American Thoracic Society/Infectious Diseases Society of America. Guide- lines for the ... ease, cardiovascular disease, and cancer (1, 2). Based on this ... nancy and postnatal ETS exposure on childhood lung function. (8). More than half the ...
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deep tracheal aspirate in the diagnosis of ventilator associated pneumonia. J Trauma 2005;59:891–895. 13. Ibrahim EH, Ward S, Sherman G, Schaiff R, Fraser VJ, Kollef MH. Experience with a clinical guideline for the treatment of ventilatorassociated pneumonia. Crit Care Med 2001;29:1109–1115. 14. Shorr AF, Sherner JH, Jackson WL, Kollef MH. Invasive approaches to the diagnosis of ventilator-associated pneumonia: a meta-analysis. Crit Care Med 2005;33:46–53. 15. American Thoracic Society/Infectious Diseases Society of America. Guidelines for the management of adults with hospital-acquired, ventilator-
associated, and health care–associated pneumonia. Am J Respir Crit Care Med 2005;171:388–416. 16. Croce MA, Fabian TC, Waddle-Smith L, Melton SM, Minard G, Kudsk KA, Pritchard FE. Utility of Gram’s stain and efficacy of quantitative cultures for posttraumatic pneumonia: a prospective study. Ann Surg 1998;227:743–751. 17. Kollef MH, Kollef KE. Antibiotic utilization and outcomes for patients with clinically suspected ventilator-associated pneumonia and negative quantitative BAL culture results. Chest 2005;128:2706–2713. DOI: 10.1164/rccm.2603004
Passive Smoking, Lung Function, and Public Health Decades of research have established that environmental tobacco smoke (ETS) has serious negative consequences for health. Exposure to ETS has been linked to a broad array of diseases, including asthma, chronic obstructive pulmonary disease, cardiovascular disease, and cancer (1, 2). Based on this research, many countries and localities have passed laws prohibiting smoking in the workplace, which includes bars and restaurants. Workplace smoking restrictions have been implemented in ten U.S. states, nine Canadian provinces, five European nations, New Zealand, Uruguay, and other locations around the world. Supporting these efforts, there is mounting evidence that smoking bans are effective in reducing ETS exposure and its consequences: chronic respiratory symptoms, pulmonary function impairment, and cardiovascular disease (3–7). Although these trends are encouraging, the findings of Moshammer and colleagues in this issue of the Journal (pp. 1255–1263) are a stark reminder that the population that is most vulnerable to the effects of ETS exposure on lung function—young children—is not being adequately protected by current legislative efforts (8). Children are primarily exposed to tobacco smoke in the home, where legal restrictions do not apply. Exposure to parental smoking has been repeatedly associated with reduced lung function among children in both crosssectional and cohort studies (9). Maternal smoking, compared with smoking by other household members, has been most strongly linked with deleterious effects on childhood respiratory health. Despite the already extensive literature, however, it has been difficult to elucidate the relative effects of smoking during pregnancy versus postnatal ETS exposure on pulmonary function. This is because women who smoke during pregnancy tend to continue smoking after the child’s birth and to smoke more heavily than nonsmoking mothers. In their elegant pooled analysis of approximately 20,000 children from nine countries in Europe and North America, Moshammer and colleagues evaluated the independent effects of maternal smoking during pregnancy and postnatal ETS exposure on childhood lung function (8). More than half the children were exposed to passive smoking. The proportion of children exposed to maternal smoking during pregnancy alone was small (2.3%), but many children were exposed to both in utero smoking and current household ETS exposure (17.5%) or current ETS exposure alone (38.2%). Maternal smoking during pregnancy had a substantive negative impact on all spirometric indices, ranging from ⫺0.9% for FEV1 to ⫺5.1% for MEF25, even after controlling for potential confounding factors and the effects of current ETS exposure. Both current ETS exposure and ETS exposure during the first 2 years of life were also associated with reduced lung function, although the effects were smaller in magnitude. Given the structure of the data, it is likely that the estimated effect of “maternal smoking during pregnancy” included airway injury that occurred dur-
