© 2007 American Thoracic Society doi: 10.1164/rccm.200705-684ED
Indoor Air, Passive Smoking, and COPDUniversity of California, San Francisco San Francisco, California Indoor air quality has assumed greater importance for health. As levels of outdoor ambient pollution have decreased in many geographic areas, the relative impact of indoor air pollution has grown. Residents of developed countries spend the majority of their time indoors, which provides more potential for indoor exposures (1). At the same time, changes in home and office building construction have resulted in lower air exchange rates, increasing personal exposure to pollutants emitted indoors (2). Secondhand smoke (SHS) is a major source of indoor air pollution. In this issue of the Journal (pp. 465–472), Osman and colleagues quantified the impact of SHS on fine particulate pollution (PM2.5) in the homes of Scottish patients with chronic obstructive pulmonary disease (COPD) (3). Both the maximum and average levels of PM2.5 measured in the living room were nearly ten times higher in homes where smoking was allowed than in nonsmoking homes. In fact, maximum living room PM2.5 levels were more than four times the U.S. Environmental Protection Agency (EPA) maximum ambient air standard. Recent work confirms that tobacco smoke is a major, if not the major, indoor source of fine particulate pollution in developed countries. Before the Irish workplace smoking ban, PM2.5 levels in Dublin pubs were six times higher than in outdoor air (4). After the ban went into effect, indoor PM2.5 levels declined by 84% and became similar to outdoor concentrations. Because outdoor PM2.5 concentrations did not change during the study period, these results strongly implicate SHS as the major indoor source of PM2.5. Although the California EPA recently concluded that SHS is a cause of asthma induction and exacerbation in children and adults, the role of SHS exposure in the clinical course of COPD has received little attention (5). Perhaps this is because personal direct cigarette smoking is such a dominant risk factor for developing COPD that other factors have been largely ignored. Osman and colleagues have added important new information about the effects of SHS exposure on patients with established COPD (3). They found that higher indoor PM2.5 levels were associated with greater respiratory symptoms, as measured by the Saint George's Respiratory Questionnaire symptom score. Interestingly, the impact of PM2.5 levels on respiratory symptoms was particularly great among current smokers, although effects were also seen in nonsmokers. Because they used an objective measure of SHS exposure, these results provide strong new evidence linking SHS with worse COPD health status. In a prospective population-based cohort study of adults with COPD, we previously studied the impact of directly measured SHS exposure on health outcomes (6). The highest tertile of urine cotinine was longitudinally associated with greater dyspnea, worse COPD severity, and worse health status among adults with COPD. Taken together with the results from the current report in the Journal, the evidence now indicates that SHS exposure may indeed negatively affect the health of patients with COPD. The finding that indoor PM2.5 concentrations had negative respiratory health effects among both smokers and nonsmokers has important implications for future research (3). We also found that SHS exposure had adverse respiratory health effects in both smoking and nonsmoking bartenders (7). Most previous research on the health effects of SHS exposure, however, has excluded smokers. These studies have implicitly assumed that the effects of passive smoking are inconsequential when compared with those of direct personal smoking. SHS exposure can cause very high levels of particulate and other pollution, especially in bars and other workplaces (8). Moreover, studies of outdoor pollution indicate that smokers are actually more susceptible to the respiratory effects of some pollutants (9). In sum, the evidence now indicates that both smokers and nonsmokers should be included in studies of SHS exposure, other pollutants, and respiratory health. The study by Osman and colleagues provides new data about the impact of NO2 in COPD (3). NO2 is another major indoor pollutant produced from combustion, particularly during gas stove or gas heater use. Among adults with asthma, gas stove use or indoor NO2 exposure has not been consistently associated with more severe respiratory symptoms or pulmonary function impairment (10–13). In the Osman study, there was also no convincing evidence that indoor NO2 levels negatively affected COPD-related health status. This is an area, however, that requires further study. Because outdoor NO2 concentrations appear to have negative health effects in COPD, further evaluation of indoor NO2 effects, especially on pulmonary function, will be needed before NO2 exposures can definitively be declared safe for patients with COPD (14, 15). On a global scale, a large burden of obstructive lung disease symptoms is attributable to indoor combustion (16). The burning of biomass fuel for heating and cooking is a major source of indoor pollution in the developing world. Biomass smoke contains high levels of particulate and other pollutants, which are often released into poorly ventilated spaces. Although the evidence is mounting that biomass smoke may be a cause of COPD, its effects on persons with established obstructive lung disease are poorly understood. Obstructive lung disease appears to predispose to a higher risk of adverse health effects from indoor particulate pollutants, especially SHS. Further research is needed to elucidate the prospective effects of indoor pollutants on adults with COPD, including pulmonary function endpoints. Studies that simultaneously consider a broad range of indoor exposures, including allergens and pollutants, would help to fully characterize the health effects of the indoor environment in COPD. In developing countries, more research is needed to determine the effects of biomass smoke on the development and clinical course of obstructive lung disease. FOOTNOTES Conflict of Interest Statement: M.D.E does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. REFERENCES
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