and childhood cancers.

Quality of life and costs — The morbidity associated with SHS exposure is a significant public health issue for children that affects both quality of life and health care costs. As an example, the 1991 United States National Health Interview Survey (including 17,448 children) found that children who were exposed to SHS had, on average, two more days of restricted activity, one more day of bed confinement, and 1.4 more days of school absence than did those who were not exposed, even after controlling for age, socioeconomic status, race, sex, and family size [29]. Analysis of the Third National Health and Nutrition Examination Survey (NHANES) data, conducted from 1988 to 1994 and including 5400 United States children aged 4 to 16 years, showed associations between high cotinine levels and wheezing, increased school absence, and reduced lung function [30]. These results come from an era when SHS exposures in the United States were generally much higher than at present. Exposure of children to SHS has dropped greatly over the ensuing decades but persists, with longstanding racial and economic inequities. Based on serum cotinine level, 37.9 percent of United States children aged 3 to11 years were exposed to SHS in the 2013 to 2014 NHANES data, with the highest prevalence among non-Hispanic Black children [31].

Prematurity and perinatal mortality — For the fetus of a smoking mother, many of the tobacco smoke components cross the placenta, including nicotine. Maternal smoking is associated with increased perinatal mortality (stillbirths and neonatal deaths). (See "Cigarette and tobacco products in pregnancy: Impact on pregnancy and the neonate", section on 'Adverse outcomes'.)

Fetal growth and neurologic development

●Effects of maternal smoking during pregnancy – Active smoking by pregnant women, resulting in passive smoking for the developing fetus, increases risk for a variety of adverse health effects in children; these effects are hypothesized to result primarily from transplacental exposure of the fetus to tobacco smoke components [32,33]. In particular, maternal smoking during pregnancy reduces birth weight by approximately 200 g on average [27,34,35]. A systematic review of studies published from 1959 through 2010 found that maternal active smoking was associated with increased risk of several non-chromosomal congenital malformations, including modest effects (odds ratios [ORs] 1.09 to 1.19) on cardiovascular/heart defects, musculoskeletal defects, and cryptorchidism, and slightly larger effects (ORs 1.25 to 1.50) on limb reduction defects, clubfoot, craniosynostosis, orofacial clefts, eye anomalies, and gastrointestinal defects (including gastroschisis and abdominal hernias) (table 1) [36].The 2014 Report of the Surgeon General concluded that the association of orofacial clefts with maternal smoking is causal [11]. (See "Cigarette and tobacco products in pregnancy: Impact on pregnancy and the neonate", section on 'Adverse outcomes'.)

Adverse effects of in utero or postnatal exposure to maternal smoking on neuropsychological development also have been postulated but have not been established. Numerous components of tobacco smoke, including nicotine and carbon monoxide, may produce these effects. In a 2015 review, most studies found cognitive deficits of various types among children whose mothers smoked during pregnancy [37]. Another review found associations of maternal smoking during pregnancy with brain structural changes in the offspring, as detected by imaging [38]. However, the sizes of the effects were small, and the long-term consequences remain unclear. Accordingly, the 2014 Report of the Surgeon General concluded that nicotine exposure during fetal development has "lasting adverse consequences for brain development" [11].

Other studies report adverse effects of SHS exposure on neurodevelopmental outcomes without distinguishing between maternal smoking during pregnancy and postnatal exposure of the child to SHS. One study suggested that maternal exposure to SHS during pregnancy is associated with modest impairment in gross motor function in her offspring, measured at 18 months of age [39]. A separate report found that serum cotinine concentrations (used as an index of SHS exposure) were associated with impairment of motor function in school-aged children [28]. Effects of maternal smoking on neurodevelopmental outcomes in the offspring are discussed separately. (See "Cigarette and tobacco products in pregnancy: Impact on pregnancy and the neonate", section on 'Long-term effects'.)

