Biomonitoring exposure to environmental tobacco smoke (ETS): A critical reappraisal

Abstract

<jats:p> 1 The most frequently used biomarkers for exposure to environmental tobacco smoke (ETS) are cotinine and thiocyanate in body fluids, carboxyhaemoglobin in red blood cells (COHb) and carbon monoxide in the expired air. Although not ideal, cotinine in blood, saliva or urine is an established biomarker for ETS exposure within the past 1-3 days. Comparison with cotinine concentrations in cigarette smokers reveals that passive smokers take up less than 1/100 of the nicotine dose of smokers. </jats:p><jats:p> 2 Biomonitoring data available for the ETS-related exposure to genotoxic substances comprise uptake of benzene, polycyclic aromatic hydrocarbons (PAH), aromatic amines, tobacco-specific nitrosamines (TSNA), electrophilic compounds giving rise to ur inary thioethers, mutagens causing urinary mutagenic activity and the formation of various DNA adducts. With the exception of TSNA, these biomarkers are related to chemicals occurring ubiquitously in the environment and in the food. As a consequence, the background levels in unexposed nonsmokers are high compared to the observed increases (if any) associated with ETS exposure. </jats:p><jats:p> 3 Some markers of biological effects, which, by defini tion, are non-specific with regard to the underlying exposure, have also been investigated in relation to ETS exposure. These markers comprise cytogenetic effects, aryl hydrocarbon hydroxylase (AHH) induc tion, urinary hydroxyproline excretion and various factors indicative of cardiovascular risks. The avail able data suggest that passive smoking is associated with a small induction of placental AHH and also with effects on cardiovascular risk markers. The latter findings in particular may be confounded by other risk factors, which have been observed to be more frequent in passive smokers than in unexposed nonsmokers. </jats:p>

Predictors of environmental exposure to polycyclic aromatic hydrocarbons among pregnant women — Prospective cohort study in Poland

“…Smoking is the major source for PAH exposure for subjects not occupationally exposed to PAH, so in the studies evaluating the impact of such exposure (relating to ambient air pollution) on pregnancy outcome, verification of smoking status in pregnancy period seems to be the standard. Smokers excreted significantly higher amounts of 1-HP compared to non-smokers and the number of cigarettes smoked correlated rather well with urinary 1-HP concentration [1][2][3].…”

Long-Term Exposure to Nicotine Modulates the Level and Activity of Acetylcholine Receptors in White Blood Cells of Smokers and Model Mice

“…Ideal smoking cessation programs involve a combination of comprehensive medical, psychiatric, and substance-abuse evaluations. Current tests include the assessment of nicotine-dependence severity (e.g., Fagerström Test for Nicotine Dependence) and measurements of smoking and nicotine intake, including expired breath carbon monoxide and cotinine (a nicotine metabolite) levels in the plasma, saliva, or urine (Scherer and Richter, 1997;Benowitz, 1999). However, these routine methods are not fully satisfactory, because they are often not precise.…”

Immunoperoxidase detection of polycyclic aromatic hydrocarbon-DNA adducts in mouth floor and buccal mucosa cells of smokers and nonsmokers

“…We should also acknowledge that the determined levels of adducts in nonsmokers could mainly reflect their exposure to other sources of PAHs, e.g., diet, environmental tobacco smoke, etc. [Scherer and Richter, 1997] as our specificity examination ensured the PAHderived nature of these adducts. Furthermore, we observed a significant correlation between the levels of adducts in mouth floor cells and those in buccal mucosa cells in the overall study group.…”