Biomarkers increase detection of active smoking and secondhand smoke exposure in critically ill patients.

Active smoking and secondhand smoke (SHS) exposure can cause or worsen many acute and chronic cardiovascular and pulmonary diseases (1, 2). SHS is a combination of mainstream smoke (exhaled by smokers) and sidestream smoke given off by the burning end of the tobacco product. Even brief exposure to SHS has significant immediate effects on endothelial cell function, inflammation, and lung function (3). Despite public health efforts to discourage smoking, U.S. smoking prevalence has recently plateaued at 20%, and the number of smokers internationally is increasing (4, 5). In addition, even though smoking has been increasingly restricted in public places and workplaces, an estimated 40% of U.S. nonsmokers have biological evidence of significant SHS exposure (6). Thus, cigarette smoke exposure remains an important cause of preventable chronic and acute disease in both smokers and those exposed to SHS. The association between recent tobacco smoke exposure and critical illness has been poorly studied. The lack of accurate methods to quantify exposure to tobacco smoke, and SHS in particular, in the critically ill has been a major hindrance. Historically, studies have commonly used questionnaires to measure exposure to tobacco smoke. This method is particularly difficult to use in the intensive care unit, because most critically ill patients have altered levels of consciousness or are endotracheally intubated or both. When patients are unable to provide a history, surrogate and chart reporting are often substituted; however, these sources can be subject to social desirability bias and are frequently inaccurate, out of date, or missing (7–9). Thus, to study the effects of cigarette smoke exposure on the incidence or outcomes of critical illness, a more quantitative approach to measuring cigarette smoke exposure in critically ill patients is needed. Biomarkers of cigarette smoke exposure quantify the biologically active dose of nicotine and toxins to which patients have been exposed, overcoming the subjectivity and inaccuracy of self-reporting or surrogate reporting. Such markers have been used to distinguish active and passive smokers from nonsmokers in epidemiologic studies and to establish causal relationships between both active smoking and SHS exposure and cardiovascular and lung disease (1, 10, 11). Nicotine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (a potent lung carcinogen), and their metabolites are markers specific for tobacco exposure in smokers, smokeless tobacco users, and nonsmokers exposed to SHS. Determining the optimal biomarker or combination of biomarkers for measuring cigarette smoke exposure in critically ill patients will be key for future studies of this population. The primary objective of our study was to compare cigarette smoke exposure, as measured by biomarkers, to exposure by self-report in a cohort of critically ill patients. A secondary objective was to determine how well biomarkers of exposure taken from different biological specimens (serum, urine, hair, and nails) correlate with each other in this population.