Emma Busenkell1, Christina M Collins1, Marilyn L Moy2, Jaime E Hart3, Stephanie T Grady4, Brent A Coull5, Joel D Schwartz6, Petros Koutrakis7, Eric Garshick8. 1. Research and Development Service, VA Boston Healthcare System, Boston, MA, USA. 2. Pulmonary, Allergy, Sleep, and Critical Care Medicine Section, Medical Service, VA Boston Healthcare System, Boston, MA, USA; Harvard Medical School, Boston, MA, USA. 3. Harvard Medical School, Boston, MA, USA; Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA; Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, USA. 4. Boston University School of Public Health, Boston, MA, USA. 5. Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, MA, USA. 6. Harvard Medical School, Boston, MA, USA; Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA; Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, USA; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA. 7. Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, USA. 8. Pulmonary, Allergy, Sleep, and Critical Care Medicine Section, Medical Service, VA Boston Healthcare System, Boston, MA, USA; Harvard Medical School, Boston, MA, USA; Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA. Electronic address: eric.garshick@va.gov.
Abstract
RATIONALE: Little is known about personal characteristics and systemic responses to particulate pollution in patients with COPD. OBJECTIVES: Assess whether diabetes, obesity, statins and non-steroidal anti-inflammatory medications (NSAIDs) modify associations between indoor black carbon (BC) and fine particulate matter ≤2.5 μm in diameter (PM2.5) on systemic inflammation and endothelial activation. METHODS: 144 individuals with COPD without current smoking and without major in-home combustion sources were recruited at Veterans Affairs Boston Healthcare System. PM2.5 and BC were measured in each participant's home seasonally for a week (up to 4 times; 482 observations) and plasma biomarkers of systemic inflammation [C-reactive protein (CRP); interleukin-6 (IL-6)] and endothelial activation [soluble vascular adhesion molecule-1 (sVCAM-1)] measured. Linear mixed effects regression with a random intercept was used, and effect modification assessed with multiplicative interaction terms and stratum specific estimates. RESULTS: Median (25%ile, 75%ile) indoor BC and PM2.5 were 0.6 (0.5,0.7) μg/m3 and 6.8 (4.8,10.4) μg/m3, respectively. Although p-values for effect modification were not statistically significant, there were positive associations (%-increase/interquartile range; 95% CI) between CRP and BC greater among non-statin (18.8%; 3.6-36.3) than statin users (11.1%; 2.1-20.9). There were also positive associations greater among non-statin users between PM2.5 and CRP. For IL-6, associations with BC and PM2.5 were also greater among non-statin users. Associations between CRP and BC were greater (20.3%; 4.5-38.5) in persons with diabetes than without diabetes (10.3%; 0.92-20.6) with similar effects of PM2.5. There were no consistent associations that differed based on obesity. Effect modification was not observed for NSAID use, or with any factor considered with sVCAM-1. CONCLUSIONS: Associations between indoor BC and PM2.5 and CRP were greater in patients with diabetes and those not taking statins, and with IL-6 if not taking statins. These results suggest that these characteristics may modify the systemic response to indoor BC and PM2.5 in persons with COPD.
RATIONALE: Little is known about personal characteristics and systemic responses to particulate pollution in patients with COPD. OBJECTIVES: Assess whether diabetes, obesity, statins and non-steroidal anti-inflammatory medications (NSAIDs) modify associations between indoor black carbon (BC) and fine particulate matter ≤2.5 μm in diameter (PM2.5) on systemic inflammation and endothelial activation. METHODS: 144 individuals with COPD without current smoking and without major in-home combustion sources were recruited at Veterans Affairs Boston Healthcare System. PM2.5 and BC were measured in each participant's home seasonally for a week (up to 4 times; 482 observations) and plasma biomarkers of systemic inflammation [C-reactive protein (CRP); interleukin-6 (IL-6)] and endothelial activation [soluble vascular adhesion molecule-1 (sVCAM-1)] measured. Linear mixed effects regression with a random intercept was used, and effect modification assessed with multiplicative interaction terms and stratum specific estimates. RESULTS: Median (25%ile, 75%ile) indoor BC and PM2.5 were 0.6 (0.5,0.7) μg/m3 and 6.8 (4.8,10.4) μg/m3, respectively. Although p-values for effect modification were not statistically significant, there were positive associations (%-increase/interquartile range; 95% CI) between CRP and BC greater among non-statin (18.8%; 3.6-36.3) than statin users (11.1%; 2.1-20.9). There were also positive associations greater among non-statin users between PM2.5 and CRP. For IL-6, associations with BC and PM2.5 were also greater among non-statin users. Associations between CRP and BC were greater (20.3%; 4.5-38.5) in persons with diabetes than without diabetes (10.3%; 0.92-20.6) with similar effects of PM2.5. There were no consistent associations that differed based on obesity. Effect modification was not observed for NSAID use, or with any factor considered with sVCAM-1. CONCLUSIONS: Associations between indoor BC and PM2.5 and CRP were greater in patients with diabetes and those not taking statins, and with IL-6 if not taking statins. These results suggest that these characteristics may modify the systemic response to indoor BC and PM2.5 in persons with COPD.
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