Effect of particulate matter exposure on patients with COPD and risk reduction through behavioural interventions: the protocol of a prospective panel study

Park, Shinhee; Won, Seung; Kang, Sung Yoon; Kim, Hwan‐Cheol; Lee, Sei Won

doi:10.1136/bmjopen-2020-039394

Cited by 9 publications

(5 citation statements)

References 28 publications

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“…The above results demonstrated that CS could promote the cellular uptake of PS-NPs and evoke higher ROS level in a strain-dependent manner, which caused cellular oxidative stress and even cell apoptosis. These results were consistent with the view that atmospheric particulate matter exposure contributed significantly to the development and exacerbation of acute respiratory distress syndrome (pathological strain). , …”

Section: Results and Discussionsupporting

confidence: 91%

“…These results were consistent with the view that atmospheric particulate matter exposure contributed significantly to the development and exacerbation of acute respiratory distress syndrome (pathological strain). 56,57 Real-Time Monitoring of PS-NPs-Induced H 2 O 2 Release from Alveolar Cells during Cyclic Stretching.…”

Section: Fabrication and Characterization Of Stretchablementioning

confidence: 99%

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Real-Time Quantification of Nanoplastics-Induced Oxidative Stress in Stretching Alveolar Cells

Zhao,

Fan,

Jin

et al. 2024

ACS Nano

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Nanoplastics from air pollutants can be directly inhaled into the alveoli in the lungs and further enter blood circulation, and numerous studies have revealed the close relation between internalized nanoplastics with many physiological disorders via intracellular oxidative stress. However, the dynamic process of nanoplastics-induced oxidative stress in lung cells under breathmimicked conditions is still unclear, due to the lack of methods that can reproduce the mechanical stretching of the alveolar and simultaneously monitor the oxidative stress response. Here, we describe a biomimetic platform by culturing alveoli epithelial cells on a stretchable electrochemical sensor and integrating them into a microfluidic device. This allows reproducing the respiration of alveoli by cyclic stretching of the alveoli epithelial cells and monitoring the nanoplastics-induced oxidative stress by the built-in sensor. By this device, we prove that cyclic stretches can greatly enhance the cellular uptake of nanoplastics with the dependencies of strain amplitude. Importantly, oxidative stress evoked by internalized nanoplastics can be quantitatively monitored in real time. This work will promote the deep understanding about the cytotoxicity of inhaled nanoplastics in the pulmonary mechanical microenvironment.

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Section: Results and Discussionsupporting

confidence: 91%

Section: Fabrication and Characterization Of Stretchablementioning

confidence: 99%

Real-Time Quantification of Nanoplastics-Induced Oxidative Stress in Stretching Alveolar Cells

Zhao,

Fan,

Jin

et al. 2024

ACS Nano

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“…We conducted a prospective cohort study at four referral hospitals in South Korea between 2019 and 2020, to assess the association between ambient PM 2.5 concentrations and clinical parameters in patients with COPD over 1-year period. The detailed protocols [ 30 , 31 ] and preliminary results [ 32 ] have been previously published. The study was individually approved by the Institutional Review Boards.…”

Section: Methodsmentioning

confidence: 99%

Fine particulate matter aggravates smoking induced lung injury via NLRP3/caspase-1 pathway in COPD

Chung,

Park,

Huh

et al. 2024

J Inflamm

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Background Exposure to noxious particles, including cigarette smoke and fine particulate matter (PM2.5), is a risk factor for chronic obstructive pulmonary disease (COPD) and promotes inflammation and cell death in the lungs. We investigated the combined effects of cigarette smoking and PM2.5 exposure in patients with COPD, mice, and human bronchial epithelial cells. Methods The relationship between PM2.5 exposure and clinical parameters was investigated in patients with COPD based on smoking status. Alveolar destruction, inflammatory cell infiltration, and pro-inflammatory cytokines were monitored in the smoking-exposed emphysema mouse model. To investigate the mechanisms, cell viability and death and pyroptosis-related changes in BEAS-2B cells were assessed following the exposure to cigarette smoke extract (CSE) and PM2.5. Results High levels of ambient PM2.5 were more strongly associated with high Saint George’s respiratory questionnaire specific for COPD (SGRQ-C) scores in currently smoking patients with COPD. Combined exposure to cigarette smoke and PM2.5 increased mean linear intercept and TUNEL-positive cells in lung tissue, which was associated with increased inflammatory cell infiltration and inflammatory cytokine release in mice. Exposure to a combination of CSE and PM2.5 reduced cell viability and upregulated NLRP3, caspase-1, IL-1β, and IL-18 transcription in BEAS-2B cells. NLRP3 silencing with siRNA reduced pyroptosis and restored cell viability. Conclusions PM2.5 aggravates smoking-induced airway inflammation and cell death via pyroptosis. Clinically, PM2.5 deteriorates quality of life and may worsen prognosis in currently smoking patients with COPD. Graphical Abstract

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“…This study was approved by the Institutional Review Boards of Asan Medical Center (2019-0476), Ulsan University Hospital (2019–07–049), Gangneung Asan Hospital (2019-06-049), and Gil Medical Center (GBirb2019-290). The detailed study design was published previously 13 .…”

Section: Methodsmentioning

confidence: 99%

“…All questionnaires were completed twice, at enrollment and the end of the study (1 year). Information about educational level and economic status was also collected 13 . Patients attending Asan Medical Center underwent serial impulse oscillometry.…”

Section: Methodsmentioning

confidence: 99%

Lifestyle practices that reduce seasonal PM2.5 exposure and their impact on COPD

Kim

Huh

et al. 2023

Sci Rep

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Particulate matter (PM) is a major air pollutant that has led to global health concerns and can cause and exacerbate chronic obstructive pulmonary disease (COPD). We asked patients with COPD to complete a detailed questionnaire about their lifestyle practices to reduce PM2.5 exposure and analyzed the relationship between ambient PM2.5 concentrations and lifestyle practices. We prospectively enrolled 104 COPD patients from four hospitals in different areas of Korea. They completed detailed questionnaires twice (at enrollment and the end of the study) and Internet of Things-based sensors were installed in their homes to continuously measure PM2.5 for 1 year. The relationship between PM2.5 concentrations, lifestyle practices, and COPD exacerbations were analyzed in each season. The PM2.5 concentration was higher outdoors than indoors in all seasons except summer, and the difference was largest in winter. The six lifestyle practices that significantly lowered the annual indoor PM2.5 concentration compared with the outdoors. The higher the economic status and educational level of patients, the lower the indoor PM2.5 concentration. Some lifestyle practices were associated with reduced small airway resistance, presented as R5–R20 determined by impulse oscillometry, and scores of the St. George’s Respiratory Questionnaire. Some lifestyle practices are associated with reduced indoor PM2.5 concentrations and can even affect clinical outcomes, including small airway resistance and quality of life of COPD patients.

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Effect of particulate matter exposure on patients with COPD and risk reduction through behavioural interventions: the protocol of a prospective panel study

Cited by 9 publications

References 28 publications

Real-Time Quantification of Nanoplastics-Induced Oxidative Stress in Stretching Alveolar Cells

Real-Time Quantification of Nanoplastics-Induced Oxidative Stress in Stretching Alveolar Cells

Fine particulate matter aggravates smoking induced lung injury via NLRP3/caspase-1 pathway in COPD

Lifestyle practices that reduce seasonal PM2.5 exposure and their impact on COPD

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