Abstract

BackgroundWe hypothesized that particulate matter (PM) gamma activity (gamma radiation associated with PM) is associated with systemic effects. ObjectiveExamine short-term relationships between ambient and indoor exposures to PM gamma activities with systemic inflammation and endothelial activation in chronic obstructive pulmonary disease (COPD) patients. MethodsIn 85 COPD patients from Eastern Massachusetts, USA from 2012 to 2014, plasma C-reactive protein (CRP), interleukin-6 (IL-6), and soluble vascular cell adhesion molecule-1 (sVCAM-1) were measured seasonally up to four times. We used US EPA RadNet data measuring ambient gamma radiation attached to PM adjusted for background radiation, and estimated in-home gamma radiation exposures using the ratio of in-home-to-ambient sulfur in PM2.5. Linear mixed-effects regression models were used to determine associations between moving averages of PM gamma activities through the week before phlebotomy with these biomarkers. We explored ambient and indoor PM2.5, black carbon (BC), and NO2 as confounders. ResultsAmbient and indoor PM gamma activities measured as energy spectra classes 3 through 9 were positively associated with CRP and IL-6. For example, averaged from phlebotomy day through previous 6 days, each IQR increase in indoor PM gamma activity for each spectra class, was associated with an CRP increase ranging from 7.45% (95%CI: 2.77, 12.4) to 13.4% (95%CI: 5.82, 21.4) and for ambient exposures were associated with an increase of 8.75% (95%CI: −0.57, 18.95) to 14.8% (95%CI: 4.5, 26.0). Indoor exposures were associated with IL-6 increase of 3.56% (95%CI: 0.31, 6.91) to 6.46% (95%CI:1.33, 11.85) and ambient exposures were associated with an increase of 0.03% (95%CI: −6.37, 6.87) to 3.50% (95%CI: −3.15, 10.61). There were no positive associations with sVCAM-1. Sensitivity analyses using two-pollutant models showed similar effects. ConclusionsOur results demonstrate that short-term exposures to environmental PM gamma radiation activities were associated with systemic inflammation in COPD patients.

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