Background and Objectives: Electronic cigarette (e-cigarette) is a device that generate vapor by heating e-cigarettes liquid. E-cigarette damages the respiratory immune system and renders the respiratory tract vulnerable to inflammations. However, there are no studies on how the inflammatory reactions in respiratory epithelial cells caused by e-cigarette occur, and the effects of Korean red ginseng (KRG) and saponin on inflammation induced by e-cigarette are unknown. This study aimed to compare the inflammatory reactions caused by e-cigarette and lipopolysaccharide (LPS), and to investigate the effects of KRG and saponin on cytokine and mucin expression induced by e-cigarette in respiratory epithelial cells.Subjects and Method In bronchoalveolar lavage fluid and lung tissue of mice, the effects of KRG and saponin on cytokines (interleukin [IL]-1β, IL-6, IL-8) and mucin 5AC/5B (MUC5AC/5B) expression induced by e-cigarette were investigated using real-time polymerase chain reaction, enzyme linked immunosorbent assay, and immunohistochemistry staining. Results: Inflammatory cells, cytokines (IL-1β, IL-6, IL-8) and MUC5AC/5B messenger RNA expression and protein production were increased by e-cigarette, similar to LPS. KRG and saponin decreased the expression of cytokines (IL-1β, IL-6, IL-8) and MUC5AC/5B induced by e-cigarette. KRG and saponin showed effects similar to that of dexamethasone. Conclusion E-cigarette causes inflammation similar to that caused by LPS. KRG and saponin regulate the expression of cytokine and MUC5AC/5B increased by e-cigarette in respiratory epithelial cells. KRG and saponin may be an effective therapeutic option for inflammatory responses induced by e-cigarette in respiratory epithelial cells.

Background and Objectives: Electronic cigarette (e-cigarette) is a device that generate vapor by heating e-cigarettes liquid. E-cigarette damages the respiratory immune system and renders the respiratory tract vulnerable to inflammations. However, there are no studies on how the inflammatory reactions in respiratory epithelial cells caused by e-cigarette occur, and the effects of Korean red ginseng (KRG) and saponin on inflammation induced by e-cigarette are unknown. This study aimed to compare the inflammatory reactions caused by e-cigarette and lipopolysaccharide (LPS), and to investigate the effects of KRG and saponin on cytokine and mucin expression induced by e-cigarette in respiratory epithelial cells.Subjects and Method In bronchoalveolar lavage fluid and lung tissue of mice, the effects of KRG and saponin on cytokines (interleukin [IL]-1β, IL-6, IL-8) and mucin 5AC/5B (MUC5AC/5B) expression induced by e-cigarette were investigated using real-time polymerase chain reaction, enzyme linked immunosorbent assay, and immunohistochemistry staining. Results: Inflammatory cells, cytokines (IL-1β, IL-6, IL-8) and MUC5AC/5B messenger RNA expression and protein production were increased by e-cigarette, similar to LPS. KRG and saponin decreased the expression of cytokines (IL-1β, IL-6, IL-8) and MUC5AC/5B induced by e-cigarette. KRG and saponin showed effects similar to that of dexamethasone. Conclusion E-cigarette causes inflammation similar to that caused by LPS. KRG and saponin regulate the expression of cytokine and MUC5AC/5B increased by e-cigarette in respiratory epithelial cells. KRG and saponin may be an effective therapeutic option for inflammatory responses induced by e-cigarette in respiratory epithelial cells.

Background and Objectives: Electronic cigarette (e-cigarette) is a device that generate vapor by heating e-cigarettes liquid. E-cigarette damages the respiratory immune system and renders the respiratory tract vulnerable to inflammations. However, there are no studies on how the inflammatory reactions in respiratory epithelial cells caused by e-cigarette occur, and the effects of Korean red ginseng (KRG) and saponin on inflammation induced by e-cigarette are unknown. This study aimed to compare the inflammatory reactions caused by e-cigarette and lipopolysaccharide (LPS), and to investigate the effects of KRG and saponin on cytokine and mucin expression induced by e-cigarette in respiratory epithelial cells.Subjects and Method In bronchoalveolar lavage fluid and lung tissue of mice, the effects of KRG and saponin on cytokines (interleukin [IL]-1β, IL-6, IL-8) and mucin 5AC/5B (MUC5AC/5B) expression induced by e-cigarette were investigated using real-time polymerase chain reaction, enzyme linked immunosorbent assay, and immunohistochemistry staining. Results: Inflammatory cells, cytokines (IL-1β, IL-6, IL-8) and MUC5AC/5B messenger RNA expression and protein production were increased by e-cigarette, similar to LPS. KRG and saponin decreased the expression of cytokines (IL-1β, IL-6, IL-8) and MUC5AC/5B induced by e-cigarette. KRG and saponin showed effects similar to that of dexamethasone. Conclusion E-cigarette causes inflammation similar to that caused by LPS. KRG and saponin regulate the expression of cytokine and MUC5AC/5B increased by e-cigarette in respiratory epithelial cells. KRG and saponin may be an effective therapeutic option for inflammatory responses induced by e-cigarette in respiratory epithelial cells.

