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Re: [samaggiphala] Efek jelek asap rokok

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  • vajra_nanda@yahoo.com
    Thanks...! Ini baru email... Sent from my BlackBerry® smartphone from Sinyal Bagus XL, Nyambung Teruuusss...! ... From: mulyasan88
    Message 1 of 2 , Feb 21, 2010
      Thanks...! Ini baru email...

      Sent from my BlackBerry� smartphone from Sinyal Bagus XL, Nyambung Teruuusss...!

      -----Original Message-----
      From: "mulyasan88" <mulyasan88@...>
      Date: Sun, 21 Feb 2010 19:21:23
      To: <samaggiphala@yahoogroups.com>
      Subject: [samaggiphala] Efek jelek asap rokok

      Teman-teman, sekedar sharing saya Copy-paste artikel yg saya ambil dari uptodate, tulisan para beliau yg berdasar berbagai penelitian terakhir dan bersumber pada 86 referensi.

      Semoga bisa membantu menjaga kesehatan pribadi dan orang-orang yg terkasih.


      Mulya


      Secondhand smoke exposure: Effects in adults

      Author
      Jonathan M Samet, MD, MS Section Editors
      Mark S Gold, MD
      Peter J Barnes, DM, DSc, FRCP, FRS Deputy Editor
      Pracha Eamranond, MD, MPH



      Last literature review version 17.3: September 2009�|�This topic last updated: December 5, 2008�(More)


      INTRODUCTION���There have been few epidemics as devastating and preventable as that caused by tobacco consumption. Cigarette smoking became highly prevalent in most developed countries through the 20th century; with a lag of several decades, the rise of smoking was followed by epidemic increases in the diseases now known to be caused by smoking, including lung and other cancers, coronary heart disease, and chronic lung disease. By mid-century, epidemiologic studies provided the initial evidence establishing that smoking caused these diseases. Mounting evidence and authoritative syntheses in the reports of the United States (US) Surgeon General soon led to definitive conclusions concerning smoking as a cause of disease. Unfortunately, as the 21st century begins, smoking is on the rise in developing countries, even as it declines in the developed countries that have had some success with tobacco control.

      The issue of secondhand smoke (SHS) and health has a much briefer history, although the irritating nature of tobacco smoke to the nonsmoker has long been chronicled. Some of the first epidemiological studies on SHS and health were reported in the late 1960s [1-3] ; there had been scattered case reports previously, and there were campaigns against smoking in public in Nazi Germany. One German physician, Fritz Lickint, used the term "passive smoking" in his 1939 book on smoking [4] . The 2006 Surgeon General's report uses the term "secondhand smoke," although the term "environmental tobacco smoke" (ETS) was used more frequently in earlier reports and discussions on the topic [5] .

      Initial epidemiological investigations focused upon parental smoking and lower respiratory illnesses in infants; studies of lung function and respiratory symptoms in children soon followed [6,7] . The first major studies on SHS smoke and lung cancer in nonsmokers were reported in 1981 [8,9] , and by 1986 the evidence supported the conclusion that SHS was a cause of lung cancer in nonsmokers, a conclusion reached by the International Agency for Research on Cancer (IARC), the US Surgeon General, and the US National Research Council [7,10,11] . Subsequently, a now substantial body of evidence has continued to identify new diseases and other adverse effects of SHS, including increased risk for coronary heart disease [6,12-15] .

      The 2006 US Surgeon General's Report leaves no doubt that any exposure to tobacco smoke is harmful to human health [5] . The findings on SHS and disease have been the foundation of the drive for smoke-free indoor environments and for educating parents concerning the effects of their smoking on their children's 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 documents. A United States Federal Court decision found the tobacco companies to be guilty of fraud and racketeering, citing their actions around SHS as one instance of such activity [16] . The industry's actions were attributable to fear of the policy implications of the findings on SHS. The tactics used to discredit the scientific evidence on SHS included the use of consultant experts who raised endless concerns about the data, sometimes without revealing their employment by the tobacco industry; support for meetings and publications speaking to limitations of the evidence on SHS; and more subtle infiltration of scientific organizations and even public health organizations, including the World Health Organization. Readers of the scientific literature need to be aware that there was an attempt to maintain seeming controversy among scientists even as the evidence mounted and supported converging conclusions by expert panels on the adverse effects of SHS [17] .

      WHAT IS SECONDHAND SMOKE?���Secondhand smoke is one of several terms used for the smoke inhaled involuntarily by nonsmokers. The smoke inhaled by nonsmokers is often referred to as secondhand smoke (SHS) or environmental tobacco smoke (ETS). At present, 1.3 billion adults worldwide are smokers, implying that SHS exposure is almost unavoidable for children and for the two-thirds of adults who do not smoke.

