We found an association between traffic-related pollution (NO2
) and asthma diagnosis only among children with elevated ETV, after controlling for potential confounders. Of multiple exposure intervals, year-of-diagnosis NO2
best predicted asthma (with some evidence for NO2
after first violence exposure), supporting a theoretical model wherein individuals may become susceptible or “primed” through social pathways to some environmental triggers, including traffic-related pollutants. Despite limitations of our data sets, these results agree with evidence elsewhere that chronic stress may shape biologic response in early life (Wright et al. 2004a
) and potentiate effects of air pollution through common physiologic systems.
Our findings contribute to the existing environmental justice literature by identifying potential changes in pollution susceptibility within communities affected by violence and other stressors. We also indicate ancillary effects of violence on children in urban communities, in addition to direct injury and post-traumatic stress. Sampson et al. (1997)
identified associations among neighborhood deterioration, violence, and low collective efficacy (social control of neighborhoods through residents’ collective effort); we observed that a heightened susceptibility to pollution, associated with violence exposures or fear thereof, may lead to synergistic health effects of social and physical environmental conditions.
Although our findings are biologically plausible and highly suggestive, there are potential limitations in interpreting our models. A clear limitation is our small sample size for investigating multiplicative effects; despite the relatively high asthma prevalence (26%), a larger cohort would be required to consider interactions across numerous potential risk factors. The pollution model relies on NO2 data, commonly used as a marker of primary vehicular emissions, but not necessarily representative of all pollutants of interest. Road construction and airplane technology changes made it unclear a priori whether NO2 could be predicted by spatial indicators in this neighborhood, particularly using 1990 traffic data, though our model proved robust. We lacked complete residential history, likely creating some misclassification in a cohort with significant residential instability. However, we found no difference in asthma prevalence or exposures between movers and nonmovers; thus we expect misclassification to be nondifferential, biasing results toward the null and making our significant results more noteworthy.
The interpretation of our interaction model is complicated by the fact that behaviors may differ in violent neighborhoods, where parents often keep children indoors due to fear of violence. Therefore, children may be more exposed to indoor NO2
, which is generally higher than outdoor NO2
, and is influenced both by infiltration from outdoors and by smoking, gas stoves, and other sources which may be more prevalent in lower-income communities (Baxter et al. 2006
; Spengler et al. 1983
). Future studies should examine differential susceptibility to a wider range of pollution exposures, including indoor allergens and environmental tobacco smoke; although we accounted for maternal smoking, we did not examine the effect of other smokers in the home. Likewise, ETV may proxy for other social exposures responsible for the susceptibility effect we found; children witnessing violence may have greater family instability (Overstreet and Braun 2000
) or may be directly victimized, potentially leading to injury-related susceptibilities.
We aimed to investigate whether a psychosocial stressor modifies pollution effects on asthma, and would prefer a long-term stress measure to corroborate the ETV scale. The CCDS elicits distress using a 6-month symptoms recall, inappropriate to our goal of capturing life-course stress. The correlation between CCDS and violence does, however, corroborate an association, supporting the plausibility of stress pathways to pollution susceptibility, and should be investigated further.
Reporting bias—generally underreporting by survivors, perpetrators, and witnesses—hampers quantitative violence research (Gordon and Riger 1991
), particularly for domestic and intimate violence. Our questionnaire focused largely on within-community events, potentially more accurately reported. A prior analysis indicated that parents underestimate older children’s exposures, but are better corroborated for near-home events, potentially due to shared experience (Thomson et al. 2002
). We were unable to examine direct victimization because very little was reported, owing either to low prevalence or underreporting, and thus we likely have some misclassification of true ETV. Most asthma cases were reported during longitudinal follow-up, limiting recall bias in diagnoses, but our retrospective violence report is subject to recall bias. To assess recall bias in violence reports, we asked the caregiver to report on asthma episodes triggered by violence; because very few parents associated violent events with asthma symptoms, recall bias in ETV by asthma status is unlikely.
Despite these limitations, our study provides evidence of a synergistic effect between social and physical factors in asthma etiology. The study also provides a model for retrospectively estimating traffic-related exposures, accounting for intracommunity heterogeneity and temporal trends using GIS. We were able to create temporally calibrated estimates using a spatially dense and temporally rich pollution data set of NO2
measurements collected throughout our epidemiologic study period. Though few studies will have access to such data, existing models provide insight about site characteristics influencing exposure variability, and spatially resolved satellite pollution data may prove useful in some settings (Liu et al. 2005
In future studies, a wider and more frequently assessed suite of social stressors and perceived stress measures should be employed to examine stress trajectories over time and temporality in susceptibility to environmental triggers. The roles of social support and health beliefs in mediating the effects of perceived stress on health outcomes should be considered as buffers in the pathway from stressor to stress response, the latter of which may influence contaminant susceptibility and health (Chen et al. 2003
). We observed no correlation between ETV and pollution levels, but suggest that longitudinal investigation of multiple exposures, and multiple pathways, are needed to further elucidate these effects. The spatial correlation across multiple exposures deserves greater investigation, and should be addressed in larger studies investigating spatial autocorrelations across, and potential synergies among, social and physical environmental factors.