Secondhand smoke exposure: Effects in adults

INTRODUCTION — There have been few epidemics as devastating and preventable as that caused by tobacco consumption. Cigarette smoking and exposure to secondhand smoke (SHS) became highly prevalent in most resource-abundant countries through the 20^th century. With a lag of several decades, the rise of smoking was followed by epidemic increases in the major diseases now known to be caused by smoking, including lung and other cancers, coronary heart disease, and chronic lung disease. By midcentury, epidemiologic studies provided the initial evidence establishing that smoking caused these diseases. Mounting evidence and authoritative syntheses in the reports of the United States Surgeon General led to definitive conclusions concerning smoking as a cause of disease. Unfortunately, in the first decades of the 21^st century, smoking is on the rise in some resource-limited countries, even as it declines in the higher-income countries that have had success with tobacco control. More recently, tobacco control has been further complicated by the emergence of a host of electronic products that deliver nicotine.

This topic will focus on the health consequences of SHS in adults. Issues related to SHS exposure to a fetus/child and effects of active cigarette smoking are discussed separately. (See "Secondhand smoke exposure: Effects in children" and "Cardiovascular risk of smoking and benefits of smoking cessation".)

BACKGROUND — The issue of SHS and health has a relatively brief history compared with active smoking, although the irritating nature of tobacco smoke to the nonsmoker has long been chronicled. Some of the first epidemiologic studies on SHS and health were reported in the late 1960s [1-3]. The 2006 US Surgeon General's report uses the term "secondhand smoke," although the term "environmental tobacco smoke," originating within the tobacco industry, was used more frequently in earlier reports and discussions on the topic [4].

Initial epidemiologic investigations focused upon parental (household) smoking and lower respiratory illnesses in infants; studies of lung function and respiratory symptoms in children soon followed [5,6]. The first major studies on SHS and lung cancer in nonsmokers were reported in 1981 [7,8], and by 1986, the evidence suggested that SHS caused lung cancer in nonsmokers, a conclusion reached by the International Agency for Research on Cancer, the United States Surgeon General, and the United States National Research Council [6,9,10]. Subsequently, a substantial body of evidence has continued to identify additional diseases and other adverse effects of SHS, including increased risk for coronary heart disease and stroke [5,11-15].

The evidence considered in the 2006 United States Surgeon General's report leaves no doubt that any exposure to tobacco smoke is harmful to human health [4]. The findings on SHS and disease have been the foundation of the drive for smoke-free indoor environments and for educating caregivers concerning the effects of their smoking on their children's health. As smoking bans are implemented, an increasing body of evidence documents reduction of SHS exposure and benefits for cardiovascular and respiratory health.

The tobacco industry's campaign to discredit the evidence on active smoking initially, and on SHS subsequently, is now well documented, as legal actions against the tobacco industry have led to the release of millions of industry documents. The tobacco industry attempted to maintain seeming controversy among scientists even as the evidence mounted and supported conclusions by expert panels on the adverse effects of SHS [16,17]. Industry websites now acknowledge the conclusions on SHS by public health authorities, and corrective statements have now been made as an outcome of the federal litigation.

WHAT IS SECONDHAND SMOKE? — SHS is one of several terms used for the smoke inhaled involuntarily by individuals who do not smoke. The smoke is often referred to as "secondhand smoke" or occasionally still as "environmental tobacco smoke." At present, one billion adults worldwide smoke cigarettes, implying that SHS exposure is almost unavoidable for children and for the two-thirds of adults who do not smoke [18].

SHS is a mixture of sidestream (SS) smoke given off by the smoldering cigarette (or pipe or cigar) and of mainstream (MS) smoke that is exhaled back into the air by those who are actively smoking. SS smoke, generated under the lower temperature conditions in the smoldering cigarette, has higher concentrations of many of the toxic compounds found in MS smoke. However, it is quickly diluted as it moves away from the cigarette to contaminate the immediate environment. While there are quantitative differences between SHS and the MS smoke inhaled by the person who is actively smoking, there is sufficient qualitative similarity to have warranted concern that the health of others may be injured by SHS, just as those who smoke are harmed by MS smoke. (See "Cigarette smoking and other possible risk factors for lung cancer" and "Patterns of tobacco use".)