      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 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 MS. 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 inhaled by the active smoker, there is sufficient qualitative similarity to have warranted concern that the health of nonsmokers may be injured by SHS, just as active smokers are harmed by MS. (See "Cigarette smoking and other risk factors for lung cancer" and see "Patterns of tobacco use and benefits of smoking cessation").

      Measurement of secondhand smoke���In environments where smoking takes place, components of tobacco smoke can readily be measured in the air, including small particles in the size range that penetrates into the lung, carbon monoxide, nicotine, and benzene. Concentrations of the smoke components depend upon the number of smokers and their smoking patterns, the size of the space where smoking is taking place, the rate of exchange of the air of the space with outdoor air, and the presence and efficiency of air cleaning devices. The exposures of nonsmokers will also depend upon proximity to smokers, particularly during the time that they are actively smoking. A baby held by a smoking mother might be inhaling dense and virtually undiluted SS, while older children could leave a room if annoyed by the smoking of their parents.

      Measurements of several 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 Environmental Protection Agency. Concentrations of particles in homes with smokers are typically at least double those of homes without smokers [18] .

      Nicotine, present as a gas in SHS, can be readily measured in indoor air using either active or passive samplers. Its presence is highly specific for tobacco smoke, as there are no other sources. Abundant nicotine measurements made over the last several decades confirm that SHS has been widely prevalent in the workplace and in homes [19] . A 31-country study showed that median air nicotine levels were 17-fold higher in homes where smoking takes place compared to those without smoking [20] .

      The secondhand smoker also inhales other components of tobacco smoke. Benzene, which causes leukemia, is generated by tobacco combustion and may contribute to the increased risk of leukemia in active smokers compared with nonsmokers. Secondhand smoke 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 in hair. Studies using biomarkers show clearly that SHS-exposed nonsmokers absorb, metabolize, and excrete tobacco smoke components, including nicotine and tobacco-specific carcinogens [18] . 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 of women and children to SHS at home, levels of hair nicotine in children living with smokers were about 2-fold higher compared to those not living with smokers [20] .

      Cotinine, the principal metabolite of nicotine, has been the most studied biomarker. Levels of cotinine in nonsmokers reach several percent of those in active smokers. 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 [18] . There is strong evidence that SHS exposure is decreasing in the United States, suggesting that these control strategies are having important effects [21,22] . In the 2002 data from the National Health and Human Nutrition Examination Survey, the proportion of US nonsmokers with cotinine concentrations of 0.05 ng/mL or greater fell by 43 percent in comparison with data from 1988-90 [21] . More recent data from the National Health and Nutrition Examination Survey (NHANES) in 2003 to 2004 show a further decrease of 36 percent [23] .

      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 smokers [24] . These observations, together with studies of biomarkers confirm the wide extent of SHS and support the plausibility of adverse effects of SHS by demonstrating uptake of tobacco smoke components by exposed nonsmokers. The 2006 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" [5] .

      HEALTH CONSEQUENCES OF SECONDHAND SMOKE���Evidence of the health risks of involuntary smoking comes from epidemiological studies, which have directly assessed the associations of measures of SHS exposure with disease outcomes. Judgments about the causality of associations between SHS exposure and health outcomes are based not only upon this epidemiological evidence, but also upon the extensive evidence derived from epidemiological and toxicological investigation of the health consequences of active smoking. (See "Patterns of tobacco use and benefits of smoking cessation").

      The literature on SHS and health has been periodically reviewed [7,11-14,25,26] . The most recent reviews were completed in 2005 by the California Environmental Protection Agency [15] and in 2006 by the office of the US Surgeon General [5] . 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 [10] , the US Surgeon General [7] , and the US National Research Council [11] . Each of these reports interpreted the available epidemiologic evidence in the context of the 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 nonsmokers. This and subsequent causal conclusions have had broad public health impact. (See "Cigarette smoking and other risk factors for lung cancer").

      In 1986, the reports of the US Surgeon General and the National Research Council also addressed the then-mounting evidence of adverse respiratory effects of SHS exposure for children. Subsequent reports, including the 2006 Surgeon General's report, identified further effects of SHS exposure on children, and the more recent reports have classified SHS as causing a number of adverse effects for exposed children [5] .

      Annoyance and irritation, although not representing an illness or disease, are also firmly linked to exposure to SHS [7,27] . Surveys document discomfort involving the eye and upper airways; confirmatory evidence has been provided by studies involving exposures of volunteers to SHS in chambers.