●Maternal exposure to SHS during pregnancy – Exposure of nonsmoking mothers to SHS is associated with reduced birth weight, although the extent of the reduction is far less than that for active maternal smoking during pregnancy. In a meta-analysis, the summary estimate of the reduction of birth weight associated with paternal smoking was 28 g [40]. A randomized trial showed that a counseling intervention to reduce SHS exposure in a group of pregnant women markedly reduced rates of very low birthweight and very preterm birth [41]. Of note, 26 percent of the women in the intervention group reporting only SHS exposure had cotinine levels consistent with active smoking (salivary cotinine levels ≥20 ng/mL), suggesting that active smoking was underreported by this group of pregnant women. Nonetheless, the counseling intervention was effective in reducing SHS exposure and improving pregnancy outcomes regardless of baseline cotinine levels. (See "Tobacco and nicotine use in pregnancy: Cessation strategies and treatment options".)

Other perinatal health effects possibly associated with exposure of a nonsmoking woman to SHS during pregnancy are growth retardation [42-44], stillbirth, congenital malformations [45], and executive function problems in the offspring [46]. The few studies conducted to assess the association between paternal smoking and congenital malformations have demonstrated risks ranging from 1.2 to 2.6 for exposed compared with nonexposed children [47,48].

Sudden infant death syndrome — Sudden infant death syndrome (SIDS) refers to the unexpected death of a seemingly healthy infant while asleep. Maternal smoking during pregnancy has been causally associated with SIDS. An estimated 25 to 40 percent of SIDS cases are related to smoking during pregnancy [49]. The relationship between smoking during pregnancy and SIDS was studied prospectively in 24,986 Danish infants [50]. Compared with the children of nonsmokers, the children of smokers had more than three times the risk of SIDS; the risk increased with the number of cigarettes smoked per day. (See "Sudden infant death syndrome: Risk factors and risk reduction strategies", section on 'Maternal risk factors'.)

It is important to determine whether maternal smoking after pregnancy, or paternal smoking and household smoking generally, are also causally associated with SIDS. Isolating the effects of prenatal smoking on SIDS risk is difficult because most women who smoke during pregnancy continue to smoke after delivery, and initial reports failed to establish a causal association between postnatal exposure to tobacco smoke and SIDS [27]. However, findings of subsequent reports supported a causal association between exposure to SHS and SIDS [33,51,52]. In addition, an ecologic analysis found that for every 1 percent increase in the state-level prevalence of smoke-free homes with infants, the SIDS rates for the states decreased by 0.4 percent, while controlling for the rate of use of the supine sleep position [53]. These data suggest that the increase in smoke-free homes has contributed to the observed decline in SIDS deaths between 1995 and 2006. The 2006 Surgeon General's report goes on to state that tobacco smoke exposure is one of the major preventable risk factors for SIDS and that all measures should be taken to protect infants from SHS exposure.

Respiratory symptoms and illness — Numerous surveys demonstrate a greater frequency of the most common respiratory symptoms (cough, phlegm, and wheeze) in the children of smokers [5,11,25,54]. A meta-analysis of relevant studies reported pooled ORs for a parent smoking ranging from 1.23 and 1.5 for asthma, wheeze, cough, increased phlegm, or breathlessness [52]. The highest risks for these symptoms occurred in children with two parents who smoked (table 2).

Participants in these studies generally have been school-aged children. The less prominent effects of SHS in comparison with the studies of lower respiratory illness in infants may reflect lower exposures to SHS by older children who spend less time with their parent(s).

Lower respiratory tract illnesses — Infants with parents who smoke have an increased risk of lower respiratory tract illness, including a significantly increased frequency of bronchitis and pneumonia during the first year of life [32,55-59], and increased severity of respiratory syncytial virus infection, a leading cause of bronchiolitis [60]. Presumably, this association represents an increase in frequency or severity of illnesses that are infectious in etiology, perhaps related to increased nasopharyngeal and oropharyngeal colonization with respiratory pathogens [61], and not as a direct response of the lung to the toxic components of SHS. Effects of exposure in utero on the airways also may play a role in the effect of postnatal exposure on risk for lower respiratory illnesses.

