exposed to ETS were not distinguishable from those nonsmokers free of tobacco smoke exposure (Pekkanen et al., 1976).
In another study, mean serum thiocyanate levels were reported to be significantly higher (p<0.002) for children and adolescents with exposure to cigarette smoke at home (n=14; SCN−=97.3±45.4 µmol/L) than for those not exposed (n=10; SCN−=54.2±11.3 µmol/L). The authors of the latter study also reported a weak correlation between thiocyanate concentration and number of cigarettes smoked per family (Poulton et al., 1984). This study was criticized because some of the determined thiocyanate levels were within the range reported for heavy cigarette smokers. It is likely that there was deceptive reporting of adolescent smoking status (Jarvis, 1985). Based on the observations to date, the level of thiocyanate in saliva, serum, and/or urine is not useful as an indicator for the uptake of ETS by a nonsmoker.
Carbon monoxide (CO) in the body originates from endogenous processes as well as environmental sources. The endogenous production of CO is primarily a consequence of the breakdown of hemoglobin and of other heme-containing pigments. Healthy adults produce about 0.4 ml of CO per hour (0.5 mg/h; Coburn et al., 1964). This provides the major portion of CO that is found as carboxyhemoglobin (COHb) in nonsmokers. In nonsmokers without occupational exposure to CO, COHb ranges from 0.5 to 1.5% (National Research Council, 1981; Wald et al., 1981).
The inhalation of CO from the environment is followed by an increase of the CO concentration in the alveolar gas and by diffusion from the gas phase through the pulmonary membrane into the blood. CO is complexed with blood to form COHb and, as such, is transported throughout the body. Complexing it with hemoglobin occurs with a strong coordination bond with the iron of heme, a bond that is about 200 times stronger than that with molecular oxygen. CO is only slowly released from the blood in the process of exhaling. In the case of nonsmokers who have been exposed to elevated levels of CO in the air for a few hours, the half-life of COHb lasts 2–4 hours (National Research Council, 1981).
Monitoring of absorbed CO in the blood is done primarily by the analysis of CO in alveolar gas and by the analysis of COHb