      Effects in children���There is an extensive list of adverse effects that various groups have concluded are causally associated with exposure of infants and children to SHS. Exposure to SHS has been found to be a cause of slightly reduced birth weight, lower respiratory illnesses, chronic respiratory symptoms, middle ear disease, reduced lung function, ever having asthma among children of school age, and the onset of wheeze illness in early childhood [5] . Maternal smoking has been characterized as a major cause of sudden infant death syndrome (SIDS), as has exposure to SHS generally. The conclusions of other reports, including those from the California Environmental Protection Agency [15] and the United Kingdom's Scientific Committee on Tobacco [13] are similar. These health consequences of SHS exposure in childhood are discussed in detail elsewhere. (See "Secondhand smoke exposure: effects in children", section on Effects in childhood).

      Effects in adults

      Lung cancer���The doses of carcinogens received from SHS exposure are far less than with active smoking. On the other hand, exposure to SHS can begin in childhood and extend across the full lifespan. (See "Cigarette smoking and other risk factors for lung cancer").

      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 active smokers [10,28] . Furthermore, genotoxic activity, the ability to damage DNA, has been demonstrated for many components of SHS [29-31] . As mentioned above, experimental exposure of nonsmokers to SHS results in the urinary excretion of NNAL, a tobacco-specific carcinogen, and living with a smoker also leads to a higher level of NNAL in nonsmokers [32] . Nonsmokers, including children, exposed to SHS also have increased concentrations of adducts of tobacco-related carcinogens [33,34] .

      A number of studies have shown that SHS is associated with lung cancer, and various review panels, including the 2006 Surgeon General's report, have concluded that SHS exposure causes lung cancer in nonsmokers [7-11,35-37] . There appears to be a dose-response relationship between intensity of exposure and relative risk.

      Results of a meta-analysis including 52 studies and prepared for the 2006 Surgeon General's report showed that the relative risk of lung cancer among male and female nonsmokers who were ever exposed to SHS from the spouse was 1.21 (95% CI 1.13-1.30). The magnitude of the effect was comparable for men (odds ratio 1.37 [95% CI 1.05-1.79]) and women (odds ratio 1.22 [95% CI 1.13-1.31]), with no significant difference by geographic area [37] .

      A meta-analysis of 25 studies of lung cancer and exposure to SHS in the workplace prepared for the 2006 US Surgeon General's report estimated a pooled relative risk of 1.22 (95% CI 1.13-1.33) [37] .

      Another exposure of concern is that of adults exposed as children to smoking parents. A meta-analysis of 24 studies found that, for men and women exposed during childhood to smoking by either parent, the odds ratio of lung cancer was 1.11 (95% CI 0.94-1.31) [37] . For maternal exposure only, the odds ratio was 1.15 (95% CI 0.86-1.52), while for paternal exposure only, the odds ratio was 1.10 (95% CI 0.89-1.36). In a prospective cohort study of 91,540 nonsmoking women in Japan, standardized mortality ratios (SMRs) for lung cancer increased significantly with the amount smoked by the husbands [8] . The findings could not be explained by confounding factors and were unchanged when follow-up of the study group was extended [35] . There was also a significantly increased risk for nonsmoking men married to wives smoking one to 19 cigarettes and 20 or more cigarettes daily. 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 [38] . It was estimated that 17 percent of lung cancer in nonsmokers is attributable to high levels of environmental smoke exposure during childhood and adolescence. In another similarly designed study, tobacco use by the spouse was associated with a 30 percent increase in risk of lung cancer [39] . The risk rose with increasing levels of pack-year exposure from the spouse; 80 or more pack-years of exposure was associated with an 80 percent excess risk of lung cancer.

      A meta-analysis of 37 published studies involving 4626 people with lung cancer found an excess risk of lung cancer of 24 percent (95% CI 13-36 percent) if an individual lived with a smoker [40] . Adjustment for potential bias and confounding by diet did not alter the estimate. A significant dose-response relationship with the number of cigarettes smoked by the spouse and the duration of exposure was also documented. A more recent meta-analysis, involving 55 studies, gave an estimate for women of a 27 percent increase in risk [41] .

      A cohort study subsequent to the above meta-analysis did not find an excess risk of lung cancer in spouses of smokers after 39 years of follow-up; however, the results of this study are weakened by its limited data on spousal smoking, which was only fully assessed at the start of the study without subsequent updating [42] . Inclusion of this study in subsequent meta-analyses had little effect on the point estimate [41,43] .

      Based upon the available data, the United Kingdom's Scientific Committee on Tobacco and Health concluded that exposure to SHS is a cause of lung cancer [13] . The US Environmental Protection Agency has classified SHS as a Group A carcinogen, that is, a known human carcinogen [26] . The International Agency for Research on Cancer (IARC) reached the same conclusion in 2002 [44] , as did the 2006 Report of the Surgeon General [37] .