Background and Objectives: Electronic cigarette (e-cigarette) is a device that generate vapor by heating e-cigarettes liquid. E-cigarette damages the respiratory immune system and renders the respiratory tract vulnerable to inflammations. However, there are no studies on how the inflammatory reactions in respiratory epithelial cells caused by e-cigarette occur, and the effects of Korean red ginseng (KRG) and saponin on inflammation induced by e-cigarette are unknown. This study aimed to compare the inflammatory reactions caused by e-cigarette and lipopolysaccharide (LPS), and to investigate the effects of KRG and saponin on cytokine and mucin expression induced by e-cigarette in respiratory epithelial cells.Subjects and Method In bronchoalveolar lavage fluid and lung tissue of mice, the effects of KRG and saponin on cytokines (interleukin [IL]-1β, IL-6, IL-8) and mucin 5AC/5B (MUC5AC/5B) expression induced by e-cigarette were investigated using real-time polymerase chain reaction, enzyme linked immunosorbent assay, and immunohistochemistry staining. Results: Inflammatory cells, cytokines (IL-1β, IL-6, IL-8) and MUC5AC/5B messenger RNA expression and protein production were increased by e-cigarette, similar to LPS. KRG and saponin decreased the expression of cytokines (IL-1β, IL-6, IL-8) and MUC5AC/5B induced by e-cigarette. KRG and saponin showed effects similar to that of dexamethasone. Conclusion E-cigarette causes inflammation similar to that caused by LPS. KRG and saponin regulate the expression of cytokine and MUC5AC/5B increased by e-cigarette in respiratory epithelial cells. KRG and saponin may be an effective therapeutic option for inflammatory responses induced by e-cigarette in respiratory epithelial cells.

Background and Objectives: Electronic cigarette (e-cigarette) is a device that generate vapor by heating e-cigarettes liquid. E-cigarette damages the respiratory immune system and renders the respiratory tract vulnerable to inflammations. However, there are no studies on how the inflammatory reactions in respiratory epithelial cells caused by e-cigarette occur, and the effects of Korean red ginseng (KRG) and saponin on inflammation induced by e-cigarette are unknown. This study aimed to compare the inflammatory reactions caused by e-cigarette and lipopolysaccharide (LPS), and to investigate the effects of KRG and saponin on cytokine and mucin expression induced by e-cigarette in respiratory epithelial cells.Subjects and Method In bronchoalveolar lavage fluid and lung tissue of mice, the effects of KRG and saponin on cytokines (interleukin [IL]-1β, IL-6, IL-8) and mucin 5AC/5B (MUC5AC/5B) expression induced by e-cigarette were investigated using real-time polymerase chain reaction, enzyme linked immunosorbent assay, and immunohistochemistry staining. Results: Inflammatory cells, cytokines (IL-1β, IL-6, IL-8) and MUC5AC/5B messenger RNA expression and protein production were increased by e-cigarette, similar to LPS. KRG and saponin decreased the expression of cytokines (IL-1β, IL-6, IL-8) and MUC5AC/5B induced by e-cigarette. KRG and saponin showed effects similar to that of dexamethasone. Conclusion E-cigarette causes inflammation similar to that caused by LPS. KRG and saponin regulate the expression of cytokine and MUC5AC/5B increased by e-cigarette in respiratory epithelial cells. KRG and saponin may be an effective therapeutic option for inflammatory responses induced by e-cigarette in respiratory epithelial cells.

