In this select population of inner-city children with asthma living with a smoker, fine particulate matter and air nicotine concentrations were highly correlated with urine cotinine concentrations. Additionally, children with a greater number of symptom days had the highest urine cotinine concentrations. Direct environmental measures of SHS, however, had minimal, if any, relationships with asthma symptom outcomes. Taken together, these findings lend support for the continued use of urine cotinine to assess SHS exposure in children.
Although direct environmental measures of SHS are attractive because they are not influenced by individual variability in the metabolism of nicotine as urine cotinine is, these measures of SHS had no correlation with asthma symptoms in our study population. This may be due to the fact that urine cotinine concentrations are explicitly linked to SHS exposure in the child independent of the site of SHS exposure. This is important given that exposure for school age children may occur in a variety of community settings of the child's social network including parents, child care providers, extended family and neighbors.
The predominant household smoker was the child's caregiver in over two-thirds and the mother in over half of the families, comparable to a hospital-based sample of low income children with asthma, [37
] yet significantly higher than the 31–39% detected in low-income, predominantly African American families [10
]. Our data indicate over a two-fold increase in child urine cotinine concentrations when the caregiver was the household smoker. This confirms that caregiver smoking contributes more to the child's SHS exposure than other household smokers [5
]. Caregiver smoking results in close proximity between the smoker and child and prolonged exposure, especially since children spend most time indoors. Moreover, most caregivers reported smoking in their own bedroom, likely in close proximity to the child.
We observed levels of indoor PM2.5
that are on average twice as high as the EPA standard for outdoor PM2.5
concentrations and are significantly higher than the 13.3 μg/ml PM2.5
levels reported in school age children with asthma residing in nonsmoking homes [39
]. Although mean air nicotine concentrations of all homes were elevated, air nicotine concentrations were not highly correlated with the number of smokers in the household. Caregiver estimation of child SHS exposure based only on total household number of cigarettes smoked resulted in some misclassification of low SHS exposure in our population. A subgroup of children with high air nicotine concentrations (>1 μg/m3
) were associated with caregiver reports of low SHS exposure, i.e. less than ½ pack of cigarettes smoked by all household smokers, suggesting the low reliability of caregiver report of SHS exposure and the underestimation of the harm of SHS to their child [40
]. Although the use of targeted questions about household smoking to identify significant SHS exposure for children with asthma has been proposed, [10
] our data indicate that caregiver report could not be relied upon to accurately distinguish children with high versus low SHS exposure.
On a local level, pediatric health care providers are in a key position to consistently influence child SHS exposure when parents are willing to disclose their own smoking behavior and quit attempts [28
]. Caregivers in our study had a median of greater than two quit attempts over the past year. Nationally 70% of smokers report a desire to quit each year, yet only 34% attempt to quit and only 10% succeed and remain tobacco-free for a year [42
]. Moreover, quit rates are lowest in less educated adults [5
] represented by over one-third of caregivers in this study population. Higher number of quit attempts are associated with increased likelihood of successful smoking cessation [43
]. Therefore, opportunities to address caregiver smoking cessation are numerous with the frequency of well child and asthma care visits that increase the likelihood of a visit coinciding with high caregiver readiness to quit smoking [28
More importantly, stronger policies are needed for restricting SHS exposure in private spaces for children. Although US tobacco control policies restrict smoking in public spaces including restaurants, workplaces, schools and hospitals, [45
] children are not protected from SHS in environments where they spend the majority of their time. A child's social network is often limited to their homes, extended family and neighbor homes and child care settings [8
]. Voluntary home smoking bans by parents may not offer complete protection to the child even if neighbors or extended family members smoke outside of the home. Partial home smoking bans have been reported to lower SHS exposure, yet not as significantly as a total home smoking ban [37
]. Promoting a larger ecological change in culture that includes community-wide change in restricting smoking in private residences may be more effective in reducing SHS exposure for children than ongoing smoking cessation services for parents [8
] as reported by caregivers in this study.
There are potential limitations to this study to consider. Urine cotinine levels reflect SHS exposure at one point in time and may not reflect long term exposure. However, caregiver report of SHS exposure among children with asthma remained relatively stable over time based on cotinine levels up to 9 months later [11
]. Factors such as size, layout, air volume and ventilation of the household that influence indoor air nicotine and particulate matter concentrations were not measured in this study and may have influenced our results. Finally, we purposely enrolled high risk children with asthma residing in homes with a smoker to detect a difference in our intervention groups and may have enrolled children with higher SHS exposure levels not applicable to non-urban children who do not live with a smoker.