Margaret T Hicken1, J Timothy Dvonch2, Amy J Schulz3, Graciela Mentz3, Paul Max4. 1. Institute for Social Research, University of Michigan, United States. Electronic address: mhicken@umich.edu. 2. Department of Environmental Health Sciences, University of Michigan, United States. 3. Department of Health Behavior and Health Education, University of Michigan, United States. 4. Environmental Affairs Unit, Building, Safety Engineering, and Environmental Department, City of Detroit, United States.
Abstract
BACKGROUND: Consensus is growing on the need to investigate the joint effects of psychosocial stress and environmental hazards on health. Some evidence suggests that psychosocial stress may be an important modifier of the association between air pollution respiratory outcomes, but few have examined cardiovascular outcomes. OBJECTIVES: We examined the modifying effect of psychosocial stress on the association between fine particulate matter air pollution (PM2.5) and blood pressure (BP). METHODS: Our data came from the Detroit Healthy Environments Partnership (HEP) 2002-2003 survey. Of 919 participants, BP was collected at two time points in a subset of 347. Building on previous work reporting associations between PM2.5 and BP in this sample, we regressed systolic (SBP) and diastolic (DBP) BP and pulse pressure (PP), in separate linear models, on the interaction among psychosocial stress, PM2.5, and HEP neighborhood (Southwest, Eastside, Northwest). RESULTS: The association between PM2.5 and SBP was stronger for those who reported high levels of stress, but this interaction was significant only in the Southwest Detroit neighborhood. Southwest Detroit residents who reported low stress showed 2.94 mmHg (95% CI: -0.85, 6.72) increase in SBP for each 10 μg/m(3) increase in 2-day prior PM2.5 exposure. Those who reported high stress showed 9.05 mmHg (95% CI: 3.29, 14.81) increase in SBP for each 10 μg/m(3) increase in PM2.5 exposure. CONCLUSIONS: These results suggest that psychosocial stress may increase vulnerability to the hypertensive effects of PM2.5. This work contributes to an understanding of the ways in which the social and physical environments may jointly contribute to poor health and to health disparities.
BACKGROUND: Consensus is growing on the need to investigate the joint effects of psychosocial stress and environmental hazards on health. Some evidence suggests that psychosocial stress may be an important modifier of the association between air pollution respiratory outcomes, but few have examined cardiovascular outcomes. OBJECTIVES: We examined the modifying effect of psychosocial stress on the association between fine particulate matter air pollution (PM2.5) and blood pressure (BP). METHODS: Our data came from the Detroit Healthy Environments Partnership (HEP) 2002-2003 survey. Of 919 participants, BP was collected at two time points in a subset of 347. Building on previous work reporting associations between PM2.5 and BP in this sample, we regressed systolic (SBP) and diastolic (DBP) BP and pulse pressure (PP), in separate linear models, on the interaction among psychosocial stress, PM2.5, and HEP neighborhood (Southwest, Eastside, Northwest). RESULTS: The association between PM2.5 and SBP was stronger for those who reported high levels of stress, but this interaction was significant only in the Southwest Detroit neighborhood. Southwest Detroit residents who reported low stress showed 2.94 mmHg (95% CI: -0.85, 6.72) increase in SBP for each 10 μg/m(3) increase in 2-day prior PM2.5 exposure. Those who reported high stress showed 9.05 mmHg (95% CI: 3.29, 14.81) increase in SBP for each 10 μg/m(3) increase in PM2.5 exposure. CONCLUSIONS: These results suggest that psychosocial stress may increase vulnerability to the hypertensive effects of PM2.5. This work contributes to an understanding of the ways in which the social and physical environments may jointly contribute to poor health and to health disparities.
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