The risk for lower respiratory illness is increased by approximately 50 percent if a parent smokes, with a somewhat greater increase for smoking by the primary caregiver specifically (OR 1.70, 95% CI 1.56-1.84) [52]. Although measures of adverse health outcomes have varied somewhat among the various studies, the relative risks associated with involuntary smoking were similar, and dose-response relationships with the extent of parental smoking were demonstrable.

Most studies have shown that maternal smoking rather than paternal smoking contributes the predominant component of the increased risk associated with parental smoking. Nonetheless, studies from China and Vietnam, where women rarely smoke, show that paternal smoking alone can increase the incidence of lower respiratory illness [58,62,63]. In most studies, the effect of SHS is noted during the first year of life; this finding may be explained by higher exposures during the first year because of the time-activity patterns of young infants, which place them in close proximity to cigarettes smoked by their mothers. However, effects of SHS on lower respiratory infections in toddlers and school-age children have also been noted [24]. A global study of disease burden from exposure to SHS estimated that 165,000 children younger than age five die annually because of lower respiratory infections attributable to SHS [24]. Most of the attributable deaths were in Africa and South Asia, suggesting that the effect of SHS may be amplified by poverty-related poor health and malnutrition.

Asthma — Exposure to SHS is associated with increased prevalence and severity of asthma and wheezing [11,27,32,51,64,65]. In a systematic review, pre- or postnatal exposure to SHS was associated with a 20 to 85 percent increased risk for asthma [66]. This association with onset of asthma might be a consequence of the increased frequency of lower respiratory infection in early childhood or other pathophysiologic mechanisms, including inflammation of the respiratory epithelium by SHS [67,68]. In utero exposures from maternal smoking also may affect lung development and increase the risk for asthma. In the systematic review cited above, there was a particularly strong effect from prenatal maternal smoking on asthma in children younger than two years [66]. In addition, newborn infants whose mothers smoked during pregnancy have increased airways responsiveness, a characteristic of asthma, compared with those whose mothers did not smoke [69]. Maternal smoking during pregnancy also reduces ventilatory function measured shortly after birth [70]. A pooled analysis of eight European birth cohorts comprising 21,600 children found that exposure to maternal smoking only during pregnancy and not after birth increased risk of both wheezing and asthma at four to six years of age [71].

SHS may promote allergic sensitization, thereby increasing risk for asthma. A meta-analysis addressing this association found modest increases in immunoglobulin E (IgE) concentrations and positive skin prick testing among children exposed to SHS, but this finding was based on a small number of studies [72]. Total IgE levels increased by 27.7 IU/mL (95% CI 7.8-47.7) among SHS-exposed children compared with non-exposed children [72]. Exposure to SHS moderately increased the overall risk of atopic sensitization with the most pronounced effect in children <7 years of age [72]. Tobacco hypersensitivity, defined by skin test reaction to a tobacco leaf extract, does not correlate well with allergic symptoms, and testing for such sensitivity does not appear to be clinically warranted [73].

Thus, although the underlying mechanisms remain to be identified, the epidemiologic evidence linking SHS exposure and childhood asthma is substantial [11,25,30,51,52,54,74,75]. A significant excess of childhood asthma occurs if the parent(s) smoke (table 2) [54]. A dose-response relationship exists between SHS and childhood asthma, and no defined threshold level of exposure is without risk [76]. The 2006 Surgeon General's report concluded that SHS exposure was causally associated with asthma prevalence, but the evidence was classified as less certain for asthma incidence [52]. Exposure to SHS during childhood is also associated with increased prevalence of asthma in adults [77]. (See "Risk factors for asthma".)