The term "thirdhand smoke" (THS) has been used to refer to smoke components deposited on surfaces and volatilized into the air, along with metabolites of these components generated through oxidative chemistry [19]. There is potential public health impact through dermal or oral absorption of the smoke components and metabolites, which include carcinogens and irritants [20].

Measurement of secondhand smoke — In environments where smoking takes place, components of tobacco smoke can readily be measured in the air, including carbon monoxide, nicotine, benzene, and small particles in the size range that penetrates into the lung.

Concentrations of the smoke components depend upon the number of people who smoke, their smoking patterns, the size of the space where smoking is taking place, the rate of air exchange with outdoor air, and the presence and efficiency of air-cleaning devices. The exposures of nonsmokers also depends upon proximity to those who smoke, particularly during the time that they are actively smoking. As examples, a baby held by a smoking person might be inhaling dense and virtually undiluted SS smoke, while older children may leave the room while someone is smoking and thus reduce exposure.

Measurements of several airborne components of SHS have been made in homes, workplaces, and public places to characterize the contribution of smoking to indoor air pollution. These studies have shown that cigarette smoking is a strong source of small particles in the air, the same size of particles that are regulated in outdoor air by the US Environmental Protection Agency (PM_2.5, airborne particles less than 2.5 micrometers in aerodynamic diameter). Concentrations of particles in smoking homes are typically two or more times higher than those of nonsmoking homes [21]. For example, fine particulate pollution in Scottish homes where smoking was permitted was approximately 10 times higher than in nonsmoking homes [22]. These measurements were made in an era when smoking was more widespread and still accepted in indoor places; nonetheless, they document the strength of smoking as a source of indoor air pollution.

Nicotine, present as a gas in SHS, can be readily measured in indoor air using either active or passive samplers. Because normal indoor air sources do not contain nicotine, its presence is highly specific for emissions from nicotine-containing tobacco products, including combustible tobacco products and e-cigarettes. Abundant nicotine measurements made over the last several decades confirm that SHS has been widely prevalent in workplaces and in homes [23]. A 31-country study showed that median air nicotine levels were 17-fold higher in homes where smoking takes place compared with those without smoking [24]. Nicotine can also be present on surfaces in rooms where there has been smoking, as a component of THS.

The individual exposed to SHS also inhales the other byproducts of tobacco combustion. For example, benzene, which causes leukemia, is generated by tobacco combustion and may contribute to the increased risk of leukemia in individuals who smoke long term compared with those who do not smoke. SHS is one of the major sources of benzene exposure for nonsmokers, making a contribution to exposure that rivals that from filling a car with gasoline and exceeding the contribution of petrochemical plants in nearby residences.

Exposure to SHS can also be documented by the measurement of biomarkers, that is, tobacco smoke components or metabolites of these components in body fluids of nonsmokers, including blood, urine, saliva, and also hair. Airborne and surface concentrations of nicotine and various biomarkers of SHS exposure are measurable; however, those measurements are largely for research. Consequently, validated measures are not available to clinicians for advising patients about whether they are exposed and the extent to which they are exposed.

Studies using biomarkers show clearly that SHS-exposed nonsmokers absorb, metabolize, and excrete tobacco smoke components, including nicotine and tobacco-specific carcinogens [21]. Although small amounts of nicotine may be ingested in certain foods, most of the nicotine and its metabolites detectable in body fluids reflect exposure to active or passive tobacco smoke. In the 31-country study of exposures to SHS in the home, levels of hair nicotine in children living in smoking households were approximately twofold higher compared with those living in nonsmoking households [24].

