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Secondhand smoke: the evidence of danger keeps growing

2004; Elsevier BV; Volume: 116; Issue: 3 Linguagem: Inglês

10.1016/j.amjmed.2003.11.005

1555-7162

Joaquín Barnoya, Stanton A. Glantz,

Smoking Behavior and Cessation

Secondhand smoke increases the risk of fatal and nonfatal coronary heart disease by about 30% (1He J. Vupputuri S. Allen K. Prerost M.R. Hughes J. Whelton P.K. Passive smoking and the risk of coronary heart disease–a meta-analysis of epidemiologic studies.N Engl J Med. 1999; 340: 920-926Crossref PubMed Scopus (493) Google Scholar, 2Law M. Morris J. Wald N. Environmental tobacco smoke exposure and ischaemic heart disease An evaluation of the evidence.Br Med J. 1997; 315: 973-980Crossref PubMed Scopus (477) Google Scholar). This effect, while appearing consistently in many epidemiologic studies, is larger than one would expect based on the dose of smoke that passive smokers receive compared with smokers (2Law M. Morris J. Wald N. Environmental tobacco smoke exposure and ischaemic heart disease An evaluation of the evidence.Br Med J. 1997; 315: 973-980Crossref PubMed Scopus (477) Google Scholar): the effect is about one third that observed in smokers whereas the relative dose of smoke is much smaller. Previous investigators have shown that this apparent disparity may be because several aspects of the cardiovascular system, including platelets (3Burghuber O. Punzengruber C. Sinzinger H. Haber P. Silberbauer K. Platelet sensitivity to prostacyclin in smokers and non-smokers.Chest. 1986; 90: 34-38Crossref PubMed Scopus (91) Google Scholar, 4Glantz S. Parmley W. Passive smoking and heart disease Mechanisms and risk.JAMA. 1995; 273: 1047-1053Crossref PubMed Scopus (390) Google Scholar) and endothelial function (5Celermajer D.S. Adams M.R. Clarkson P. et al.Passive smoking and impaired endothelium-dependent arterial dilatation in healthy young adults.N Engl J Med. 1996; 334: 150-155Crossref PubMed Scopus (833) Google Scholar, 6Otsuka R. Watanabe H. Hirata K. et al.Acute effects of passive smoking on the coronary circulation in healthy young adults.JAMA. 2001; 286: 436-441Crossref PubMed Scopus (318) Google Scholar, 7Glantz S.A. Parmley W.W. Even a little secondhand smoke is dangerous.JAMA. 2001; 286: 462-463Crossref PubMed Scopus (70) Google Scholar), are very sensitive, even to the comparatively low doses of smoke (compared with smoking) that nonsmokers inhale when around secondhand smoke. Indeed, some of the effects of secondhand smoke on the cardiovascular system in nonsmokers are comparable to the effects of smoking in smokers, perhaps because the effects of the toxins in the smoke saturate at relatively low exposures. In this issue of the Journal, Panagiotakos et al (8Panagiotakos D, Pitsavos C, Chrysoohoou C, et al. Effect of exposure to second hand smoke on inflammation markers: The ATTICA epidemiological study. Am J Med. 2003;116:145–150Google Scholar) document one more effect of secondhand smoke: an increase in inflammation, which is a precursor of atherosclerotic plaque (9Libby P. Ridker P.M. Maseri A. Inflammation and atherosclerosis.Circulation. 2002; 105: 1135-1143Crossref PubMed Scopus (5970) Google Scholar). In particular, they showed not only that white blood cells, C-reactive protein, homocysteine, fibrinogen, and oxidized low-density lipoprotein (LDL) cholesterol levels were increased among those exposed to secondhand smoke, but that the increases were similar to what was observed in smokers. The mechanisms by which secondhand smoke increases the risk of heart disease are multiple and include an increase in oxidized LDL cholesterol, increase platelet adherence, mitochondrial damage, and oxidative damage (4Glantz S. Parmley W. Passive smoking and heart disease Mechanisms and risk.JAMA. 1995; 273: 1047-1053Crossref PubMed Scopus (390) Google Scholar, 10Ballinger S.W. Patterson C. Knight-Lozano C.A. et al.Mitochondrial integrity and function in atherogenesis.Circulation. 2002; 106: 544-549Crossref PubMed Scopus (387) Google Scholar). Rather than happening in isolation, these mechanisms interact with each other. In addition, secondhand smoke damages the endothelium, a vital layer of coronary arteries (11Puranik R. Celermajer D.S. Smoking and endothelial function.Prog Cardiovasc Dis. 2003; 45: 443-458Abstract Full Text Full Text PDF PubMed Scopus (131) Google Scholar). The endothelium secretes vasodilating substances such as nitric oxide and prevents inflammatory cells from attaching to the vessel wall. Secondhand smoke interferes with the production of nitric oxide (12Hutchison S. Sudhir K. Sievers R. et al.Effects of L-arginine on atherogenesis and endothelial dysfunction due to secondhand smoke.Hypertension. 