Exposure to SHS also appears to worsen the severity of asthma in children and increases health care utilization [65], as demonstrated by the following observations:

●In an evaluation of asthmatic children followed in a clinic, level of lung function, symptom frequency, and responsiveness to inhaled histamines were adversely affected by maternal smoking [78,79].

●Population studies also have shown increased airways responsiveness for SHS-exposed children with asthma [80,81].

●Exposure to smoking in the home increases the number of emergency department visits made by asthmatic children [82].

●Asthmatic children with smoking mothers are more likely to use asthma medications [83].

All guidelines for the management of asthma urge elimination of SHS exposure at home [84].

Lung growth and development — During childhood, measures of lung function increase with height. Parental smoking adversely affects growth of lung function during childhood [5,25,52,85-87]. A study of 193 high school athletes, for example, found a fourfold increase in prevalence of low forced expiratory flow at 25 to 75 percent of the forced vital capacity and/or cough in athletes exposed to SHS compared with athletes who were not exposed [86]. Children with pulmonary problems such as cystic fibrosis may experience greater adverse effects on lung function from regular SHS exposure [88,89].

It is difficult to distinguish the effects of in utero exposure from those of childhood SHS exposure [27]. However, a growing number of studies suggests that in utero exposure to maternal smoking is independently associated with decreased lung function in childhood [70,90-92]. These epidemiologic findings are supported by animal models, which point to nicotine as having a key role [93]. The magnitude of the effect is small, and it is unknown whether these children will have decreased lung function at the completion of lung growth as adults; nonetheless, SHS-exposed children enter adulthood with less pulmonary reserve [94].

Middle ear disease — The United States Surgeon General's Office [5,11], United States National Research Council [10], United States Environmental Protection Agency [95], and American Academy of Pediatrics (AAP) [32] all have reviewed the literature on SHS and otitis media and concluded that an association exists between SHS exposure and otitis media in children. The evidence supports a causal relationship [11,27,96].

Positive associations between SHS and otitis media have been demonstrated consistently in prospective cohort studies, but not as consistently in case-control studies. This difference in findings may reflect the focus of the cohort studies on the first two years of life, the peak age of risk for middle ear disease. The case-control studies, on the other hand, have been directed at older children who are at lower risk for otitis media. Exposure to SHS has been associated most consistently with recurrent otitis media and not with incident or single episodes [97]. One meta-analysis found a pooled OR of 1.37 (95% CI 1.10-1.70) for recurrent otitis media, 1.33 (95% CI 1.12-1.58) for middle ear effusions, and 1.20 (95% CI 0.90-1.60) for clinical referrals or operative interventions for middle ear effusions, if a parent smoked [52]. Another meta-analysis, which reviewed studies published through December 2012, found that maternal smoking nearly doubled the risk of the child developing middle ear disease requiring surgery (OR 1.86, 95% CI 1.31-2.63) [96].

SHS exposure is also associated with sensorineural hearing loss later in childhood. This was shown in a study using data from NHANES (2005 to 2006), in which hearing loss was associated with serum cotinine levels in a dose-related fashion [98]. The mechanism for this association remains unclear. Of note, the majority of teens did not recognize the hearing difficulties.

Dental caries — Exposure to SHS may be associated with an increased risk of dental caries in children [11,99,100]. For example, a cross-sectional study of dental caries and serum cotinine levels in more than 3000 children ages 4 to 11 found that elevated cotinine levels were associated with caries in deciduous but not permanent teeth [101]. In a 2014 study of 500 children aged 5 to14 years in Pakistan, 67.2 percent of the children had dental caries and 30.8 percent of their family members reported smoking [102]. After adjusting for other risk factors for dental caries (junk food intake, in-between meals, age, plaque index, dental visits, and socioeconomic status), the association between SHS and dental caries remained statistically significant.

