Short-term exposure to ozone and cause-specific mortality risks and thresholds in China: Evidence from nationally representative data, 2013-2018

Environment International, Journal Year: 2022, Volume and Issue: 171, P. 107666 - 107666

Published: Nov. 28, 2022

Ambient ozone pollution is steadily increasing and becoming a major environmental risk factor contributing to the global disease burden. Although association between short-term exposure mortality has been widely studied, results are mostly reported on deaths from non-accidental or total cardiopulmonary rather than spectrum of causes. In particular, knowledge gap still exists for potential thresholds in risks.This nationwide time-series study China included 323 counties totaling 230,266,168 residents. Daily maximum 8-hour average was calculated as metric. A two-stage statistical approach adopted assess effects 21 cause-specific 2013-2018. The subset threshold were utilized explore thresholds, stratification analysis used evaluate population susceptibility.On average, annual mean concentration 93.4 μg/m3 across counties. 10-μg/m3 increase lag 0-1 day associated with increases 0.12 % disease, 0.11 circulatory 0.09 respiratory 0.29 urinary system 0.20 nervous disease. There may be "safe" ozone-mortality association, which 60 100 μg/m3, vary by cause death. Women older adults (especially those over 75) more affected exposure. Populations North had higher ozone-related mortality, while populations South mortality.National findings link premature death circulatory, respiratory, neurological, diseases, provide evidence mortality. These have important implications helping policymakers tighten relevant air quality standards developing early warning systems public health protection China.

Language: Английский

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The NLRP3 inflammasome in fibrosis and aging: The known unknowns

Ageing Research Reviews, Journal Year: 2022, Volume and Issue: 79, P. 101638 - 101638

Published: May 5, 2022

Language: Английский

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Polyphenols, flavonoids and inflammasomes: the role of cigarette smoke in COPD

European Respiratory Review, Journal Year: 2022, Volume and Issue: 31(164), P. 220028 - 220028

Published: June 14, 2022

COPD is predicted to become the third leading cause of morbidity and mortality worldwide by 2030. Cigarette smoking (active or passive) one its chief causes, with about 20% cigarette smokers developing from smoke (CS)-induced irreversible damage sustained inflammation airway epithelium. Inflammasome activation leads cleavage pro-interleukin (IL)-1β pro-IL-18, along release pro-inflammatory cytokines via gasdermin D N-terminal fragment membrane pores, which further triggers acute phase responses concurrent pyroptosis. There currently intense interest in role nucleotide-binding oligomerisation domain-like receptor family, pyrin domain containing protein-3 inflammasomes chronic inflammatory lung diseases such as their potential for therapeutic targeting. Phytochemicals including polyphenols flavonoids have phyto-medicinal benefits CS-COPD. Here, we review published articles last decade regarding known associations between inflammasome-mediated ameliorations pre-clinical manifestations CS-COPD polyphenol flavonoid treatment, a focus on underlying mechanistic insights. This article will potentially assist development drugs prevention therapy COPD, particularly smokers.

Language: Английский

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Vanadium exposure exacerbates allergic airway inflammation and remodeling through triggering reactive oxidative stress

Frontiers in Immunology, Journal Year: 2023, Volume and Issue: 13

Published: Jan. 11, 2023

Background Metal components of environmental PM2.5 are associated with the exacerbation allergic diseases like asthma. In our recent hospital-based population study, exposure to vanadium is shown pose a significant risk for current asthma, but causal relationship and its underlying molecular mechanisms remain unclear. Objective We sought determine whether co-exposure can aggravate house dust mite (HDM)-induced airway inflammation remodeling, as well investigate related mechanisms. Methods Asthma mouse model was generated by using either pentoxide (V 2 O 5 ) or HDM alone in combination, which remodeling investigated. The effect V on HDM-induced epithelial-derived cytokine release oxidative stress (ROS) generation also examined vitro analyses. role ROS co-exposure-induced inhibitors antioxidant. Results Compared alone, exacerbated increased infiltration inflammatory cells elevated levels Th1/Th2/Th17 (IL-25, TSLP) cytokines bronchoalveolar lavage fluids (BALFs). Intriguingly, potentiated remodeling. Increased further supported analysis human bronchial epithelial (HBECs). Mechanistically, ROS, particularly mitochondrial-derived significantly enhanced HBECs after compared challenge alone. Inhibition inhibitor N-acetyl-L-cysteine (NAC) mitochondrial-targeted antioxidant MitoTEMPO blocked caused co-exposure. Furthermore, vitamin D 3 an found inhibit Conclusions Our findings suggest that exacerbates contribute

Language: Английский

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ROS induced the Rab26 promoter hypermethylation to promote cigarette smoking-induced airway epithelial inflammation of COPD through activation of MAPK signaling

Free Radical Biology and Medicine, Journal Year: 2023, Volume and Issue: 195, P. 359 - 370

Published: Jan. 5, 2023

Language: Английский

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