Polycyclic aromatic hydrocarbons are pervasive in the atmosphere, originating from sources like vehicle emissions and incomplete combustion. Exposure to PAHs occurs through diet, tobacco smoke, and air pollutants, and they are recognized as carcinogens. This study, conducted from July to October 2021 in Seoul, Gyeonggi, and Ulsan regions, focused on taxi drivers, a group with elevated PAH exposure due to prolonged vehicle use. The study involved 19 male taxi drivers and 46 control participants (18 male, 28 female). LC-MS/MS analysis was employed to quantify urinary levels of 18 hydroxy-PAHs, oxidative damage markers (MDA, 8-OHdG), and cotinine. The detection rates of OH-PAHs were 1-naphthol (96.9 %), 2-naphthol (90.8 %), 2-hydroxyfluorene (86.2 %), and 1-hydroxypyrene (80.0 %). Compared to the male controls, taxi drivers showed higher median concentrations of 2-OH-Na (1.698 ng/mL), 1-OH-Na (0.666 ng/mL), 2-OH-Flu (0.067 ng/mL), and 1-OHP (0.045 ng/mL). Similarly, significant differences were observed between taxi drivers and female controls for 1-OH-Na, 2-OH-Na, 2-OH-Flu, 3-OH-Phe, and 1-OHP. MDA and 8-OHdG were detected in over 90% of all groups, with significant differences between taxi drivers. Strong positive correlations were revealed between urinary OH-PAHs, MDA, and 8-OHdG (r ranging from 0.589 to 0.770, p<0.01). The findings suggest that taxi drivers, due to prolonged exposure to traffic-related air pollutants, have elevated levels of PAH metabolites and oxidative stress, especially among smokers. Further studies with larger sample sizes are recommended to validate these results and explore the long-term health implications of occupational PAH exposure in urban transportation workers..

Polycyclic aromatic hydrocarbons are pervasive in the atmosphere, originating from sources like vehicle emissions and incomplete combustion. Exposure to PAHs occurs through diet, tobacco smoke, and air pollutants, and they are recognized as carcinogens. This study, conducted from July to October 2021 in Seoul, Gyeonggi, and Ulsan regions, focused on taxi drivers, a group with elevated PAH exposure due to prolonged vehicle use. The study involved 19 male taxi drivers and 46 control participants (18 male, 28 female). LC-MS/MS analysis was employed to quantify urinary levels of 18 hydroxy-PAHs, oxidative damage markers (MDA, 8-OHdG), and cotinine. The detection rates of OH-PAHs were 1-naphthol (96.9 %), 2-naphthol (90.8 %), 2-hydroxyfluorene (86.2 %), and 1-hydroxypyrene (80.0 %). Compared to the male controls, taxi drivers showed higher median concentrations of 2-OH-Na (1.698 ng/mL), 1-OH-Na (0.666 ng/mL), 2-OH-Flu (0.067 ng/mL), and 1-OHP (0.045 ng/mL). Similarly, significant differences were observed between taxi drivers and female controls for 1-OH-Na, 2-OH-Na, 2-OH-Flu, 3-OH-Phe, and 1-OHP. MDA and 8-OHdG were detected in over 90% of all groups, with significant differences between taxi drivers. Strong positive correlations were revealed between urinary OH-PAHs, MDA, and 8-OHdG (r ranging from 0.589 to 0.770, p<0.01). The findings suggest that taxi drivers, due to prolonged exposure to traffic-related air pollutants, have elevated levels of PAH metabolites and oxidative stress, especially among smokers. Further studies with larger sample sizes are recommended to validate these results and explore the long-term health implications of occupational PAH exposure in urban transportation workers..

Polycyclic aromatic hydrocarbons are pervasive in the atmosphere, originating from sources like vehicle emissions and incomplete combustion. Exposure to PAHs occurs through diet, tobacco smoke, and air pollutants, and they are recognized as carcinogens. This study, conducted from July to October 2021 in Seoul, Gyeonggi, and Ulsan regions, focused on taxi drivers, a group with elevated PAH exposure due to prolonged vehicle use. The study involved 19 male taxi drivers and 46 control participants (18 male, 28 female). LC-MS/MS analysis was employed to quantify urinary levels of 18 hydroxy-PAHs, oxidative damage markers (MDA, 8-OHdG), and cotinine. The detection rates of OH-PAHs were 1-naphthol (96.9 %), 2-naphthol (90.8 %), 2-hydroxyfluorene (86.2 %), and 1-hydroxypyrene (80.0 %). Compared to the male controls, taxi drivers showed higher median concentrations of 2-OH-Na (1.698 ng/mL), 1-OH-Na (0.666 ng/mL), 2-OH-Flu (0.067 ng/mL), and 1-OHP (0.045 ng/mL). Similarly, significant differences were observed between taxi drivers and female controls for 1-OH-Na, 2-OH-Na, 2-OH-Flu, 3-OH-Phe, and 1-OHP. MDA and 8-OHdG were detected in over 90% of all groups, with significant differences between taxi drivers. Strong positive correlations were revealed between urinary OH-PAHs, MDA, and 8-OHdG (r ranging from 0.589 to 0.770, p<0.01). The findings suggest that taxi drivers, due to prolonged exposure to traffic-related air pollutants, have elevated levels of PAH metabolites and oxidative stress, especially among smokers. Further studies with larger sample sizes are recommended to validate these results and explore the long-term health implications of occupational PAH exposure in urban transportation workers..