Childhood cancers — SHS, including maternal smoking during pregnancy, has been evaluated as a risk factor for the major childhood cancers, including in the 2014 Surgeon General's Report [11]. The evidence is limited and is inadequate to infer the presence or absence of a causal relationship between prenatal and postnatal exposure to SHS and childhood cancers. For the specific cases of childhood leukemias, lymphomas, and brain tumors, the evidence was suggestive but not strong enough to infer a causal association [52,103]. In a meta-analysis, the pooled estimate of the relative risk for any childhood cancer associated with maternal smoking was 1.10 (95% CI 1.03-1.19) and that for all leukemias was 1.05 (95% CI 0.82-1.34) [104]. In a subsequent meta-analysis, an association was found between paternal smoking and risk for childhood acute myeloid leukemia [105].

Renal function — Exposure to tobacco smoke may be associated with reduced renal function during adolescence. In a cross-sectional study of adolescents in the United States, the estimated glomerular filtration rate (eGFR) decreased linearly with increasing serum cotinine concentrations, after adjustment for body mass index and sociodemographic characteristics [106]. Moreover, in a large prospective study in the Netherlands, maternal smoking during pregnancy was associated with smaller kidney volume and lower eGFR in school-aged offspring [107]. Effects were seen in adolescents with cotinine levels consistent with SHS exposure as well as active smoking. These observations complement previously recognized associations between tobacco smoke exposure and chronic kidney disease in adults but require replication before effects during adolescence can be established. (See "Epidemiology of chronic kidney disease".)

Smoking initiation — SHS exposure during childhood (from household and peer smoking) is a well-recognized predictor of smoking initiation during adolescence. This has generally been presumed to be due to social modeling. However, emerging literature suggests that it may be related to airborne nicotine exposure [108].

Atherogenesis — Environmental exposure to tobacco smoke is associated with acute and chronic changes in endothelial function, which are in turn associated with atherogenesis [13,32,109]. In a longitudinal study of children, tobacco smoke exposure (as measured by cotinine levels) was associated with endothelial dysfunction (as measured by endothelium-dependent vasodilatory responses of the brachial artery) in a dose-dependent manner [110]. The trends were not explained by low-density lipoprotein (LDL) cholesterol, blood pressure, body mass index, or other cardiovascular risk factors. Similarly, data from two prospective cohorts showed that exposure to parental smoking during childhood or adolescence was associated with greater carotid intima-media thickness (IMT) in adulthood after adjustment for confounders. IMT is an important index of atherogenesis, and the reported increase in IMT if two parents smoked corresponds to advancing the "vascular age" of the offspring by 3.3 years [111]. In another prospective study, children with significant SHS exposure from parental smoking, as documented by a detectable level of serum cotinine, had substantially increased risk of having carotid atherosclerotic plaque 26 years later compared with unexposed children (relative risk [RR] 4.0, 95% CI 1.7-9.8) [112]. The association persisted even after adjusting for other cardiovascular risk factors such as blood pressure, lipids, and personal smoking status.

Effects first noted in adulthood — The magnitude of exposure to carcinogens and other toxins from SHS is far less than the exposure that occurs with active smoking. However, exposure to SHS usually begins much earlier in life than active smoking, and the duration of exposure to carcinogens occurs over a longer period of time.

The following health consequences during adulthood have been linked to childhood exposure to SHS. The evidence linking the risk for these adult health problems to household exposure to SHS is discussed in detail elsewhere. (See "Secondhand smoke exposure: Effects in adults".)

Lung cancer — Numerous authoritative reviews have concluded that SHS is a cause of lung cancer [11,52]. Household exposure to SHS during childhood and adolescence specifically increases the long-term risk for lung cancer in a dose-response relationship in some studies. In a population based, case-control study, household exposure to 25 or more smoker-years during childhood and adolescence doubled the risk of lung cancer, whereas exposure to fewer than 25 smoker-years did not increase the risk [113]. An estimated 17 percent of lung cancer in nonsmokers is attributable to high levels of SHS exposure during childhood and adolescence.

