Urinary Cotinine and Exposure to Parental Smoking in a Population of Children with Asthma (Drug Monitoring and Toxicology‪)‬

Increased attention has been focused on the potential health effects of environmental tobacco smoke (ETS) [6] on adults and children (1, 2). Increased symptoms such as chronic cough, chronic wheezing, and respiratory infections are observed in children exposed to parental smoking (3, 4). The long-term prevalence of these symptoms is unknown, hence new studies are required (5). Studies on smoking and health have estimated exposure on the basis of the reported number of cigarettes smoked daily (6), which is subject to bias and limitations in accuracy. Several biochemical tests, such as plasma or saliva thiocyanate, expired carbon monoxide, and carboxyhemoglobin (7), have been evaluated to measure cigarette smoke intake. However, they are not suitable because they lack sensitivity and specificity. Cotinine, one of the major metabolites of nicotine, provides more advantages because it is specific for exposure to nicotine from tobacco smoke, it is chemically stable, and urinary pH influences the excretion of cotinine less than it influences nicotine excretion (8). In addition, its longer half-life (19-40 h compared with 2 h for nicotine) (9-11) means that it reflects long-term exposure, whereas nicotine reflects recent exposure.