| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
0-103 |
Sentence |
denotes |
Sensitive inflammatory biomarkers of acute fine particulate matter exposure among healthy young adults: |
| T2 |
104-179 |
Sentence |
denotes |
Findings from a randomized, double-blind crossover trial on air filtration. |
| T3 |
180-344 |
Sentence |
denotes |
The short-term alteration of peripheral cytokines may be an early adverse health effect of PM2.5 exposure and may be further associated with cardiovascular disease. |
| T4 |
345-657 |
Sentence |
denotes |
We conducted a randomized, double-blind crossover trial using true or sham air filtration among 54 healthy college students in Beijing to investigate the potential benefits of short-term indoor air filtration and the adverse health effects of time-weighted personal PM2.5 exposure through inflammatory cytokines. |
| T5 |
658-808 |
Sentence |
denotes |
The participants randomly received true or sham air filtration intervention for a week, and the treatment was changed after a two-week washout period. |
| T6 |
809-917 |
Sentence |
denotes |
Peripheral blood samples were collected after each intervention period to measure 38 inflammatory cytokines. |
| T7 |
918-1054 |
Sentence |
denotes |
A linear mixed-effects model was applied to estimate the impacts of air purification or a 10 μg/m3 PM2.5 exposure increase on cytokines. |
| T8 |
1055-1146 |
Sentence |
denotes |
Lag effects of PM2.5 exposure were analyzed using single-day and moving average lag models. |
| T9 |
1147-1318 |
Sentence |
denotes |
Air filtration reduced indoor and time-weighted average personal PM2.5 concentrations by 69.0% (from 33.6 to 10.4 μg/m3) and 40.3% (from 40.6 to 24.3 μg/m3), respectively. |
| T10 |
1319-1436 |
Sentence |
denotes |
We observed a significant association of PM2.5 exposure with growth-regulated alpha protein (GRO-α) of -11.3% (95%CI: |
| T11 |
1437-1451 |
Sentence |
denotes |
17.0%, -5.4%). |
| T12 |
1452-2025 |
Sentence |
denotes |
In the lag models, significant associations between personal PM2.5 exposure and interleukin-1 receptor antagonist (IL-1Ra), monocyte chemotactic protein (MCP-1), and eotaxin were obtained at lag0, while associations with cytokines including vascular endothelial growth factor (VEGF), epidermal growth factor (EGF), fibroblast growth factor-2 (FGF-2), granulocyte colony-stimulating factor (G-CSF), macrophage inflammatory protein-1β (MIP-1β), IL-4, tumor necrosis factor-α (TNF-α), and interferon-γ (IFN-γ) were noted at relatively long lagged exposure windows (lag5-lag6). |
| T13 |
2026-2117 |
Sentence |
denotes |
No significant alteration in cytokines was observed under true air filtration intervention. |
| T14 |
2118-2200 |
Sentence |
denotes |
Our study indicates the effectiveness of air filtration on indoor PM2.5 reduction. |
| T15 |
2201-2294 |
Sentence |
denotes |
PM2.5 exposure may decrease GRO-α levels and change different cytokine levels time-varyingly. |
| T16 |
2295-2398 |
Sentence |
denotes |
Further study is still needed to explore the mechanisms of PM2.5 exposure on the inflammatory response. |
| T1 |
0-103 |
Sentence |
denotes |
Sensitive inflammatory biomarkers of acute fine particulate matter exposure among healthy young adults: |
| T2 |
104-179 |
Sentence |
denotes |
Findings from a randomized, double-blind crossover trial on air filtration. |
| T3 |
180-344 |
Sentence |
denotes |
The short-term alteration of peripheral cytokines may be an early adverse health effect of PM2.5 exposure and may be further associated with cardiovascular disease. |
| T4 |
345-657 |
Sentence |
denotes |
We conducted a randomized, double-blind crossover trial using true or sham air filtration among 54 healthy college students in Beijing to investigate the potential benefits of short-term indoor air filtration and the adverse health effects of time-weighted personal PM2.5 exposure through inflammatory cytokines. |
| T5 |
658-808 |
Sentence |
denotes |
The participants randomly received true or sham air filtration intervention for a week, and the treatment was changed after a two-week washout period. |
| T6 |
809-917 |
Sentence |
denotes |
Peripheral blood samples were collected after each intervention period to measure 38 inflammatory cytokines. |
| T7 |
918-1054 |
Sentence |
denotes |
A linear mixed-effects model was applied to estimate the impacts of air purification or a 10 μg/m3 PM2.5 exposure increase on cytokines. |
| T8 |
1055-1146 |
Sentence |
denotes |
Lag effects of PM2.5 exposure were analyzed using single-day and moving average lag models. |
| T9 |
1147-1318 |
Sentence |
denotes |
Air filtration reduced indoor and time-weighted average personal PM2.5 concentrations by 69.0% (from 33.6 to 10.4 μg/m3) and 40.3% (from 40.6 to 24.3 μg/m3), respectively. |
| T10 |
1319-1436 |
Sentence |
denotes |
We observed a significant association of PM2.5 exposure with growth-regulated alpha protein (GRO-α) of -11.3% (95%CI: |
| T11 |
1437-1451 |
Sentence |
denotes |
17.0%, -5.4%). |
| T12 |
1452-2025 |
Sentence |
denotes |
In the lag models, significant associations between personal PM2.5 exposure and interleukin-1 receptor antagonist (IL-1Ra), monocyte chemotactic protein (MCP-1), and eotaxin were obtained at lag0, while associations with cytokines including vascular endothelial growth factor (VEGF), epidermal growth factor (EGF), fibroblast growth factor-2 (FGF-2), granulocyte colony-stimulating factor (G-CSF), macrophage inflammatory protein-1β (MIP-1β), IL-4, tumor necrosis factor-α (TNF-α), and interferon-γ (IFN-γ) were noted at relatively long lagged exposure windows (lag5-lag6). |
| T13 |
2026-2117 |
Sentence |
denotes |
No significant alteration in cytokines was observed under true air filtration intervention. |
| T14 |
2118-2200 |
Sentence |
denotes |
Our study indicates the effectiveness of air filtration on indoor PM2.5 reduction. |
| T15 |
2201-2294 |
Sentence |
denotes |
PM2.5 exposure may decrease GRO-α levels and change different cytokine levels time-varyingly. |
| T16 |
2295-2398 |
Sentence |
denotes |
Further study is still needed to explore the mechanisms of PM2.5 exposure on the inflammatory response. |