1999; 34: 44-50Crossref PubMed Scopus (37) Google Scholar, 13Sun Y. Zhu B. Sievers R. Glantz S. Deedwania P. Parmley W. L-arginine preserves endothelial dependent relaxation during environmental tobacco smoke in lipid fed rabbits.Circulation. 1994; 90: I-459Google Scholar, 14Schwarzacher S.P. Hutchison S. Chou T.M. et al.Antioxidant diet preserves endothelium-dependent vasodilatation in resistance arteries of hypercholesterolemic rabbits exposed to environmental tobacco smoke.J Cardio Pharm. 1998; 31: 649-653Crossref PubMed Scopus (14) Google Scholar). The study of Panagiotakos et al (8Panagiotakos D, Pitsavos C, Chrysoohoou C, et al. Effect of exposure to second hand smoke on inflammation markers: The ATTICA epidemiological study. Am J Med. 2003;116:145–150Google Scholar) has several strengths but also some limitations. The size of the random sample, the ability to control for potential confounders (e.g., diet, physical activity), and assessment of secondhand smoke exposure at home and at work, are some of the strengths of this study. The facts that the data are cross-sectional, that there was no biochemical validation of secondhand smoke exposure (e.g., cotinine levels), and that levels of exposure are classified only as regular or occasional, are some limitations of the study. The percentage of people who report current exposure (38% of never-smoking men and 33% of women) seems low, given that the prevalence of current smoking in the sample (48% of men and 38% of women) is high. This fact raises the possibility that the authors are underestimating actual exposure. The effects of this underestimation, however, will bias the results towards the null. The elevated levels of inflammatory markers found in this study are surrogate markers of inflammation that would lead to atherosclerotic disease and ultimately to an increase in the risk of heart disease. To validate their results, it would be desirable to have the results of a prospective study. Although Panagiotakos et al (8Panagiotakos D, Pitsavos C, Chrysoohoou C, et al. Effect of exposure to second hand smoke on inflammation markers: The ATTICA epidemiological study. Am J Med. 2003;116:145–150Google Scholar) studied the effect of long-term exposure to secondhand smoke, it is important to note that some of the cardiovascular effects occur very quickly, some within minutes. Using the coronary flow velocity reserve as a surrogate of endothelial function, Otsuka et al (6Otsuka R. Watanabe H. Hirata K. et al.Acute effects of passive smoking on the coronary circulation in healthy young adults.JAMA. 2001; 286: 436-441Crossref PubMed Scopus (318) Google Scholar) showed that after 30 minutes of breathing secondhand smoke, the endothelial function of coronary arteries of nonsmokers is compromised to a level similar to what is observed in a regular smoker. Platelet function (15Glantz S.A. Parmley W.W. Passive smoking and heart disease Epidemiology, physiology, and biochemistry.Circulation. 1991; 83: 1-12Crossref PubMed Scopus (535) Google Scholar) and oxidation of LDL cholesterol (16Valkonen M. Kuusi T. Passive smoking induces atherogenic changes in low-density lipoprotein.Circulation. 1998; 97: 2012-2016Crossref PubMed Scopus (128) Google Scholar) show similar rapid responses. In addition, heart rate variability (a predictor of cardiac death or arrythmic events after myocardial infarction) in healthy people has been shown to decrease by 12% after 2 hours of breathing secondhand smoke in an airport lounge (17Pope C.I. Eatough D. Gold D. et al.Acute exposure to environmental tobacco smoke and heart rate variability.Environ Health Perspect. 2001; 109: 711-716Crossref PubMed Scopus (158) Google Scholar). Three hours of secondhand smoke exposure leads to significant increases in the circulating white blood cell counts (18Anderson R. Theron A.J. Richards G.A. Myer M.S. van Rensburg A.J. Passive smoking by humans sensitizes circulating neutrophils.Am Rev Respir Dis. 1991; 144: 570-574Crossref PubMed Google Scholar). It would be desirable to know if other inflammatory markers, such as C-reactive protein, fibrinogen, and homocysteine, respond as quickly to secondhand smoke and how long it takes the effect to resolve after the exposure ends. Even if only about 35% of the people in the study (conducted in Greece) are exposed to secondhand smoke at work or in their daily lives, this exposure still represents an important public health problem. In addition to heart disease, secondhand smoke increases the risk of lung and other cancers and of respiratory problems, thereby accounting for 53,000 deaths annually in the United States (15Glantz S.A. Parmley W.W. Passive smoking and heart disease Epidemiology, physiology, and biochemistry.Circulation. 