Cotinine, the principal metabolite of nicotine, has been the most studied biomarker. Levels of cotinine in nonsmokers previously reached several percent of those who actively smoked. In an analysis of blood from a national survey in the United States during the late 1980s, cotinine could be detected in almost the entire sample using a very sensitive assay procedure [21]. There is strong evidence that SHS exposure is decreasing in the United States, suggesting that tobacco-control strategies have important effects [25,26]. In the 2002 data from the National Health and Nutrition Examination Survey (NHANES), the proportion of United States nonsmokers with cotinine concentrations of 0.05 ng/mL or greater fell by 43 percent compared with data from 1988 to 1990 [25]. Data from NHANES show a further decrease of 36 percent in 2003 to 2004 [27], and an additional 25 percent decrease through 2011 to 2012 [28]. However, there was no further detectable decrease in the percentage of United States nonsmokers with SHS exposure as documented by a detectable cotinine level through 2013 to 2014, with one quarter of all nonsmokers exposed to SHS [29]. Further, disparities in SHS exposure are evident, with the highest rates seen among children and those living in rental housing, poverty, or a residence with someone who smokes inside the home.

In nonsmokers, tobacco-smoke carcinogens have also been shown to be bound to cellular DNA and albumin as adducts, and nonsmokers experimentally exposed to SHS excrete NNAL, a carcinogenic nitrosamine found in tobacco smoke, as do those exposed by living with people who smoke [30]. These observations, together with studies of biomarkers, confirm the wide extent of SHS exposure and support the plausibility of adverse effects of SHS by demonstrating uptake of tobacco smoke components by exposed nonsmokers. The 2006 US Surgeon General's report concludes that "the evidence is sufficient to infer that exposure of nonsmokers to secondhand smoke causes… an increased risk for lung cancer" [4].

Electronic cigarettes — Electronic cigarettes (e-cigarettes), which do not involve the combustion of tobacco, generate an aerosol that almost always contains nicotine [31] and may contain other chemicals, including tobacco-related carcinogens [32], albeit at far lower concentrations than in tobacco smoke. The nicotine in the aerosol could be inhaled by others and/or absorbed across the skin. Effects of e-cigarettes are described separately. (See "Vaping and e-cigarettes", section on 'Secondhand aerosol exposure'.)

HEALTH CONSEQUENCES OF SECONDHAND SMOKE — Evidence of the health risks of involuntary smoking comes from epidemiologic studies, which have directly assessed the associations of SHS exposure with disease outcomes. Judgments about the causality of the relationship between SHS exposure and health outcomes are also based upon extensive evidence derived from the biologic and toxicologic investigation of the health consequences of active smoking. (See "Patterns of tobacco use".)

The literature on SHS and health has been periodically reviewed [6,10-13,15,33-35]. One review was completed in 2005 by the California Environmental Protection Agency [14] and another review in 2006 by the office of the US Surgeon General with updating in the 2014 report [4]. Since then, there have not been major authoritative reviews by government agencies or international authorities. Causal conclusions were reached as early as 1986, when involuntary smoking was found to be a cause of lung cancer in nonsmokers by the International Agency for Research on Cancer [9], the US Surgeon General [6], and the US National Research Council [10]. Each of these reports interpreted the available epidemiologic evidence in the context of the already deep understanding of active smoking and lung cancer. In spite of somewhat differing approaches for reaching a conclusion, the findings of the three reports were identical: involuntary smoking is a cause of lung cancer in people who do not smoke. This and subsequent causal conclusions have had broad public health impact. (See "Cigarette smoking and other possible risk factors for lung cancer".)

In 1986, the reports of the US Surgeon General and the US National Research Council also addressed the then-mounting evidence of adverse respiratory effects of SHS exposure for children. Subsequent reports, including the 2006 and 2014 US Surgeon General's reports, identified further adverse effects of SHS exposure on children [4,15]. (See "Secondhand smoke exposure: Effects in children".)

Annoyance and irritation, although not representing an illness or disease, are also firmly linked to exposure to SHS [6,36]. Surveys document discomfort involving the eye and upper airways; confirmatory evidence has been provided by studies involving exposures of volunteers to SHS in chambers.

