Cotinine excretion as a predictor of peak flow variability.

Environmental tobacco smoke (ETS) is suspected to be an important risk factor for bronchial hyperresponsiveness. In order to test the effect of ETS, we measured expiratory flow rates and urine cotinine excretion (UCE) within a narrow time window in two consecutive years. Maternal smoking habits and medical history were ascertained by standardized questionnaires. The percentage ratio of the amplitude over the mean (AVAM) of the diurnal peak flow rates of children (complete values from at least five consecutive days) was calculated as an indicator of bronchial responsiveness. The association of UCE and log10AVAM was analyzed by multiple linear regression. Complete data were available for a sample of 417 children. The median of UCE in children of parents who smoked (3.2 ng/mg and 2.9 ng/mg creatinine, Surveys 1 and 2, respectively) was higher than the median in children of nonsmoking parents (0 ng/mg in both surveys). With increasing UCE the log10AVAM rose in the first and second surveys, as well as in the longitudinal analysis (p = 0.003). This association, however, showed up only in boys (p = 0.0001) and not in girls (p = 0.31). Our data suggest that there is a need both for further analysis of the gender difference and for more support of strategies against passive smoking as far as children are concerned, since airway hyperresponsiveness is a risk factor for chronic airway impairment.

The internal dose of passive smoking at home depends on the size of the dwelling.

As part of a longitudinal study two urine samples (survey 1 in 1991 and survey 2 in 1992) were collected from 602 elementary school children to investigate the relationship between urinary cotinine excretion (UCE) and the daily consumption of cigarettes at home (exposure). Size of the dwelling, educational level, and maternal smoking were taken into consideration as additional predictors. The history regarding parental smoking habits and confounding variables was ascertained by standardized questionnaires completed by the parents. Cotinine was measured using gas chromatography selected ion monitoring. UCE was expressed as cotinine/creatinine (ng/mg). In children with detectable UCE in survey 1 (35%) and in survey 2 (44%) the excretion ranged between 1.5 and 24.7 ng/mg (5-95%) and between 1.2 and 25.2 ng/mg, respectively. UCE measurements in both surveys were highly correlated (r = 0.65, P = 0.0001), and 59.6% of the UCE in survey 2 can be explained in linear regression by the UCE in survey 1. Using multiple linear regression, the categorized number of cigarettes reported to be consumed at home (20 cigarettes and more: 1991, P = 0.0001; 1992, P = 0.0003) and low educational level of the parents (P = 0.011 in 1991, P = 0.04 in 1992) were positively associated with UCE, whereas the size of the dwelling turned out to be negatively associated with UCE (P = 0.12 in 1991, P = 0.001 in 1992). In small dwellings (< or = 80 m2) the effect of exposure on UCE was much more pronounced. In conclusion, a single UCE measurement provides information which is widely stable within a yearly interval and is related to passive smoke history as well as to socio-economic status and the size of the dwelling. The latter variable should be considered as an effect modifier of exposure on internal dose and should be taken into account in future studies on passive smoke exposure.