1991; 83: 1-12Crossref PubMed Scopus (535) Google Scholar, 19Wells A.J. An estimate of adult mortality in the United States from passive smoking.Environ Int. 1988; 14: 249-265Crossref Scopus (87) Google Scholar, 20National Cancer Institute. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protectional Agency (Smoking and Health Monograph 10). Bethesda, Maryland: National Cancer Institute; 1999. Report No.: NIH Pub. No. 88-4645. Available at: http://rex.nci.nih.gov/NCI_MONOGRAPHS/MONO10/MONO10.HTM. Accessed October 27, 2003Google Scholar). The solution for secondhand smoke exposure is simple and straight forward: smoke-free environments. In addition to protecting nonsmokers from the toxins in secondhand smoke, smoke-free environments lead to a 3.8% decrease in the absolute prevalence of smoking and a three cigarette per day decrease among continuing smokers—a 29% drop in total cigarette consumption (21Fichtenberg C.M. Glantz S.A. Effect of smoke-free workplaces on smoking behaviour systematic review.BMJ. 2002; 325: 188Crossref PubMed Google Scholar). Because the risks of heart disease fall so quickly when exposure to tobacco smoke ends, the California tobacco control program, which stressed smoke-free laws, not only reduced cigarette consumption, but also led to a large decrease in heart disease mortality (22Fichtenberg C.M. Glantz S.A. Association of the California Tobacco Control Program with declines in cigarette consumption and mortality from heart disease.N Engl J Med. 2000; 343: 1772-1777Crossref PubMed Scopus (256) Google Scholar, 23Fichtenberg C.M. Glantz S.A. Controlling tobacco use.N Engl J Med. 2001; 344: 1798-1799Google Scholar). Although creation of smoke-free environments makes a valuable contribution to public health, it costs the tobacco industry billions of dollars in lost sales (21Fichtenberg C.M. Glantz S.A. Effect of smoke-free workplaces on smoking behaviour systematic review.BMJ. 2002; 325: 188Crossref PubMed Google Scholar, 22Fichtenberg C.M. Glantz S.A. Association of the California Tobacco Control Program with declines in cigarette consumption and mortality from heart disease.N Engl J Med. 2000; 343: 1772-1777Crossref PubMed Scopus (256) Google Scholar, 23Fichtenberg C.M. Glantz S.A. Controlling tobacco use.N Engl J Med. 2001; 344: 1798-1799Google Scholar). For more than 3 decades, the tobacco industry has worked in the shadows to generate a false controversy about the fact that secondhand smoke is dangerous. Through scientific consultants around the world who have been hired and managed by industry lawyers to obscure their connection to the tobacco industry, the industry has financed research that supports its political position (24Barnes D.E. Bero L.A. Why review articles on the health effects of passive smoking reach different conclusions.JAMA. 1998; 279: 1566-1570Crossref PubMed Scopus (365) Google Scholar) that secondhand smoke is just another indoor air contaminant and should not be regulated (25Barnoya J. Glantz S. Tobacco industry success in preventing regulation of secondhand smoke in Latin America the "Latin Project".Tob Control. 2002; 11: 305-314Crossref PubMed Scopus (88) Google Scholar, 26Muggli M.E. Forster J.L. Hurt R.D. Repace J.L. The smoke you don't see uncovering tobacco industry scientific strategies aimed against environmental tobacco smoke policies.Am J Public Health. 2001; 91: 1419-1423Crossref PubMed Scopus (120) Google Scholar). Despite the industry's well-orchestrated secondhand smoke campaign, the scientific evidence behind the harmful effects of secondhand smoke keeps growing and the pressure for smoke-free environments continues to spread. Although most of the attention and justification for creating smoke-free workplaces and public places has been to prevent cancer, the fact is that the effects of secondhand smoke on the heart and vascular system occur more quickly and account for the largest fraction of the disease and death that is caused by secondhand smoke (15Glantz S.A. Parmley W.W. Passive smoking and heart disease Epidemiology, physiology, and biochemistry.Circulation. 1991; 83: 1-12Crossref PubMed Scopus (535) Google Scholar, 19Wells A.J. An estimate of adult mortality in the United States from passive smoking.Environ Int. 1988; 14: 249-265Crossref Scopus (87) Google Scholar, 20National Cancer Institute. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protectional Agency (Smoking and Health Monograph 10). Bethesda, Maryland: National Cancer Institute; 1999. Report No.: NIH Pub. No. 88-4645. Available at: http://rex.nci.nih.gov/NCI_MONOGRAPHS/MONO10/MONO10.HTM. Accessed October 27, 2003Google Scholar) Clinicians and public health advocates should educate their patients about the dangers that secondhand smoke poses to heart health and urge them to take appropriate personal and public policy steps to end this exposure.