Lung cancer — SHS exposure is associated with an increased risk of lung cancer. While the doses of carcinogens received from SHS exposure are far less than with active smoking, exposure to SHS can begin at birth and extend across the full lifespan. A number of studies have shown that SHS is associated with lung cancer in different populations [4,7,8,10,37,38]. After reviewing the available data, national and international expert panels have all concluded that SHS causes cancer [4,12,15,34,39].

A 2014 pooled analysis of 18 case-control studies found that, among those who never smoked, individuals exposed to SHS had an odds ratio for lung cancer of 1.31 (95% CI 1.17-1.45) [37]. Among histologic types of cancer, there was a stronger association with small-cell lung cancer. Another study estimated that exposure to SHS was responsible for 21,400 lung cancer deaths worldwide in 2004 [40]. There appears to be a dose-response relationship between intensity of exposure and relative risk, with household partners, children, and workplace contacts at increased risk:

●Spousal exposure – A 2006 meta-analysis including 52 studies found that the relative risk of lung cancer among nonsmokers who were ever exposed to SHS from the smoking of their partner was 1.21 (95% CI 1.13-1.30) [4]. A 2007 meta-analysis, involving 55 studies, found that females had a 27 percent increase in risk if partnered with an individual who smokes [38].

●Childhood exposure – Household exposure to SHS during childhood is associated with an increased risk for lung cancer. This is discussed in detail elsewhere. (See "Secondhand smoke exposure: Effects in children", section on 'Lung cancer'.)

●Workplace exposure – A 2006 meta-analysis of 25 studies of lung cancer and exposure to SHS in the workplace estimated a pooled relative risk of 1.22 (95% CI 1.13-1.33) [4].

An association between involuntary smoking and lung cancer is biologically plausible based upon the presence of carcinogens in sidestream smoke and the lack of a documented risk-free threshold dose for respiratory carcinogens in those who actively smoke [9,41]. Furthermore, genotoxic activity, the ability to damage DNA, has been demonstrated for many components of SHS [42-44]. Experimental exposure of nonsmokers to SHS results in the urinary excretion of NNAL, a tobacco-specific carcinogen, and living with an individual who smokes also leads to a higher level of NNAL in nonsmokers [45]. Nonsmokers, including children, exposed to SHS also have increased concentrations of tobacco-related carcinogens [46,47].

The risk for the development of lung cancer in response to SHS may be influenced by genetics. One study found a significant increase in polymorphisms in the gene glutathione S-transferase M1 (GSTM1) among 51 nonsmoking females with SHS exposure who developed lung cancer compared with 55 nonsmoking females with lung cancer who did not have exposure [48]. In another population-based study among never smokers, in those with high SHS exposure, GSTM1 and GSTP1 polymorphisms were associated with over a fourfold increased risk of developing lung cancer [49]. GST is believed to play a role in detoxifying carcinogens in tobacco smoke; therefore, mutations which decrease its activity could serve to promote tumorigenesis.

Other respiratory tract illness — Several cross-sectional studies have investigated the association between respiratory symptoms in adult nonsmokers and involuntary exposure to tobacco smoke. These studies have primarily considered exposure outside the home. Consistent evidence of an effect of passive smoking on chronic respiratory symptoms in adults has not been found [50-56], although the small particles in SHS would be anticipated to reach the airways and alveoli and potentially cause injury. Several studies suggest that passive smoking may cause acute respiratory morbidity (ie, illnesses and symptoms) [57-63].

People with asthma and chronic obstructive pulmonary disease (COPD) may be at increased risk from SHS exposure. However, experimental studies have not clearly demonstrated a role of SHS in exacerbating asthma in adults. The acute responses of asthmatics to SHS have been assessed by exposing persons with asthma to tobacco smoke in a chamber. This experimental approach cannot be readily controlled because of the impossibility of blinding subjects to exposure to SHS. However, suggestibility does not appear to underlie physiologic responses of asthmatics of SHS [64]. Of three studies involving exposure of unselected people with asthma to SHS, only one showed a definite adverse effect [65-68]. One study recruited 21 people with asthma who reported exacerbation with exposure to SHS [69]. With challenge in an exposure chamber at concentrations much greater than typically encountered in indoor environments, seven of the subjects experienced a more than 20 percent decline in FEV1.

