Published Online: Febraury 4, 2013
Exposure to tobacco smoke (ETS) is a well-known risk factor for childhood asthma and impaired lung function, but the effect on airway inflammation in preschool-age children is unclear. Most of the studies on ETS and children are based on parental reports of their daily smoking habits. Measurement of cotinine, a major nicotine me-tabolite, in blood, urine, saliva, or hair offers a more objective way to monitor passive smoking also in young children.
In a study recently published in The Journal of Allergy and Clinical Immunology, Kal-liola et al hypothesized that parental smoking affects lung function and may increase airway inflammation in young children. Exposure to tobacco smoke was assessed by parental reports and children’s urinary cotinine concentrations. Lung function was examined by impulse oscillometry and fractional concentration of exhaled nitric oxide (FeNO) as a marker of airway inflammation was measured.
The researchers studied ninety-six 3 to 7 year old children prone to wheezing triggered by environmental factors and infections. Forty-three percent of these children were exposed to tobacco smoke by parental reports. The airway inflammation measured by FeNO was higher and lung function lower in children exposed to maternal ETS. Smoking of father did not have similar effect on children’s lung function or FeNO. Children’s urinary cotinine concentrations reflected well parental reports on their daily smoking habits and correlated also with the FeNO.
Our findings clearly show the detrimental effects of ETS on developing lungs particu-larly in children prone to wheezing. Further studies are needed to enlighten on the mechanisms, but the message of this study is clear – young children should not be exposed to ETS.
The Journal of allergy and Clinical Immunology (JACI) is an official scientific journal of AAAAI, and is the most-cited journal in the field of the allergy and clinical immu-nology.