Periodontal health in children exposed to passive smoking Erdemir EO, So¨nmez IS, Oba AA, Bergstrom J, C ¸agˇlayan O. Periodontal health in children exposed to passive smoking. J Clin Periodontol 2010; 37: 160–164. doi: 10.1111/j.1600-051X.2009.01510.x. Abstract Aim: To determine (1) the cotinine levels of saliva, urine and gingival crevicular fluid (GCF) of children in families with and without smoking members and (2) a possible association between the periodontal health of the children and exposure to passive smoking. Material and Methods: The study population comprised of 109 children in the age range 6–12 years. Children were classified as exposed to passive tobacco smoking (PTS-exposed, n 5 51) and as unexposed controls (PTS-unexposed, n 5 58). Plaque index, gingival index, bleeding on probing, probing depth and clinical attachment level (CAL) were recorded. GCF, saliva and urine samples were also collected. The levels of cotinine in these fluids were determined by enzyme-linked immunosorbent assay. Results: The mean salivary cotinine concentration was significantly increased in PTS- exposed children compared with PTS-unexposed children (po0.05). Further, in a dose-dependent way, the mean salivary concentration was significantly higher in children whose father or mother was a smoker (po0.05) as compared, respectively, with children whose fathers and mothers were non-smokers. The mean CAL was significantly less in PTS-exposed children compared with non-PTS-exposed children (0.09 mm; po0.05) and also in children whose father was a smoker (po0.05), but not in children whose mother was a smoker as compared with non-smoker fathers and mothers, respectively. The GCF cotinine levels were below the detection limits with the assay method that was used. Conclusions: We have observed that children who are exposed to passive smoking have elevated cotinine levels in their saliva concomitant with a lowered CAL. Key words: children; cotinine; passive smoking; periodontal health Accepted for publication 23 October 2009 Smoking is generally accepted as a major preventable risk factor in the incidence and progression of periodontal disease (Schenkein et al. 1995, Gonzalez et al. 1996, Bergstrom et al. 2000, Johnson & Hill 2004, Borrell & Papapanou 2005, Heitz-Mayfield 2005, Palmer et al. 2005, Tonetti & Claffey 2005). Recently, it was reported that among adults who had never smoked cigarettes, the odds of having periodontal disease were 1.6 times greater for persons exposed to passive smoking than for persons not exposed, after con- trolling for known risk factors for perio- dontal disease (Arbes et al. 2001). This result suggested that passive smoking may also have a harmful effect on perio- dontal health. Passive smoking has been associated with a number of negative health out- comes in children. It is causally associated with asthma induction and exacerbation, middle ear infections, chronic respiratory symptoms and acute lower respiratory tract infections such as bronchitis and pneumonia (California Environmental Protection Agency 2007). Although self-reported smoking is the most widely used strategy to classify smokers and non-smokers, quantification of the exposure to smoking based on self- reports may at times be unreliable (Gon- zalez et al. 1996). A number of biochem- ical markers have been used to validate claims of non-smoking, including mea- sures based on thiocyanate, nicotine, cotinine and carbon monoxide. Levels of thiocyanate and carbon monoxide are easier to determine but may be elevated through exposures unrelated to smoking, such as traffic emissions and diet (Jarvis et al. 1987, Patrick et al. 1994). Cotinine, a major metabolite of nicotine, is the most commonly used biochemical marker of tobacco use (Armitage et al. 1975, Benowitz 1996); its plasma half-life is longer than that of nicotine, ranging from 10 to 30 h (Beno- witz et al. 1983, Curvall & Enzell 1986). A few reports have documented an association between cotinine level in Ebru Olgun Erdemir 1 , Is -ıl Sarog ˇ lu So ¨ nmez 2 , Aylin Akbay Oba 2 , Jan Bergstrom 3 and Osman C ¸ ag ˇ layan 4 1 Department of Periodontology, Faculty of Dentistry, Kirikkale University, Kirikkale, Turkey; 2 Department of Pedodontics, Faculty of Dentistry, Kirikkale University, Kirikkale, Turkey; 3 Karolinska Institutet, Institute of Odontology, Stockholm, Sweden; 4 Department of Biochemistry, Faculty of Medicine, Kirikkale University, Kirikkale, Turkey Conflict of interest and source of funding statement None declared. Institutional support has been taken. J Clin Periodontol 2010; 37: 160–164 doi: 10.1111/j.1600-051X.2009.01510.x 160 r 2009 John Wiley & Sons A/S