Other cancers — A retrospective case-control study examined the association between cancer in adulthood and transplacental or childhood SHS exposure [114]. Cancer risk was increased 50 percent among children of men who smoked. The relative risk for hematopoietic cancers was increased when two parents were smokers (from 1.7 to 4.6). An analysis from a large European cohort study found no association of childhood exposure with risk for diverse cancer types in adulthood, including breast cancer [115].

Cardiovascular disease — Causal associations between active smoking and fatal and nonfatal cardiovascular disease (CVD) outcomes have long been demonstrated [11,116]. The risk of CVD in active smokers increases with the amount and duration of cigarette smoking and decreases quickly with cessation. In addition, there is growing concern regarding the risk of CVD from SHS exposure in nonsmoking adults and children. (See "Cardiovascular risk of smoking and benefits of smoking cessation", section on 'Cigarette smoking and CVD'.)

The association between childhood SHS exposure and risks for developing CHD is illustrated by the following studies:

●The relationship between plasma cotinine concentration and cholesterol level was studied in healthy nonsmoking adolescents [117]. SHS exposure was associated with decreased high-density lipoprotein cholesterol (HDL-C) and increased ratio of total cholesterol to HDL-C.

●A twin study followed a cohort of 408 11-year-old twin pairs through age 15 years [118]. Among children with a family history of cardiovascular disease, HDL-C levels were inversely related to SHS exposure and were lower in White children compared with Black children.

●A large study in Germany determined that parental smoking is a risk factor for high blood pressure in preschool-aged children, independent of the child's body mass index, parental hypertension, or birth weight [119].

●A cross-sectional study of 10- to 12-year-old Australian children examined the influence of parental health behaviors on children's health behaviors [120]. An association was observed between parental smoking and the child ingesting a high-fat diet and reporting lower physical activity. The authors suggest that higher-risk lifestyle diseases (eg, coronary artery disease) may be related to a clustering of adverse health-related behaviors, including sedentary lifestyle and higher intake of fat.

●Atherogenesis is another important risk factor for cardiovascular disease; the contribution of SHS to atherogenesis is discussed above. (See 'Atherogenesis' above.)

The cited studies and other evidence support statements from several societies on the association between SHS exposure and cardiovascular disease. In 1992, the American Heart Association (AHA)'s Council on Cardiopulmonary and Critical Care also concluded that SHS both increases the risk of heart disease and is "a major preventable cause of cardiovascular disease and death" [121]. This conclusion was echoed in 1998 by the Scientific Committee on Tobacco and Health in the United Kingdom [30], another AHA statement in 2004 [122], and again in the 2006 and 2014 Surgeon General's reports [11,52].

The association between SHS exposure during adulthood and risks for CVD, and the potential mechanisms for this association, are discussed separately. A meta-analysis estimated that the excess risk of coronary heart disease in nonsmokers exposed to SHS is 27 percent (95% CI 19-36) [52]. (See "Secondhand smoke exposure: Effects in adults", section on 'Cardiovascular disease and stroke'.)

Atrial fibrillation — Evidence from a long-term prospective population study indicates an association between childhood SHS exposure and development of atrial fibrillation in adulthood, after adjusting for genetic contributors and other important risk factors for atrial fibrillation [123]. For every pack/day increase in parental smoking, there was an 18 percent increase in the risk of atrial fibrillation in the offspring. Some, but not all, of the increased risk was mediated by offspring smoking. These findings are consistent with the known association between active smoking and atrial fibrillation [124], but further studies are needed on childhood SHS exposure.

