Evaluation of Passive Smoking by Measuring Urinary Trans, trans-muconic Acid and Exhaled Carbon Monoxide Levels.

Abstract

No method has yet been established to evaluate the exposure to tobacco smoke in passive smoking (PS). We therefore conducted a study on the possibility that the levels of urinary trans, trans-muconic acid (MA) and the exhaled carbon monoxide (CO) could be indices of the passive exposure to tobacco smoke. The moderate correlation was observed between urinary MA levels and the number of consumed cigarettes per day in smokers. The mean urinary MA level of the PS (+) group was significantly higher than that with the PS (-) group. Among the PS (+) group, the mean MA level in the urine obtained in the afternoon was higher than that obtained in the morning . A high correlation was observed between the exhaled CO levels and the number of consumed cigarettes per day in smokers. Like the urinary MA level, the mean exhaled CO level in the PS (+) group, too, gave a significantly higher level than in the PS (-) group. Because the biological half life of MA (7.5 ± 0.85 h) was longer than that of CO (3.0 ± 0.36 h), the measurement of urinary MA level is recommended for evaluating the exposure of passive smoking. The measurement of exhaled CO levels is useful only for chain smokers and nonsmokers with PS just before measurement .

Assessment of smoking behaviour in the dental setting. A study comparing self-reported questionnaire data and exhaled carbon monoxide levels

“…The cut-off value for the categorization of individuals as either positive or negative for smoking has been recommended to be 8-10 ppm [29]. CO measurements are reported to be reasonably specific for detecting heavy cigarette smokers, but especially for light smokers, environmental sources of CO of similar magnitude can pose problems in diagnosis and monitoring of smoking behaviour [30].…”

Carbon monoxide and respiratory symptoms in young adult passive smokers: A pilot study comparing waterpipe to cigarette

“…Although urine cotinine and carboxyhemoglobin levels were not evaluated in this study, we chose CO as a biological marker of SHS because it is quick and easy to measure, cheaper than performing a series of laboratory assays, non-invasive, thus more acceptable to the participant [36,37]. Despite the non-specificity of CO to tobacco smoke, the latter remains the most important source of CO in indoor places, and it can be used as a biomarker for passive tobacco exposure [38][39][40]. In fact, using carbon monoxide to evaluate passive smoking has been useful in case of cigarettes: carbon monoxide could be considered one of the most toxic substances present in the gas-phase of second-hand tobacco smoke [41].…”

Validation of smoking status in clinical research into inflammatory periodontal disease

“…Biochemical assessment of current smoking status can be achieved by measurement of systemic levels of cotinine, nicotine, thiocyanate (Jarvis et al 1987, Yamanaka et al 1991), or other constituents or metabolites of tobacco smoke (Caldwell et al 1992, Scherer & Richter 1997, Taniguchi et al 1999). Plasma, serum, saliva and urine are all suitable fluids in which to measure tobacco smoke exposure.…”