Several studies have shown improvement in the status of people with asthma after the implementation of workplace bans on smoking [63,70]. In Scotland, following the national smoking ban in 2006, the respiratory health of bar workers with and without asthma improved [70].

Exposure to SHS has been associated with reduction of several lung function measures [4,71]. One observational study found that after adjusting for known risk factors, increased SHS exposure in nonsmokers was associated with increased COPD prevalence and concluded that SHS exposure in multiple settings could have an effect comparable to smoking up to 14 cigarettes per day [72]. However, the findings have not been consistent and methodologic issues constrain interpretation of the findings. Thus, a conclusion cannot yet be reached on the effects of SHS exposure on lung function in adults.

In a matched case-control study, SHS was associated with chronic rhinosinusitis, particularly at the workplace [73]. In a population-based case-control study, exposure to SHS at home was associated with community-acquired pneumonia in nonsmoking adults ≥65 years [74].

Cardiovascular disease and stroke — Exposure to SHS increases nonsmokers' risk of cardiovascular disease. While the risk estimates for SHS and coronary heart disease (CHD) outcomes vary, most studies show modest increases in risk. Large epidemiologic studies estimate approximately a 20 percent increased risk of coronary disease and coronary death in nonsmokers exposed to SHS [75,76]. Pooled relative risks from meta-analyses indicate a 25 to 30 percent increase in the risk of CHD from exposure to SHS, with a dose-response relationship [4,77,78].

Other studies have found a higher relative risk. Data from the Nurses' Health Study found that compared with females not exposed to SHS, the relative risk of CHD, after adjustment for other cardiovascular risk factors, was 1.58 among those who reported occasional exposure and 1.91 among those reporting regular exposure [79]. Another study that measured serum cotinine concentration to assess environmental exposure found that after 20 years of follow-up, among males who were nonsmokers, the risk of CHD was increased in those with higher serum cotinine concentrations [80]. Compared with males in the lowest quartile of serum cotinine concentration, the risks in the second, third, and fourth quartiles were 1.45, 1.49, and 1.57, respectively. No consistent association was found between serum cotinine concentration and stroke. The effects of active cigarette smoking on cardiovascular risk are discussed separately. (See "Cardiovascular risk of smoking and benefits of smoking cessation".)

Studies suggest that SHS exposure among nonsmokers with cardiovascular disease is both a common and potentially modifiable risk factor. Between 29 and 40 percent of nonsmokers with cardiovascular disease being seen in inpatient or outpatient settings have detectable serum cotinine levels [81,82]. Before-after studies suggest that laws that limit public and workplace smoking may result in a rapid decrease in the risk of acute coronary syndrome (ACS) in all people, including those who smoke and those who do not [83]. One meta-analysis found that the rate of hospitalization for acute myocardial infarction decreased with time (0.83, 95% CI 0.80-0.87), following hospitalizations 12 months after implementation of smoking restriction laws [84]. A review of the evidence by an Institute of Medicine Committee led to the conclusion that bans are causally linked to a reduction in ACS [85].

Several studies show that exposure to SHS in healthy young volunteers compromises coronary artery endothelial function in a manner that is indistinguishable from that of individuals who actively smoke, suggesting that endothelial dysfunction may be an important mechanism by which SHS increases CHD risk [4,86]. A cross-sectional study found that after controlling for some potential confounders, exposure to SHS was associated with increased inflammatory markers including higher white blood cell counts and levels of C-reactive protein (CRP), homocysteine, fibrinogen, and oxidized low-density lipoprotein (LDL) cholesterol [87].

SHS is also associated with noncardiac vascular disease. For example, a large cross-sectional study of 60,377 women in China found an association between stroke in women and smoking by their husbands [88]. The prevalence of stroke increased with greater duration of smoking and with an increasing number of cigarettes smoked daily. The 2014 US Surgeon General's report concluded that exposure to SHS causes a 20 to 30 percent increased risk of stroke, based on evidence from more than 20 studies [15].

