Background: Previous research has documented effects of both physical and social environmental exposures on childhood asthma. However, few studies have considered how these two environments might interact to affect asthma.
Objective: This study aimed to test interactions between chronic exposure to traffic-related air pollution and chronic family stress in predicting biologic and clinical outcomes in children with asthma.
Method: Children with asthma (n = 73, 9-18 years of age) were interviewed about life stress, and asthma-relevant inflammatory markers [cytokine production, immunoglobulin E (IgE), eosinophil counts] were measured. Parents reported on children's symptoms. Children completed daily diaries of symptoms and peak expiratory flow rate (PEFR) measures at baseline and 6 months later. Exposure to traffic-related air pollution was assessed using a land use regression model for nitrogen dioxide concentrations.
Results: NO(2) by stress interactions were found for interleukin-5 (beta for interaction term = -0.31, p = 0.02), IgE (interaction beta = -0.29, p = 0.02), and eosinophil counts (interaction beta = -0.24, p = 0.04). These interactions showed that higher chronic stress was associated with heightened inflammatory profiles as pollution levels decreased. Longitudinally, NO(2) by stress interactions emerged for daily diary symptoms (interaction beta = -0.28, p = 0.02), parent-reported symptoms (interaction beta = -0.25, p = 0.07), and PEFR (interaction beta = 0.30, p = 0.03). These interactions indicated that higher chronic stress was associated with increases over time in symptoms and decreases over time in PEFR as pollution levels decreased.
Conclusions: The physical and social environments interacted in predicting both biologic and clinical outcomes in children with asthma, suggesting that when pollution exposure is more modest, vulnerability to asthma exacerbations may be heightened in children with higher chronic stress.
Keywords: air pollution; asthma; immune; psychosocial; stress; traffic.