Polycyclic aromatic hydrocarbons are pervasive in the atmosphere, originating from sources like vehicle emissions and incomplete combustion. Exposure to PAHs occurs through diet, tobacco smoke, and air pollutants, and they are recognized as carcinogens. This study, conducted from July to October 2021 in Seoul, Gyeonggi, and Ulsan regions, focused on taxi drivers, a group with elevated PAH exposure due to prolonged vehicle use. The study involved 19 male taxi drivers and 46 control participants (18 male, 28 female). LC-MS/MS analysis was employed to quantify urinary levels of 18 hydroxy-PAHs, oxidative damage markers (MDA, 8-OHdG), and cotinine. The detection rates of OH-PAHs were 1-naphthol (96.9 %), 2-naphthol (90.8 %), 2-hydroxyfluorene (86.2 %), and 1-hydroxypyrene (80.0 %). Compared to the male controls, taxi drivers showed higher median concentrations of 2-OH-Na (1.698 ng/mL), 1-OH-Na (0.666 ng/mL), 2-OH-Flu (0.067 ng/mL), and 1-OHP (0.045 ng/mL). Similarly, significant differences were observed between taxi drivers and female controls for 1-OH-Na, 2-OH-Na, 2-OH-Flu, 3-OH-Phe, and 1-OHP. MDA and 8-OHdG were detected in over 90% of all groups, with significant differences between taxi drivers. Strong positive correlations were revealed between urinary OH-PAHs, MDA, and 8-OHdG (r ranging from 0.589 to 0.770, p<0.01). The findings suggest that taxi drivers, due to prolonged exposure to traffic-related air pollutants, have elevated levels of PAH metabolites and oxidative stress, especially among smokers. Further studies with larger sample sizes are recommended to validate these results and explore the long-term health implications of occupational PAH exposure in urban transportation workers..

Background: Lung dysfunction and high apolipoprotein B/apolipoprotein A-I (apoB/apoA-I) ratio are both recognized risk factors for cardiovascular disease. However, few studies have examined the association between the apoB/ApoA-I ratio and lung function. Therefore, we investigated whether this ratio is associated with decreased lung function in a large healthy cohort. Methods: We performed a cohort study on 68,418 healthy Koreans (34,797 males, mean age:38.1 years) who underwent a health examination in 2019. ApoB/apoA-I ratio was categorized into quartiles. Spirometric values at the fifth percentile in our population were considered the lower limit of normal (LLN), which was used to define lung function impairment. Adjusted odds ratios (aORs) and 95% confidence intervals (CIs), using the lowest quartile as the reference, were estimated to determine lung function impairment. Results: Mean apoB/apoA-I ratio was 0.67 ± 0.21. Subjects with the highest quartile of this ratio had the lowest predicted forced expiratory volume in one second (FEV1 %) and forced vital capacity (FVC%) after controlling for covariates (P < 0.001). However, FEV1 /FVC ratio was not significantly different among the four quartiles (P = 0.059). Compared with the lowest quartile (Q1, reference), the aORs (95% CI) for FEV1 % < LLN across increasing quartiles (from Q2 to Q4) were 1.216 (1.094–1.351), 1.293 (1.156–1.448), and 1.481 (1.311– 1.672) (P for trend < 0.001), respectively. Similarly, the aORs for FVC% < LLN compared with the reference were 1.212 (1.090–1.348), 1.283 (1.147–1.436), and 1.502 (1.331–1.695) with increasing quartiles (P for trend < 0.001). However, the aORs for FEV1 /FVC < LLN were not significantly different among groups (P for trend = 0.273). Conclusion High apoB/apoA-I ratio was associated with decreased lung function. However, longitudinal follow-up studies are required to validate our findings.