Scatter plots of metabolic changes by exposure of EPA and DPA.

<p>Scatter plots illustrate the biochemical compounds that had a metabolic change significantly associated with welding fume exposure: A1) eicosapentaenoic acid (EPA); A2) EPA after removal of a potential outlier (subject ID: 358); B) docosapentaenoic acid n₃ (DPA_n3); and C) docosapentaenoic acid n₆ (DPA_n6). The <i>x</i>-axis represents total PM_2.5 exposure during the welding workshop, while the <i>y</i>-axis represents biochemical metabolic change (post-welding workshop – pre-welding workshop). Black circles represent data from Study-2011; red triangles represent data from Study-2012. Each mark is labeled with the subject ID.</p

Functional network for EPA and DPA.

<p>Network analysis revealed that intracellular and extracellular eicosapentaenoic acid (EPA) interact with 19 genes, while docosapentaenoic acid (DPA) interacts with 7 genes; EPA, DPA_n3, DPA_n6, and 24 regulated genes were used to build the illustrated functional network. The green line represents activation; the red line represents inhibition; the gray line represents unspecified effects.</p

Metabolites associated with PM_2.5 metal welding fume exposure.

*<p>Values presented as mean ± SD (min∼max).</p

Association of PM_2.5 metal welding fume exposure with metabolite pathways.

a<p>Number of biochemical compounds within the same pathway;</p>b<p>Number of biochemical compounds that have the same coefficient direction when regressed by exposure both in Study-2011 and Study-2012;</p>c<p>Number of biochemical compounds with association <i>p<</i>0.05 in combined dataset analyzed by linear mixed model with adjustment of age and medication use;</p>d<p>First principal component (PC₁) was used as response, with PM_2.5 total exposure as predictor in linear regression model or linear mixed-effects model;</p>e<p>Proportion of variance explained by PC₁;</p>f<p>PC₁ was used as response in the linear mixed model with random slope with or without adjustment of age and medication use.</p

Characteristics of the study population.^a

a<p>Values presented either as mean±SD or <i>n</i>;</p>b<p>Five subjects participated in both studies;</p>c<p>At study entry.</p

Association of PM_2.5 metal welding fume exposure with metabolite change.

a<p>Total PM_2.5 exposure as predictor, metabolite change as response;</p>b<p>Linear mixed-effects model was used with/without adjustment for age and medication use;</p>c<p><i>q</i> represented FDR adjusted <i>p</i> value using Benjamini & Hochberg method.</p

Sensitivity analysis of combined effects of thrombocytopenia and ARDS^†.

<p>ARDS = acute respiratory distress syndrome; AHR = adjusted hazard ratio.</p><p>*Each line represents a multivariate cox regression with adjustment of age, gender, APACHII score, and sepsis; Platelet count (×10³/µL) was dichotomized by cutoff point;</p>†<p>AHR was estimated by comparison with non-thrombocytopenia/non-ARDS group.</p

Survival curves of the effects of thrombocytopenia and acute respiratory distress syndrome (ARDS) on 60-day mortality.

<p>Univariate survival analyses show Kaplan-Meier curves of thrombocytopenia (platelet count <80×10³/µL) and ARDS development on 60-day mortality among critically ill patients at-risk for ARDS in the Beijing cohort (upper panel, <i>p</i> = 0.05) and the Boston cohort (lower panel, <i>p</i><0.0001). Blue: non-thrombocytopenia & non-ARDS; red: thrombocytopenia & non-ARDS; green: non-thrombocytopenia & ARDS; orange: thrombocytopenia & ARDS.</p

Multivariable analysis of mortality predictors in Beijing and Boston cohorts.

<p>ARDS = acute respiratory distress syndrome; APACHE = Acute Physiology and Chronic Health Evaluation; AHR = adjusted hazard ratio; CI = confidence intervals; NS = not selected in multivariate modeling.</p

Baseline characteristics of the Beijing cohort.

<p>ARDS = acute respiratory distress syndrome; APACHE = Acute Physiology and Chronic Health Evaluation; ICU = intensive care unit; IQR = interquartile range.</p><p>*APACHE II score was calculated with all components within 24 hours of ICU admission.</p>†<p>Pneumonia, aspiration, pulmonary contusions, or sepsis from lower pulmonary source were categorized as direct pulmonary injury; sepsis from an extrapulmonary source, trauma without pulmonary contusions, and multiple transfusions were categorized as external pulmonary lung injury. Patients with both direct and external pulmonary injuries were considered to have direct lung injury.</p