      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 women with exposure to SHS who developed lung cancer compared with 55 nonsmoking women with lung cancer who had no environmental tobacco smoke exposure [45] . In another population-based study among never smokers, in those with high SHS exposure, GSTM1 and GSTP1 polymorphisms were associated with over a 4-fold increased risk of developing lung cancer [46] . GST is believed to play a role in detoxifying carcinogens in tobacco smoke; thus, mutations which decrease its activity could serve to promote tumorigenesis.

      Cardiovascular disease���Causal associations between active smoking and fatal and nonfatal coronary heart disease (CHD) outcomes have long been demonstrated [47] . The risk of CHD in active smokers increases with amount and duration of cigarette smoking and decreases quickly with cessation. Active cigarette smoking is considered to [48] : Increase the risk of cardiovascular disease by promoting atherosclerosis Increase the tendency to thrombosis Cause coronary artery spasm Increase the likelihood of cardiac arrhythmias Decrease the oxygen-carrying capacity of the blood Affect vascular endothelial cell function

      (See "Cardiovascular risk of smoking and benefits of smoking cessation").

      It is biologically plausible that SHS could be associated with increased risk for CHD through the same mechanisms considered relevant for active smoking, although the lower exposures to smoke components of SHS have raised questions regarding the relevance of the mechanisms cited for active smoking [49,50] . 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 habitual smokers, suggesting that endothelial dysfunction may be an important mechanism by which SHS increases CHD risk [37,51] . 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, homocysteine, fibrinogen, and oxidized LDL cholesterol [52] . Animal models also indicate adverse effects of SHS on the cardiovascular system [37] .

      Findings of a cohort study published in 1985 first raised concern that passive smoking may increase risk for CHD [53] . There are now more than 20 studies on the association between SHS and cardiovascular disease. These studies assessed both fatal and nonfatal cardiovascular heart disease outcomes, and most used self-administered questionnaires to assess SHS exposure. They cover a wide range of racial and geographic populations. The majority of the studies measured the effect of SHS exposure due to spousal smoking; however, some studies also assessed exposures from smoking by other household members or occurring at work or in transit. Some studies have also included measurements of biomarkers.

      While the risk estimates for SHS and CHD outcomes vary in these studies, they range mostly from null to modestly significant increases in risk, with the risk for fatal outcomes generally higher and more significant. The meta-analysis prepared for the 2006 US Surgeon General's report estimated the excess risk from SHS exposure as 27 percent (95% CI 19-36 percent) [37] .

      A cohort study reported in 2003 did not find an excess risk of CHD in spouses of smokers after 39 years of follow-up; however, the results of this study are weakened by its limited data on spousal smoking, which was only fully assessed at the start of the study [42] .

      A prospective cohort study performed in 2004 measured serum cotinine levels [54] . The study included 4729 men in the United Kingdom who provided baseline blood samples in 1978 to 1980. After 20 years of follow-up, among the 2105 men who were nonsmokers, the risk of CHD was increased in those with higher serum cotinine concentrations. Compared with men in the lowest quartile of serum cotinine concentration, after adjusting for established CHD risk factors, 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.

      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 both smokers and nonsmokers [55-58] . Examples of well-performed observational studies showing this effect include: A study in Helena, Montana looked at the effect of a local law banning smoking in public and in workplaces; the law was in effect for six months, and then enforcement was suspended by a court order [55] . Admissions of people living in Helena for acute myocardial infarction to the single hospital serving the area decreased significantly from an average of 40 admissions during the same six months in the years before and after the ban to 24 admissions during the ban; admissions of people not living in Helena showed no significant change. Although these and other data suggest acute effects of SHS on cardiovascular risk [59] , the results in Helena could have been due to a decrease in exposure to SHS, to a decrease in active smoking caused by the ban, or both. A prospective study examined the effects of a law in 2006 that prohibited smoking in all enclosed public places in Scotland [58] . Admissions for ACS in nine hospitals were compared during a 10-month period immediately prior to implementation of the ban, and during the same 10-month period immediately after the ban. There were fewer admissions for ACS after the ban (2684 versus 3235, 17 percent reduction). England, which did not have such a ban, experienced a 4 percent reduction in admissions for ACS. Prior to the ban, Scotland had experienced a mean annual reduction in admissions for ACS of 3 percent. The reduction in admissions for ACS was seen in current smokers, former smokers, and never smokers (reductions of 14, 19, and 21 percent, respectively).