RESPONDING TO SPECIFIC CLINICAL QUESTIONS ABOUT SECONDHAND SMOKE — SHS exposure remains highly prevalent and results in exposure to respiratory irritants and carcinogens. It has clinically relevant consequences, particularly for the health of children and possibly for adults with chronic respiratory conditions, including asthma and chronic obstructive pulmonary disease. From the public health perspective, SHS contributes to the burden of childhood respiratory morbidity and mortality and increases population risk for lung cancer and heart disease in adults, perhaps with a lasting effect from early life and childhood exposures. It is a readily controllable form of environmental pollution that could be completely eliminated. Numerous situations may arise in clinical practice that provide opportunity to screen for and prevent SHS exposure, and suggested approaches are given below.

Resources to support tobacco cessation and control of SHS exposure are widely available online at BeTobaccoFree, HealthyChildren, American Cancer Society, and the Environmental Protection Agency's Indoor Air Quality website.

Specific approaches to reducing exposure to SHS, including measures to reduce smoke exposure in the home environment, are discussed in detail elsewhere. (See "Control of secondhand smoke exposure".)

Special risk groups

Pregnancy — Health care during pregnancy should include routine assessment of smoking by the parent(s) and other adults in the home. Most women stop smoking while pregnant, but a substantial percentage of smoking women (up to approximately 30 percent) continue to smoke. To encourage smoking cessation, the clinician should advise pregnant women who smoke about the adverse effects of their smoking for the fetus, including effects on growth and development, and risks of prematurity and delivery complications such as abruptio placenta. (See 'Prematurity and perinatal mortality' above and "Cigarette and tobacco products in pregnancy: Impact on pregnancy and the neonate", section on 'Adverse outcomes'.)

In addition, pregnant women should be advised about the continued adverse effects of their smoking after birth, including risks of sudden infant death syndrome (SIDS), asthma and lower respiratory tract illnesses, and middle ear disease, as detailed above. Support and referral to resources for cessation should be offered. (See "Tobacco and nicotine use in pregnancy: Cessation strategies and treatment options".)

The 2020 United States Surgeon General's report provides a detailed review of benefits of smoking cessation during pregnancy for most pregnancy outcomes [125]. The report concludes that there are causal benefits of maternal smoking cessation, both for the health of the mother and the health of her fetus and newborn.

Children at risk for asthma — Exposure to tobacco smoke should be avoided for all children but particularly for the child at risk for asthma on the basis of a family history of asthma and allergies, beginning with in utero exposure. During the first weeks after birth, studies of lung function of infants whose mothers smoke have demonstrated increased airways responsiveness, perhaps as a precursor of asthma. SHS exposure, particularly from maternal smoking, is a known risk factor for asthma in young children. Given that genetic predisposition may require environmental triggering to manifest, preventable triggers such as SHS exposure should be avoided.

Children with asthma — SHS exposure, particularly from parental smoking, is associated with increased symptoms, medication usage, and utilization of health services for asthma [126]. Guidelines for the management of asthma, for example those developed by the National Asthma Education and Prevention Program [84], call for the elimination of SHS exposure in the home for children with asthma. Intervention studies demonstrated reduced morbidity and decreased airway hyperresponsiveness with reduced parental smoking exposure [127,128]. Parents may not recognize tobacco smoke as a trigger if the child does not have immediate symptoms and may not report it as such. A useful intervention may be to point out the role of SHS as an irritant to the airways that can accentuate airway hyperresponsiveness, leaving them more vulnerable to the effects of other triggers. (See 'Respiratory symptoms and illness' above.)

Does it help to restrict smoking in the home and car? — Reducing SHS exposure in the home and vehicles is critical since the home is the major location of exposure for children and for nonsmoking adults who are not exposed elsewhere. For this purpose, policies banning or restricting smoking in the home should be recommended for families with smokers. The only approach that effectively protects nonsmokers is to make the home smoke-free [11,32,129]. While rates of smoking bans in the home have increased in the past decade, one-third of parents participating in a study reported that their child's pediatrician did not screen for tobacco use in the home or household smoking rules [130]. Other restrictions, such as creating designated smoke-free areas, restricting smoking to outside the home, and smoking only when no children are present, are far less effective. SHS cannot be controlled by either air cleaning or building ventilation [52,131]. Reduction of exposure to SHS in the home and elsewhere is discussed in detail separately. (See "Control of secondhand smoke exposure", section on 'Effect of smoking bans'.)