Diabetes — A meta-analysis of seven studies found an association between passive smoking and type 2 diabetes, reporting a pooled relative risk (RR) of 1.22 (95% CI, 1.10-1.35) compared with never smokers [89].

Active smoking is a causal risk factor for diabetes [15]. (See "Type 2 diabetes mellitus: Prevalence and risk factors", section on 'Smoking'.)

All-cause mortality — There are relatively few data on the association between all-cause mortality and SHS. One study estimated that exposure to SHS was responsible for more than 600,000 premature deaths worldwide in 2004, accounting for approximately 1 percent of total mortality [40].

CONTROL OF SECONDHAND SMOKE EXPOSURE — Exposure to SHS takes place in many different microenvironments. The contributions of different microenvironments to personal SHS exposures depend upon the time spent in those environments and the concentrations of SHS in the different locations. The contributions of different microenvironments also depend upon age, sex, and other sociodemographic factors. For children, the home is a dominant locus of exposure, while for adults the workplace and social environments may be significant loci.

Thus, control of SHS exposure is straightforward: Smoking should be banned in microenvironments where nonsmokers may be exposed to SHS. In the United States and many other countries, most public places and workplaces are covered by smoking bans, and smoke-free policies for households are common. Public education campaigns can be helpful [90].

As a result of declines in smoking rates and implementation of smoke-free policies in the United States, SHS exposure, as identified by a detectable cotinine level, decreased from 88 percent of nonsmokers exposed in 1988 to 25 percent exposed in 2014, with an estimated 58 million people exposed from 2013 to 2014 according to the National Health and Nutrition Examination Survey [29,91].

The World Health Organization (WHO) has offered policy recommendations to achieve smoke-free environments [92]. Its Framework Convention for Tobacco Control (FCTC) calls for protection of nonsmokers against exposure to SHS [93]. Most countries that have ratified the Framework Convention have implemented measures to limit SHS exposure [94]. Control of SHS exposure in the home and elsewhere is discussed in detail separately. (See "Control of secondhand smoke exposure".)

RESPONDING TO SPECIFIC CLINICAL QUESTIONS ABOUT SECONDHAND SMOKE — Exposure to SHS 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 (COPD). From the public health perspective, passive smoking contributes to the population's risk for lung cancer and heart disease. It is a readily controllable form of environmental pollution that can be completely eliminated. A number of situations that may arise in clinical practice and suggested approaches are given below. There are now extensive resources available on the health effects of passive smoking that can be used by clinicians working in public health and clinical domains.

Lung cancer and heart disease risk for adults — When the 1986 US Surgeon General's Report was released [6], Dr. Everett Koop, the Surgeon General, was asked if the causal conclusion with regard to lung cancer meant that nonsmokers should divorce smoking spouses. Of course, there are less dramatic alternatives, but reduction or elimination of such exposure is important, and is reviewed separately (see "Control of secondhand smoke exposure", section on 'The home environment'). Lung cancer in never smokers is not a rare disease [95]; there are approximately 30,000 lung cancer deaths annually in never smokers [96], of which approximately 7300 are estimated to be attributable to SHS [97]. Nonsmokers partnered with people who smoke have approximately a 20 percent greater risk for lung cancer and coronary heart disease than those partnered with nonsmokers. While this increment in risk is relatively modest, it can be reduced.

Workplace exposures — The majority of adults in the United States are now nonsmokers, and tobacco smoking in the workplace, if permitted, may be viewed as both an annoyance and a health risk. For the nonsmoker with asthma or perhaps COPD, health care providers can reasonably postulate that the exposure may exacerbate respiratory illness. Fortunately, the majority of workers now report that their workplaces are smoke-free in the United States and in other high-income countries. This move to smoke-free workplaces in the United States reflects local and state statutes and employer practices, as there is no national ban on smoking in all workplaces.

