This study assessed the relationship between ETS exposure and behavior problems among a group of inner-city children with persistent asthma. Overall, 30% of children scored >14 on the total BPI, indicating significant behavior problems that may warrant professional intervention.25
This provides further evidence that children with asthma who live in an urban community have a high prevalence of behavior problems. High rates of ETS exposure also were noted, with over half of the children living with one or more smokers in the home. We found that cotinine levels are associated with problem behaviors among this sample of urban children with asthma, even when controlling for pertinent and potentially confounding variables.
Specifically, we found that high levels of tobacco smoke exposure were associated with externalizing behaviors, including headstrong and antisocial behaviors, among urban children with asthma. Increased rates of externalizing behaviors have been found in previous samples of children exposed to tobacco smoke.18,19,33
For example, in a large longitudinal study that followed pregnant women and their children, the authors found strong associations between externalizing behavior in 4 to 6 year-olds and both prenatal and postnatal smoke exposure.19
Several studies have utilized the BPI as a parent-report measure to assess behavioral problems in children.6,18,34
For example, the BPI was administered in the 1988 National Health Interview on Child Health. A study that used these data compared behavior scores among children ages 5 to 17 years with asthma and children without chronic conditions.6
The authors found that children with significant asthma had a mean BPI score of 7.4 compared with 5.4 for children without a chronic condition. In comparison, the average BPI score for our sample of 4-to 10-year-old children with asthma was 10.9 (SD = 6.8). The higher scores found in our study may be caused in part by the different age ranges of children included in these studies and the different sampling frames.
We found a 2.3-point difference in total BPI score between children with low and high cotinine levels, representing approximately one-third of a standard deviation difference between groups. Although this difference is statistically significant, it is difficult to infer the clinical significance of this finding. The BPI score is a sum of positive responses for each behavior item, and thus the score can be interpreted as the mean number of behavioral concerns described by the parents. In our sample, children with a cotinine >1.47 ng/mL had, on average, 2.3 more items for which the parent reported that a described behavior problem was true for their child, compared with children with lower cotinine levels. This degree of difference is consistent with findings from a large nationally representative study where children exposed to maternal smoking had behavior scores 2.04 points higher than children with non-smoking mothers.18
Many factors may play a role in children’s behavior. The families included in this study are from a poor inner-city community with high rates of public health insurance and parental depression. Family characteristics, environment, and stressful life events may have an effect on children’s behavior and parental views of behavior. A strength of our study is that we are able to account for several items that may affect children’s behavior. For example, previous studies have established associations between childhood behavior and parental stress35
Parents’ education level and household income have also been linked with worse scores on the BPI.25,37
Furthermore, enrollment in Medicaid38
have been shown to be associated with worse behavior in children later in life.
The high level of smoke exposure observed in this study is consistent with previous studies that have documented smoke exposure among children living in urban areas.14
In addition, as previously reported in the literature, we found that children were more likely to have a higher cotinine value if they were African American, insured by Medicaid, or had a parent with less than a high school education.10,12
Nicotine, a key component of ETS, is a neuroteratogen with known adverse effects on the brain including fewer neurons, poor synaptic development, and poor neurobehavioral functioning.40
Thus, the harm of prenatal smoking on the developing brain has been clearly established. Children exposed to ETS in childhood often are also exposed to prenatal maternal smoking, and therefore it is difficult to separate the 2 sources of exposure and subsequent developmental outcomes in human studies. However, there is some evidence that postnatal ETS exposure in childhood, independent of prenatal exposure, may be hazardous to neurodevelopment. Studies in both rodents and rhesus monkeys have demonstrated changes in brain cell development when animals were only exposed to ETS postnatally.20,21
Although controlled trials in humans are not ethical, these animal studies indicate a potential mechanistic connection between postnatal ETS exposure and adverse neurobehavioral outcomes, thus strengthening the impetus for avoidance of ETS exposure in childhood.
There are some limitations to this study. Behavior problems were assessed at one time point by one caregiver, and they were not confirmed by physicians or teachers or with subsequent assessments. In addition, because this is a cross-sectional study, we cannot establish a causal or directional relationship between ETS exposure and behavior problems in these children. All families were recruited from an inner-city community, and many of the families experience stressful lives that may contribute to both higher smoke exposure and parental views of behavior problems. For instance, we found a high rate of parent depression in this study, which could effect both child behavior and smoking status, as described in previous studies.36,41,42
Although we were able to control for several variables including parent depression and stress in our multivariate analysis, residual confounding is possible. Further, we did not have an exact measure of income in this study, and therefore we used enrollment in Medicaid as a proxy variable. Last, our sample included children with asthma from an urban school district, and these findings can only be generalized to a similar population.
Researchers have used various cutoff values to define levels of smoke exposure.29
Because no clearly established level of cotinine has been determined to be safe, we divided the cotinine value at the mean and also considered cotinine as a continuous variable with consistent findings of increased behavior problems with higher levels of exposure. Further, when we reanalyzed the data using tertiles of cotinine levels, similar trends were seen. It is important to note that cotinine was detected in 95% of our sample. Furthermore, in children, salivary cotinine has a half-life of approximately 32 to 82 hours,43
and therefore these values reveal ETS exposure for only a few days before collection. However, studies have suggested that a single cotinine measurement is reasonably consistent with routine exposure to ETS.43,44
This study is unique in that it utilizes a brief and, easy to use behavior scale to assess childhood behavior problems. This scale could be used in pediatric clinics as a screening tool for potential behavior difficulties. Further, we used an objective measure of smoke exposure to assess the association between ETS and behavior problems among a group of vulnerable children.
Children with asthma and exposure to ETS represent a group at high risk for behavior problems. Although we cannot from this study determine whether reducing ETS exposure and improving asthma control would prevent behavior difficulties, it would be helpful for pediatric health care providers to be aware of this association and to provide appropriate screening and counseling in the primary care setting. In addition, the harmful effects of ETS on lung function and asthma morbidity are well described. Thus, tobacco counseling is needed as part of routine care for children with asthma.