Synergistic Effects of Traffic-Related Air Pollution and Exposure to Violence on Urban Asthma Etiology

The gradient of socioeconomic position (SEP) on health may be explained partly by a combination of increased contaminant exposures and greater susceptibility to their effects. Air pollution, for instance, may be higher near major roadways, power plants, and industrial sites, where property values are lower and lower-income populations reside (Graves 1988). Increased life stress among lower-SEP populations has also been proposed as a primary pathway through which SEP affects health (Gee and Payne-Sturges 2004; Morello-Frosch and Shenassa 2006). Because of this potential spatial covariance across exposures, and because stress and pollution may influence common physiologic pathways (i.e., oxidative stress) and health outcomes (i.e., respiratory disease), stronger methods are needed to disentangle their effects and investigate synergies (Gee and Payne-Sturges 2004; O’Neill et al. 2003; Weiss and Bellinger 2006). The environmental justice literature has documented significant disproportionate contaminant exposures in minority and lower-SEP communities (Brulle and Pellow 2006), and the resultant influence on asthma exacerbation patterns (Maantay 2007). However, fewer studies have considered disproportionate susceptibility among lower-SEP populations. Exposure to violence (ETV) has been conceptualized as a chronic urban stressor, potentially elevated in communities where pollution is higher. Chronic stress effects of episodic violence are grounded in trauma theory (e.g., post-traumatic stress), detailed elsewhere (Wright 2006). Episodic violence, post-traumatic stress (Augustyn et al. 2002; Overstreet and Braun 2000), and hyper-vigilance (Gordon and Riger 1991)—more prevalent in lower-SEP urban communities (Sampson et al. 1997)—may negatively influence health though physiologic alterations, including immune dysregulation, and behavioral pathways. Many urban caregivers, for example, restrict children’s behavior, keeping them indoors due to fear of violence (Levy et al. 2004; Wright et al. 2004b), making children more sedentary, increasing indoor exposures, and decreasing spatial autonomy that is important to development (Katz 1991). Chronic stress has been linked to asthma exacerbations in cross-sectional (Oh et al. 2004) and prospective (Sandberg et al. 2004) population studies. Other evidence suggests a role for stress in the onset of asthma (Wright et al. 2002, 2004a). Chronic stress may influence hypothalamic–pituitary–adrenal (HPA) axis and cortisol dysregulation (Hellhammer et al. 1997; Ockenfels et al. 1995), glucocorticoid resistance (Miller et al. 2002), sympathetic–adrenal–medullary (SAM) activation, catecholamine production (Glaser and Kiecolt-Glaser 2005), immune mediator function, inflammation (Umetsu et al. 2002), and cytokine production (Chen et al. 2003; Wright et al. 2004a). Stress and pollution affect some common physiologic systems, facilitating synergistic effects; for example, psychological stress (Epel et al. 2004) and ozone (Fugisawa 2005) both affect oxidative stress pathways. Few studies have examined the influence of stress on pollution susceptibility, though some findings suggest differential susceptibility by SEP, possibly mediated by life stress (Morello-Frosch and Shenassa 2006). Time-series studies indicate effect modification of short-term pollution exposures by SEP (Jerrett et al. 2004; Lin et al. 2004; Martins et al. 2004), though others found no significant modification (Zanobetti and Schwartz 2000). Fewer studies have considered long-term exposures, though some indicate greater associations between long-term air pollution and mortality among less-educated adults (Hoek et al. 2002; Krewski et al. 2000). In urban settings, traffic-related air pollution may be elevated along with ETV, and previous studies have linked traffic-related air pollution to asthma exacerbation and respiratory outcomes. In the United States and Europe, children living or attending school near truck routes and highways show increased asthma and allergy symptoms (Brauer et al. 2002), hospitalizations (Edwards et al. 1994; Lin et al. 2002), allergic rhinitis (Duhme et al. 1996), and reduced lung function (Brunekreef et al. 1997). Traffic-related pollutants have also been associated with asthma development (Gordian et al. 2006; Zmirou et al. 2004). Incorporating traffic-related air pollution into large-scale epidemiologic studies requires models linking traffic and ambient concentrations. Relationships between traffic and health have been examined using several different traffic indicators, with no consensus on which indictors best capture variability in traffic-related pollution or health outcomes in different settings. Prior studies have successfully extrapolated traffic exposures from sampling homes to larger cohorts using predictive land-use regression (LUR) models (Brauer et al. 2002; Brunekreef et al. 1997). LUR shows strong predictive power for intraurban nitrogen dioxide variability (Hochadel et al. 2006; Sahsuvaroglu and Jerrett 2004), using traffic and land use characteristics (i.e., population density, major sources). In this study, we explore the hypothesis that a chronic stressor (here, lifetime ETV) predicts stronger associations between traffic-related air pollution exposure and childhood asthma development. We employ data from the Maternal-Infant Smoking Study of East Boston (MISSEB), a community-based prospective pregnancy cohort examining asthma, respiratory, and cognitive development. Questionnaires were administered detailing violence exposures (both witnessing and victimization) and avoidance behaviors (staying in at night, avoiding certain areas, keeping children indoors). Because the MIS-SEB did not examine air pollution, we used geographic information systems (GIS) and LUR at the neighborhood scale to retrospectively estimate pollution exposures, using monthly NO2 data collected over 18 years in the surrounding neighborhoods.