If asked about workplace risks from these exposures, health care providers can reasonably reply that the exposure would increase risk to some extent and that it could be reduced or eliminated with a workplace smoking policy. (See "Control of secondhand smoke exposure", section on 'Public smoking bans'.)

Multiunit housing — Several studies show that people living in multiunit housing may be exposed to SHS from smoking in other units [98-100]. In some municipalities, smoking has been banned within apartment complexes or common areas of multiunit housing. In early 2017, the US Department of Housing and Urban Development (HUD) prohibited use of certain combustible tobacco products, including cigarettes, cigars, pipes, and hookahs, in public housing properties, with a requirement for public housing agencies to adopt a smoke-free policy by July 30, 2018 [101]. In one study, there was an immediate improvement in indoor air quality, but it was not maintained at 12 months [102]. In another study, there was no detectable difference in indoor nicotine levels after the policy implementation [103].

THIRDHAND SMOKE EXPOSURE — Thirdhand smoke (THS) exposure refers to exposure to smoke components and their metabolic byproducts. The smoke leaves a residue of nicotine and other toxic substances in household dust and on surfaces. The persistence of residual toxic substances from smoking represents an unappreciated health hazard through dermal exposure, dust inhalation, and ingestion.

Although not yet well studied, there is concern that exposure to THS from contact with surfaces that have adsorbed smoke, and from inhalation of resuspended dust and off-gassed SHS chemical components and metabolites, will result in absorption of toxins through the skin or lungs, or ingestion from contamination of the hands [104-107]. (See "Control of secondhand smoke exposure", section on 'Thirdhand smoke exposure'.)

After smoking behaviors end, odors and toxic chemicals from tobacco smoke may linger in homes for months or even years [108]. Repainting or replacement of drywall, carpeting, and other tobacco smoke-affected materials, or a thorough, professional cleaning of the home may mitigate THS. However, the efficacy of these mitigation methods is still unknown, particularly if there has been long-term smoking in the home [108].

OTHER SOURCES OF INFORMATION

●Reports of the US Surgeon General on the adverse health consequences of smoking and SHS exposure can be found at the US Department of Health and Human Services website, along with additional resources for the public.

●The US Centers for Disease Control and Prevention (CDC)'s Office of Smoking and Health (OSH) provides comprehensive information on the health effects of tobacco use and SHS exposure, data and statistics, as well as information on national and global tobacco control programs.

●The National Cancer Institute (NCI) provides fact sheets on tobacco and smoking cessation, as well as links to publications and other web resources.

●The American Cancer Society (ACS) provides user-friendly background on SHS, a summary of adverse health effects, and a list of resources for prevention of SHS exposure as well as quitting smoking, which can be found on the ACS website.

●The American Nonsmokers' Rights Foundation (ANRF) tracks smoke-free laws and provides a range of resources on their website.

●The Thirdhand Smoke Resource Center shares information, resources, and technical support with residents, communities, businesses, health care professionals, and policymakers about the toxic legacy of tobacco smoke residue and to achieve indoor environments that are 100 percent free of tobacco smoke toxicants.

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)")

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

SUMMARY AND RECOMMENDATIONS

●Definition and epidemiology – The smoke inhaled by nonsmokers is often referred to as secondhand smoke (SHS). At present, over 1.1 billion adults worldwide smoke, implying that SHS exposure is a common risk for children and for adults who do not smoke. (See 'What is secondhand smoke?' above.)

●Health risks of secondhand smoke

•Exposure to SHS is causally associated with an increased risk of lung cancer, coronary heart disease, and stroke among nonsmokers. (See 'Health consequences of secondhand smoke' above.)

•SHS may cause acute respiratory morbidity, particularly for people with asthma. (See 'Other respiratory tract illness' above.)

●Public health impact of regulating secondhand smoke – Implementing laws that limit public and workplace smoking may result in a rapid decrease in the risk of acute myocardial infarction in all people, including those who smoke and those who do not. (See 'Cardiovascular disease and stroke' above and 'Workplace exposures' above.)