ing both the prenatal and postnatal periods. On the other hand, the analyses that included smoking during pregnancy and current ETS exposure together in the same model likely underestimated the true effect of postnatal ETS exposure on lung function (i.e., a conservative bias). In sum, this work clearly confirms that smoking during pregnancy and postnatal childhood ETS exposure both have an independent negative impact on childhood lung function. We interpret the findings of Moshammer and colleagues as a powerful confirmation of previous studies that examined the relationship of cotinine level, which is a biomarker of recent ETS exposure, on lung function impairment among children, taking prenatal exposure into account. For example, Corbo and colleagues found that even low-level ETS exposure, as measured by urinary cotinine, had an adverse effect on lung function among healthy nonsmoking children and adolescents (10). Mannino and colleagues also found a strong association between higher serum cotinine levels and worse lung function among children aged 8 to 16 years (11). The article by Moshammer and colleagues also helps clarify the impact of early-life ETS exposure on asthma induction in childhood. A large body of epidemiologic research, which includes more than 80 studies, indicates that early exposure to passive smoking increases the risk of developing new-onset asthma in childhood (2). The high concordance between maternal smoking during pregnancy and early childhood ETS exposure, however, has made it difficult to parse out the independent effects of in utero exposure to tobacco byproducts via the placenta versus childhood passive smoking exposure. Some critics have even argued that the association between childhood ETS and asthma can be explained by smoking during pregnancy alone and not by passive smoking after birth. The current study clarifies this issue, finding that both in utero and postnatal ETS exposure were associated with poorer pulmonary function in childhood. Decreased lung function in early life, in turn, is a risk factor for persistent wheezing and childhood asthma (12, 13). Moreover, other recent work published in the Journal found that smoking during pregnancy and postnatal ETS exposure both increase the risk of asthma in adulthood (14). Taken together, the evidence supports the effects of both maternal smoking during pregnancy and childhood ETS exposure on childhood asthma induction. Because there is an asthma epidemic in the United States and much of the developed world, childhood ETS exposure represents an important target for asthma prevention. ETS exposure is a major cause of disease and suffering. It has been linked with premature death from lung cancer, ischemic heart disease, and stroke: an estimated annual excess of 50,000 and 11,000 deaths from these conditions in the United States and the United Kingdom, respectively (2, 15). In the United States alone, there are more than 200,000 childhood asthma
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episodes that are attributable to parental smoking every year (2). Consequently, the current legislative efforts to prohibit public smoking are critical priorities. Although the number of countries and localities prohibiting workplace smoking continues to grow, most adults are still vulnerable. In the United States, only one in four adults is currently protected from workplace passive smoking by such regulations (16). For children, who are especially susceptible to the health consequences of ETS exposure, the situation may be far worse, as legislative efforts to ban public smoking afford no protection in the home. To prevent ETSrelated morbidity and mortality among children, the key priorities must include elimination of ETS exposure in both public places and the home.
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9. Conflict of Interest Statement : Neither author has a financial relationship with a commercial entity that has an interest in the subject of this manuscript.
Mark D. Eisner, M.D., M.P.H. University of California, San Francisco San Francisco, California Francesco Forastiere, M.D., Ph.D. Rome E Health Authority Rome, Italy
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References 1. Eisner MD, Balmes J, Katz PP, Trupin L, Yelin EH, Blanc PD. Lifetime environmental tobacco smoke exposure and the risk of chronic obstructive pulmonary disease. Environ Health 2005;4:7. 2. Office of Environmental Health Hazard Assessment California Environmental Protection Agency. Health effects assessment for environmental tobacco smoke, 2005. Available from: ftp://ftp.arb.ca.gov/carbis/ regact/ets2006/app3part%20b.pdf (accessed March 2, 2006). 3. Allwright S, Paul G, Greiner B, Mullally BJ, Pursell L, Kelly A, Bonner B, D’Eath M, McConnell B, McLaughlin JP, et al. Legislation for smokefree workplaces and health of bar workers in Ireland: before and after study. BMJ 2005;331:1117. 4. Bates MN, Fawcett J, Dickson S, Berezowski R, Garrett N. Exposure
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DOI: 10.1164/rccm.2603002
