Background: Short-term effects of fine particulate matter (PM) exposure on lung function have been reported. However, few studies have assessed PM exposure on the personal level, and the mechanism underlying the effects of PM exposure on lung function remains less clear.
Objectives: To evaluate the association between personal PM exposure and lung function alteration in general population and to explore the roles of systematic inflammation and oxidative damage in this association.
Methods: A total of 7685 lung function tests were completed among 4697 urban adults in Wuhan, China. Plasma C-reactive protein (CRP), urinary 8-iso-prostaglandin-F (8-iso-PGF) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels were measured. Personal PM exposure levels were estimated using an estimation model from the actual measurements of individual PM levels in 191 participants. Mixed linear models were used to evaluate the association between personal PM exposure and lung function. Mediation analyses were conducted to investigate the roles of CRP, 8-iso-PGF and 8-OHdG in above associations.
Results: After adjusting for confounders, each 10 μg/m increase in the previous-day personal PM exposure was associated with 2.94 mL, 2.02 mL and 16.14 mL/s decreases in forced vital capacity (FVC), forced expiration volume in 1 s (FEV) and peak expiratory flow, respectively. The associations were more obvious among never smokers compared with current smokers. Cumulative 7-day exposure to PM led to the strongest adverse effects on lung function. Among never smokers with high PM exposure levels, a positive relationship was observed between personal PM level and urinary 8-iso-PGF, and 8-iso-PGF meditated 4.69% and 12.30% of the association between the 7-day moving PM concentration and FVC and FEV, respectively. We did not observe a significant positive association between PM exposure and plasma CRP or urinary 8-OHdG.
Conclusion: Short-term personal exposure to PM is associated with reduced pulmonary ventilation function. Urinary 8-iso-PGF partly mediates these associations.
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http://dx.doi.org/10.1016/j.scitotenv.2020.142522 | DOI Listing |
Proc Natl Acad Sci U S A
February 2025
Department of Physiology and Membrane Biology, University of California Davis, Davis, CA 95616.
The L-type Ca channel (Ca1.2) is essential for cardiac excitation-contraction coupling. To contribute to the inward Ca flux that drives Ca-induced-Ca-release, Ca1.
View Article and Find Full Text PDFPLoS One
January 2025
Department of Pulmonary Diseases, Uludag University Faculty of Medicine, Bursa, Turkey.
Background: End-stage renal disease (ESRD) patients frequently experience protein-energy wasting (PEW), which increases their morbidity and mortality rates.
Objective: This study explores the effects of nutritional status and pulmonary function on the short- and long-term mortality of ESRD patients undergoing hemodialysis.
Materials And Methods: 67 consecutive ESRD patients on maintenance hemodialysis were included in the study.
In 2019, the novel coronavirus swept the world, exposing the monitoring and early warning problems of the medical system. Computer-aided diagnosis models based on deep learning have good universality and can well alleviate these problems. However, traditional image processing methods may lead to high false positive rates, which is unacceptable in disease monitoring and early warning.
View Article and Find Full Text PDFInt J Surg
January 2025
Aging Research Center, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden.
Introduction: Lung function has been associated with cognitive decline and dementia, but the extent to which lung function impacts brain structural changes remains unclear. We aimed to investigate the association of lung function with structural macro- and micro-brain changes across mid- and late-life.
Methods: The study included a total of 37 164 neurologic disorder-free participants aged 40-70 years from the UK Biobank, who underwent brain MRI scans 9 years after baseline.
Biochem Genet
January 2025
Department of Pulmonary Disease, Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, 200071, China.
Angiotensin-converting enzyme 2 (ACE2) has been reported to exert a protective effect in acute lung injury (ALI), though its underlying mechanism remains incompletely understood. In this study, ACE2 expression was found to be upregulated in a mouse model of ALI induced by lipopolysaccharide (LPS) injection. ACE2 knockdown modulated the severity of ALI, the extent of autophagy, and the mTOR pathway in this model.
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