There are three main findings of this study. First, smoking outside the home, compared to inside the home, was related with CCR. Second, female and younger infants revealed higher CCRs than their male and older counterparts. Third, significant fluctuations in daily CCR were not apparent in infants over a seven day time period.
Infants from homes with indoor smoking had higher CCRs than infants from homes where smoking occurred on the balcony or in other places outside the home. The data support preexisting cross-sectional findings that suggest a home smoking ban may reduce infants' cotinine levels [4, 5]. According to dose-response relationships, the present data are somewhat contradictory. The cross-sectional data clearly revealed a dose-response relationship, but the longitudinal data did not. The mean CCR was higher (57.9 μg/mmol) in infants with two smokers in the home compared to infants with one smoker in the home (24.9 μg/mmol). This confirms findings from the German Environmental Survey IV that also revealed a higher geometrical mean of cotinine among infants in households with more than one smoker than in households with only one smoker . In another study urine cotinine levels of infants' aged 3 to 27 month were correlated with the number of smokers in the home, however in this study also households with no smokers were included . Our cross-sectional data clearly revealed a significant dose-response relationship between CCR and time infants spend in rooms in which smoking occurs in respect to study day 1, r
=.46, p =.01 (one-tailed), however our longitudinal data did not. Furthermore a positive but not significant relationship was revealed between CCR and cpd parents smoked in the presence of the infant in respect to study day 1, r
=.32, p =.07 (one-tailed).
Second, the present data revealed that sex and age of the infant predicted CCR. When these two predictors were included, in addition to smoking inside home, 68% of the CCR variance was explained. Only 22% of the variance was explained when only the information about smoking inside the home was used. CCRs were greater among girls than among boys. Mean creatinine was lower in girls than in boys. Whether total creatinine excretion over a 24 hours period was lower in girls is unknown. This would have required 24 hour urine volume measurements. The mean cotinine value tended to be higher in girls than in boys. This confirms former evidence about higher mean cotinine values in girls compared to boys .
Our data revealed that mean cotinine and CCRs were higher and mean creatinine values were lower in younger than in older infants. This is in accordance with the expectation that the concentration of the same amount of tobacco smoke is higher among younger than among older infants due to less body tissue of the younger [21–23]. We do not know, whether total creatinine excretion over a 24 hours period was lower in younger than in older infants. However, our finding according to which mean cotinine was greater in younger than in older children is consistent with previous evidence. It also revealed that younger children had higher urinary cotinine levels than older children . Urinary elimination half-life of cotinine seems to depend on age . However, elimination half-life of cotinine did not differ between infants and children . 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 . 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 immunoassay measures metabolites of nicotine, in particular cotinine, 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 se, it also measures other nicotine metabolites. Assessing cotinine specifically, e.g. by high-performance liquid chromatography (HPLC), may give lower results. Nevertheless, 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.