Environmental tobacco smoke (ETS) in the home is a major preventable health problem for children around the world. In children, ETS exposure (passive smoking) has been shown to be particularly associated with respiratory infection, especially lower respiratory tract infection (LRTI).1,2,3 Exposure intensity of ETS among children shows a strong correlation with indoor parental and, especially, maternal smoking, the number of cigarettes smoked, the number and volume capacity of the rooms where cigarettes are smoked and individual metabolic diversities.4 The use of cotinine, a major metabolite of nicotine, as a biological marker of smoke absorption has been suggested as an approach to strengthen the evidence of the relation between passive smoking and respiratory illness. In several studies, a strong disagreement was present between parental self reports and quantitative measures. Epidemiological studies on ETS exposure report that cotinine measurement in body fluids (especially in urine) is a more powerful predictor of actual exposure compared to parental self reports, has a higher sensitivity and indicates a longer period of exposure.5 Globally the percentage of children exposed to ETS is considerably high and has been reported at between 29% and 69%.6
With regard to cut‐off values, several limits have been proposed by investigators who compared cotinine in body fluids of smokers and non‐smokers. Henderson et al7 reported that a cut‐off cotinine:creatinine ratio (CCR) of 30 ng/mg identifies children exposed to smoking at home with a high degree of sensitivity (80%) and specificity (100%). This cut‐off point has been commonly used to compare children unexposed and exposed to ETS. The cut‐off CCR of 30 ng/mg creatinine as a passive smoking indicator may be appropriate for countries having low smoking prevalence. However, as the prevalence of passive smoking in developing countries such as Turkey is very high, this cut‐off level would be insufficient to indicate the causative effect of ETS in LRTI correctly.8,9
The case‐control study carried out by Keskinoglu et al10 was conducted between October 2003 and April 2004 in an urban district of Izmir, Turkey. The case group (n = 150) consisted of children aged 2–12 years who had been diagnosed with LRTI. The control group (n = 150) comprised healthy children during the period of the study, and these children were paired with the cases according to age, sex and street resided in by the family. In our study, according to the cut‐off CCR of 30 ng/mg, the prevalence of passive smoking was 87.3% in the case group with LRTI (n = 150) and 84.7% in the healthy children group (n = 150), with no significant difference (p = 0.618). However, a significant difference was found between passive smoking prevalence in groups at a urinary CCR of 60 ng/mg (76.7% and 50.7%, respectively) (p<0.001). The children with LRTI had more dense ETS exposure compared to the healthy children (OR = 4.72; 95% CI = 2.62 to 8.51). When the cut‐off level of urinary CCR was accepted as 60 ng/mg creatinine, it was found that passive smoking increased LRTI in children significantly (p = 0.000). This finding indicated that the causative effect on LRTI of passive smoking was dose dependent.
We believe that the evaluation of ETS exposure using a higher cut‐off level of CCR than 30 ng/mg creatinine, such as 60 ng/mg and over, to investigate whether there is any association between ETS exposure and LRTI in an intensive exposure status and to assess the dose dependent relation will be more accurate.
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