PMID- 18629323 OWN - NLM STAT- MEDLINE DCOM- 20080912 LR - 20211020 IS - 0091-6765 (Print) IS - 1552-9924 (Electronic) IS - 0091-6765 (Linking) VI - 116 IP - 7 DP - 2008 Jul TI - Chronic traffic-related air pollution and stress interact to predict biologic and clinical outcomes in asthma. PG - 970-5 LID - 10.1289/ehp.11076 [doi] AB - 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. FAU - Chen, Edith AU - Chen E AD - Department of Psychology, University of British Columbia, Vancouver, British Columbia, Canada. echen@psych.ubc.ca FAU - Schreier, Hannah M C AU - Schreier HM FAU - Strunk, Robert C AU - Strunk RC FAU - Brauer, Michael AU - Brauer M LA - eng GR - R01 HL073975/HL/NHLBI NIH HHS/United States GR - HL 073975/HL/NHLBI NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Research Support, Non-U.S. Gov't PL - United States TA - Environ Health Perspect JT - Environmental health perspectives JID - 0330411 RN - 0 (Air Pollutants) RN - 0 (Vehicle Emissions) RN - S7G510RUBH (Nitrogen Dioxide) SB - IM CIN - Environ Health Perspect. 2008 Sep;116(9):A376-7; author reply A377. PMID: 18795127 MH - Adolescent MH - Air Pollutants/*adverse effects MH - Air Pollution/*adverse effects MH - Asthma/*etiology/*psychology MH - Child MH - Environmental Exposure/adverse effects MH - Family Relations MH - Female MH - Humans MH - Male MH - Nitrogen Dioxide/analysis MH - Stress, Psychological/*complications MH - Vehicle Emissions/*toxicity PMC - PMC2453169 OTO - NOTNLM OT - air pollution OT - asthma OT - immune OT - psychosocial OT - stress OT - traffic EDAT- 2008/07/17 09:00 MHDA- 2008/09/16 09:00 PMCR- 2008/07/01 CRDT- 2008/07/17 09:00 PHST- 2007/11/15 00:00 [received] PHST- 2008/02/26 00:00 [accepted] PHST- 2008/07/17 09:00 [pubmed] PHST- 2008/09/16 09:00 [medline] PHST- 2008/07/17 09:00 [entrez] PHST- 2008/07/01 00:00 [pmc-release] AID - ehp0116-000970 [pii] AID - 10.1289/ehp.11076 [doi] PST - ppublish SO - Environ Health Perspect. 2008 Jul;116(7):970-5. doi: 10.1289/ehp.11076.