Peter E Umukoro1, Jason Y Y Wong, Jennifer M Cavallari, Shona C Fang, Chensheng Lu, Xihong Lin, Murray A Mittleman, Georg Schmidt, David C Christiani. 1. Department of Environmental Health (Dr Umukoro, Dr Wong, Dr Cavallari, Dr Fang, Dr Lu, Dr Christiani); Department of Epidemiology (Dr Wong, Dr Mittleman, Dr Christiani); Department of Biostatistics (Dr Lin); Department of Medicine, Stanford University, California (Dr Wong); Department of Community Medicine and Health Care, University of Connecticut Health Center, Farmington (Dr Cavallari); Cardiovascular Epidemiology Research Unit, Beth Israel Deaconess Medical Center/Harvard Medical School, Boston, Massachusetts (Dr Mittleman); Medical Department, Munich University of Technology (Dr Schmidt); DZHK (German Centre for Cardiovascular Research) Partner site Munich Heart Alliance, Germany (Dr Schmidt); and Pulmonary and Critical Care Unit, Massachusetts General Hospital/Harvard Medical School, Boston (Dr Christiani).
Abstract
OBJECTIVE: The aim of this study was to investigate whether associations of acceleration capacity (AC) and deceleration capacity (DC) with metal-PM2.5 are mediated by inflammation. METHODS: We obtained PM2.5, C-reactive protein, interleukin (IL)-6, 8, and 10, and electrocardiograms to compute AC and DC, from 45 male welders. Mediation analyses were performed using linear mixed models to assess associations between PM2.5 exposure, inflammatory mediator, and AC or DC, controlling for covariates. RESULTS: The proportion of total effect of PM2.5 on AC or DC (indirect effect) mediated through IL-6 on AC was 4% at most. Controlling for IL-6 (direct effect), a 1 mg/m increase of PM2.5 was associated with a decrease of 2.16 (95% confidence interval -0.36 to 4.69) msec in AC and a decrease of 2.51 (95% confidence interval -0.90 to 5.93) msec in DC. CONCLUSION: IL-6 may be mediating the effect of metal particulates on AC.
OBJECTIVE: The aim of this study was to investigate whether associations of acceleration capacity (AC) and deceleration capacity (DC) with metal-PM2.5 are mediated by inflammation. METHODS: We obtained PM2.5, C-reactive protein, interleukin (IL)-6, 8, and 10, and electrocardiograms to compute AC and DC, from 45 male welders. Mediation analyses were performed using linear mixed models to assess associations between PM2.5 exposure, inflammatory mediator, and AC or DC, controlling for covariates. RESULTS: The proportion of total effect of PM2.5 on AC or DC (indirect effect) mediated through IL-6 on AC was 4% at most. Controlling for IL-6 (direct effect), a 1 mg/m increase of PM2.5 was associated with a decrease of 2.16 (95% confidence interval -0.36 to 4.69) msec in AC and a decrease of 2.51 (95% confidence interval -0.90 to 5.93) msec in DC. CONCLUSION:IL-6 may be mediating the effect of metal particulates on AC.
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