, 1999). A weaker association was observed between EPZ-5676 msds cotinine and PSE from another smoker when reported by nonsmoking parents and compared with the association observed when smoking parents reported on their own exposure. The less accurate reports of exposure by nonsmoking parents are not surprising, as they are not the source of the child’s exposure. Nonsmoking parents may estimate exposure based on historical smoking patterns they may have observed, speculate about exposure that is not directly observed, and tend to overestimate the salient exposure episodes when reporting overall exposure. Additionally, some nonsmokers could exaggerate reports of exposure in an attempt to draw attention to the smoker’s behavior in relation to the child’s exposure and health status.
While there was general correspondence (up to ~30% in shared variance) between parental reports of exposure and urine cotinine levels in this sample, the two measures are far from perfect agreement and provide independent information. The strength of these relationships does not allow, for example, for the precise prediction of the number of cigarettes exposed based on cotinine levels. Residual variance may be accounted for by individual physiological differences, metabolic differences, sources and locations of exposure, and limitations in parental reports of exposure. Biological measures do not inform when the exposure occurred, the pattern of exposure, or the magnitude of exposure at each occurrence. Comprehensive exposure assessments in future studies of PSE involving pediatric cancer patients would, therefore, benefit from combinations of biological and reported estimates from parents.
It should be noted that only single, intermittent urine cotinine samples were obtained in this study, providing a relatively crude index of typical and maximal exposure. However, single cotinine measurements may not be sufficient to precisely characterize overall exposure level or exposure over a variable time course (Matt et al., 2007). The large CIs on predicted exposure levels obtained in our study suggest considerable variability in exposure outcomes. Given the variability of children’s exposure, estimates of exposure may be artifactually inflated or reduced if the timing of the urine samples reflects episodic high or low level exposure events.
For example, children in our sample exposed to high levels of smoke in the car during travel to the hospital may have high urine cotinine levels if the samples are collected upon arrival at the hospital. Alternatively, children being treated at the smoke-free hospital environment for greater periods of time prior to urine sample collection may have less opportunity for exposure. These factors may have affected the less than perfect correspondence Dacomitinib between cotinine and parent reports.