Kehl et al. BMC Public Health 2010, 10:424 http://www.biomedcentral.com/1471-2458/10/424 according to which mean cotinine was greater in younger than in older children is consistent with pre- vious evidence. It also revealed that younger children had higher urinary cotinine levels than older children [24]. Urinary elimination half-life of cotinine seems to depend on age [23]. However, elimination half-life of cotinine did not differ between infants and children [25]. A further explanation for higher cotine levels among younger than among older children might be that younger infants have a higher ventilation rate than older children or adults [23,24]. Parents might tend to spend more time with younger than with older infants. Furthermore, the greater lack of independent mobility and inability to detract themselves from exposure to ETS among younger infants could be a reason for higher urinary cotinine respectively CCR compared to older infants. Third, the present data revealed that daily exposure to ETS, as assessed by CCR, was stable over seven days in the total sample. No absolute difference of CCR was found between weekends and weekdays. This finding suggests that weekends, or other peak smoking days, may not distort the overall findings. Instead, mean CCR over seven consecutive days, seems to be justified. The present data suggest that a single day measurement of cotinine in urine accurately reflects infant’s exposure to ETS over one week period assuming that ETS exposure is consistent over that period. The finding may not be generalized to longer periods of time. A series of CCR assessments taken from infants during the first two years of their lives revealed variability over these two years [15]. Maturing of the infant and potential changes in exposure to smoke may explain this finding. The present study has several limitations. First, the sample was a convenience sample. However, the number of cpd among daily smokers was in accordance with other studies [5,25]. Second, data about smoking and about ETS exposure of infants might have been biased by parents’ self-reports, even though we have found CCR in the infants. Also, the sample size was large enough to test relations between parents’ self-reports of smoking and ETS in infants. Third, adjustment of urine cotinine concentration by creatinine concentration in urine of infants is problematic because creatinine levels and creatinine excretion were lower in girls than in boys and lower in younger than in older children. Despite this fact, the cross-sectional data revealed that the mean cotinine values were higher in younger infants and tended to be higher in girls. Finally, the used immunoas- say measures metabolites of nicotine, in particular coti- nine, to which it is highly specific. Cross-reactivity between cotinine and other cotinine metabolites could occur. Since the assay is used for screening purposes rather than for determining cotinine concentrations per Page 7 of 8 se, it also measures other nicotine metabolites. Assessing cotinine specifically, e.g. by high-performance liquid chromatography (HPLC), may give lower results. Never- theless, we estimated the used immunoassay to be highly adequate to examine the longitudinal relationship between infants’ exposure to environmental tobacco smoke and parents’ self-reported smoking behavior. Conclusion Smoking inside the home, together with the infant’s sex and age, is crucial in predicting CCR in infants. The finding that CCR was higher in girls than in boys needs further examination. The data suggest that significant fluctuations in daily CCR were not apparent. Measure- ment of CCR in urine on a single day might accurately reflect infants’ exposure to ETS over one week. The findings provide evidence about CCR for purposes of public health. The data speak for home smoking bans. In addition, the findings support routine cotinine mea- surement among children of smokers for purposes of feedback that might help to generate intention to quit smoking. Acknowledgements Institution where the work was performed: Ernst-Moritz-Arndt-University Greifswald, Institute of Epidemiology and Social Medicine, Walther-Rathenau- Str. 48, D-17487 Greifswald, Germany. Author details 1Ernst-Moritz-Arndt-University Greifswald, Institute of Psychology, Department Health and Prevention, Robert-Blum-Str. 13, D-17487 Greifswald, Germany. 2Ernst-Moritz-Arndt-University Greifswald, Institute of Community Medicine, Section Epidemiology of Health Care and Community Health, Ellernholzstr. 1-2, D-17487 Greifswald, Germany. 3University Hospital Greifswald, AoR, Institute of Clinical Chemistry and Laboratory Medicine, Sauerbruchstrasse, D-17475 Greifswald, Germany. 4Ernst-Moritz-Arndt- University Greifswald, Institute of Epidemiology and Social Medicine, Walther-Rathenau-Str. 48, D-17487 Greifswald, Germany. Authors’ contributions DK, JRT and UJ developed the research question and designed the study. DK conducted the literature research. DK and JRT collected data. MN and JL were responsible for the cotinine and creatinine analysis and their interpretation. DK carried out the statistical data analysis and their interpretation and was responsible for drafting the manuscript. All authors made substantial intellectual contributions to the work and participated in writing the manuscript by reviewing the drafts. All authors have approved the final manuscript. Competing interests The authors declare that they have no competing interests. Received: 23 February 2010 Accepted: 19 July 2010 Published: 19 July 2010 References 1. Boyaci H, Etiler N, Duman C, Basyigit I, Pala A: Environmental tobacco smoke exposure in school children: parent report and urine cotinine measures. Pediatrics International 2006, 48(4):382-389. 2. Gehrman CA, Hovell MF: Protecting children from environmental tobacco smoke (ETS) exposure: a critical review. Nicotine & Tobacco Research 2003, 5(3):289-301.