Can secondhand smoke exposure be measured? — The degree of exposure of the child to SHS can be estimated by measuring cotinine in blood or other body fluids or hair nicotine levels. However, this test is usually only available for research studies and the results are subject to short-term variations in SHS exposure. (See 'What is secondhand smoke?' above.)

Is exposure to e-cigarette vapor harmful? — Passive exposure to vapor released from electronic cigarettes (e-cigarettes) is expected to be less toxic to bystanders than exposure to combustible cigarette smoke. However, there are some concerns about the potential health consequences of secondhand exposure to e-cigarette vapor due to increases in environmental concentrations of nicotine and particulate matter. This issue is discussed separately. (See "Vaping and e-cigarettes", section on 'Secondhand aerosol exposure'.)

OTHER SOURCES OF INFORMATION — Valuable information designed for patient education about SHS is available from many sources, including:

●The American Thoracic Society provides a series of fact sheets designed for patients.

●The HealthyChildren website, from the American Academy of Pediatrics (AAP), includes information for patients about the risks associated with SHS and how to control or prevent exposure, in both English and Spanish. The AAP also provides policy statements on SHS [32,132,133].

●Reports from the United States Surgeon General provide information about the adverse health consequences of smoking and SHS exposure.

●The Centers for Disease Control and Prevention provides comprehensive information on the health effects of tobacco use and SHS exposure, data and statistics, and information on national and global tobacco control programs.

●The National Cancer Institute's Cancer Causes and Prevention resource contains fact sheets about smoking and tobacco use, as well as links to publications and other online resources.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Smoking cessation, e-cigarettes, and tobacco control".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topics (see "Patient education: Quitting smoking (The Basics)" and "Patient education: Smoking in pregnancy (The Basics)" and "Patient education: Secondhand smoke and children (The Basics)")

●Beyond the Basics topic (see "Patient education: Quitting smoking (Beyond the Basics)")

SUMMARY

●Definition – Secondhand smoke (SHS) is a mixture of sidestream smoke given off by smoldering tobacco and the mainstream smoke that is exhaled back into the air by active smokers. Exposure to SHS can be estimated by measuring either concentrations of smoke components in the air or by biomarkers such as cotinine. In research studies, questionnaires are also used to capture exposure to SHS. (See 'What is secondhand smoke?' above.)

●Health consequences for children – There is strong evidence that exposure to SHS is causally associated with a number of adverse health effects in children, including prematurity and perinatal mortality, fetal growth restriction, sudden infant death syndrome (SIDS), respiratory symptoms and illnesses (including asthma), atherogenesis and future risk of cardiovascular disease, renal function impairment, and middle ear disease. (See 'Health consequences of secondhand smoke' above.)

●Special-risk groups

•Pregnancy – Exposure of a nonsmoking pregnant woman to SHS is associated with reduced birth weight, although the extent of the reduction is far less than that for active maternal smoking during pregnancy. (See 'Fetal growth and neurologic development' above and "Cigarette and tobacco products in pregnancy: Impact on pregnancy and the neonate", section on 'Adverse outcomes'.)

•Children with asthma – SHS exposure, particularly from parental smoking, is associated with increased risk, symptoms, and severity of asthma in children. (See 'Children with asthma' above.)

●Counseling – Reducing SHS exposure in the home is critical since the home is the major location of exposure for children. The only approach that effectively protects nonsmokers is to make the home smoke-free. (See 'Does it help to restrict smoking in the home and car?' above and "Control of secondhand smoke exposure".)

●Health consequences for adults – SHS exposure during adulthood also has adverse health effects; these issues are discussed in a separate topic review. (See "Secondhand smoke exposure: Effects in adults".)