      SHS may also be associated with noncardiac vascular disease. A large cross-sectional study of 60,377 women in China found an association between stroke in women and smoking by their husbands [60] . The prevalence of stroke increased with greater duration of smoking and with an increasing number of cigarettes smoked daily.

      In 1997, the California Environmental Protection Agency (CalEPA) concluded that there is "an overall risk of 30 percent" for CHD due to exposure from SHS [12] . In 2005, the CalEPA established that 22,700 to 69,000 deaths from CHD were attributable to SHS in 2000 [15] . The 2006 Surgeon General's report stated that pooled relative risks from meta-analyses indicate a 25 to 30 percent increase in the risk of coronary heart disease from exposure to SHS [37] .

      Respiratory symptoms and illnesses���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 [61-67] , 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 [68-74] .

      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 physiological responses of asthmatics of SHS [75] . Of three studies involving exposure of unselected asthmatics to SHS, only one showed a definite adverse effect [76-79] . One study recruited 21 asthmatics who reported exacerbation with exposure to SHS [80] . 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 [74,81] . In Scotland, following the national smoking ban in 2006, the respiratory health of asthmatic and nonasthmatic bar workers improved [81] .

      Lung function���Exposure to SHS has been associated in cross-sectional investigations with reduction of several lung function measures. 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.

      Diabetes���Some evidence suggests that active smoking may be a risk factor for diabetes, although the association between smoking and diabetes is not clearly causal. (See "Prediction and prevention of type 2 diabetes mellitus", section on Smoking). A 15-year cohort study also found an increased incidence of glucose intolerance in young adults ages 18 to 30 exposed to SHS [82] .

      All-cause mortality���There are relatively few data on the association between all-cause mortality and SHS. Follow-up of never-smokers ages 45 to 74 years from the 1981 and 1996 censuses in New Zealand suggest that nonsmoking adults who lived with smokers had about a 15 percent increase in adjusted mortality compared with those living in a smoke-free household [83,84] .

      CONTROL OF SHS 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.

      The World Health Organization (WHO) has offered policy recommendations to achieve smokefree environments [85] . Its Framework Convention for Tobacco Control calls for protection of nonsmokers against exposure to SHS. 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���Secondhand smoking 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, 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 physicians working in the public health domain.

      Effects of SHS on children���Issues related to exposure of a fetus or child to SHS are discussed in detail elsewhere. (See "Secondhand smoke exposure: effects in children", section on Responding to specific clinical questions about secondhand smoke).

      Lung cancer and heart disease risk for adults���When the 1986 Report of the Surgeon General was released [7] , Dr. Everett Koop, the Surgeon General at the time, was asked if the causal conclusion with regard to lung cancer meant that nonsmokers should divorce smoking spouses. While divorce is a potential strategy to control exposure to SHS in the home, there are alternatives, as reviewed separately. (See "Control of secondhand smoke exposure", section on The home environment). Lung cancer in never-smokers is not a rare disease [86] ; there are approximately 10,000 cases annually, of which approximately 2,000 to 3,000 are estimated to be attributable to SHS. Nonsmokers married to smokers have about a 20 percent greater risk for lung cancer and coronary heart disease than those married to nonsmokers. While this increment in risk is relatively modest, it can be readily reduced.

      Workplace exposures���The majority of adults in the United States are now nonsmokers, and exposure to tobacco smoke in the workplace, if permitted, may be viewed as both an annoyance and a health risk. Fortunately, the majority of workers now report that their workplaces are smokefree. For the nonsmoker with asthma or perhaps chronic obstructive pulmonary disease, health care providers can reasonably postulate that the exposure may be harmful. SHS exposure would also be anticipated to increase risk for lung cancer and heart disease to an extent, although specific calculations could not be readily made. 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 Workplaces).

      Sick-building syndrome���Sick-building syndrome can be a complex clinical problem, requiring a clinical diagnosis in an individual to be based in a population context. Passive smoking should be considered as one of the factors that can contribute to the occurrence of sick-building syndrome.

      OTHER SOURCES OF INFORMATION���The American Thoracic Society (ATS) statement on cigarette smoking and health, as well as other ATS guidelines, can be accessed through the ATS web site at www.thoracic.org/sections/publications/statements/index.html.

      Reports of the Surgeon General of the US Public Health Service on the adverse health consequences of smoking and SHS exposure can be found at www.surgeongeneral.gov/library/reports/index.html.

      INFORMATION FOR PATIENTS���Educational materials on this topic are available for patients. (See "Patient information: Smoking cessation"). We encourage you to print or e-mail this topic review, or to refer patients to our public web site, www.uptodate.com/patients, which includes this and other topics.


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