Smoke Inhalation
Recently Published Documents


TOTAL DOCUMENTS

979
(FIVE YEARS 183)

H-INDEX

46
(FIVE YEARS 11)

Author(s):  
Atacan Emre KOÇMAN ◽  
Mert SEÇER ◽  
Cihan TANRIKUT ◽  
Deniz ARIK ◽  
M.cengiz ÜSTÜNER ◽  
...  

Author(s):  
Martina Linnenluecke ◽  
Mauricio Marrone

Abstract We examine 512 Australian newspaper articles published over a 5-year period (2016 to 2021) that report on air pollution due to bushfire smoke and resulting human health impacts. We analyze to what extent these articles provide information on the possible range of negative health impacts due to bushfire smoke pollution, and to what extent they report on climate change as a driver behind increased bushfire risk. A temporary surge in articles in our sample occurs during the unusually severe 2019/2020 Black Summer bushfires. However, most articles are limited to general statements about the health impacts of bushfire smoke, with only 50 articles in the sample (9%) mentioning an explicit link between bushfire smoke inhalation and cardiovascular and respiratory problems or increases in mortality risk. 148 of the 512 articles in the sample (29%) established a connection between bushfire risk and climate change. We carry out a further keyword analysis to identify differences in reporting by Australia’s two main publishing groups (News Corp Australia and Nine Entertainment), which shows that articles in News Corp Australia outlets offered the lowest climate change coverage. We suggest that more detailed communication strategies are needed to strengthen public preparedness for future impacts.


Burns ◽  
2021 ◽  
Author(s):  
Kafi N. Sanders ◽  
Jyoti Aggarwal ◽  
Jennifer M. Stephens ◽  
Steven N. Michalopoulos ◽  
Donna Dalton ◽  
...  

2021 ◽  
Vol 50 ◽  
pp. 365-368 ◽  
Author(s):  
Kirk L. Cumpston ◽  
Viviana Rodriguez ◽  
Tammy Nguyen ◽  
Adam MacLasco ◽  
Carolyn Zin ◽  
...  
Keyword(s):  

2021 ◽  
Author(s):  
Kaylie I Kirkwood ◽  
Michael W Christopher ◽  
Jefferey L Burgess ◽  
Sally R Littau ◽  
Brian S Pratt ◽  
...  

Lipids play many biological roles including membrane formation, protection, insulation, energy storage, and cell division. These functions have brought great interest to lipidomic studies for understanding their dysregulation in toxic exposure, inflammation, and diseases. However, lipids have shown to be analytically challenging due to their highly isomeric nature and vast concentration ranges in biological matrices. Therefore, powerful multidimensional techniques such as those integrating liquid chromatography, ion mobility spectrometry, collision induced dissociation, and mass spectrometry (LC-IMS-CID-MS) have recently been implemented to separate lipid isomers as well as provide structural information and increased feature identification confidence. These multidimensional datasets are however extremely large and highly complex, resulting in challenges in data processing and annotation. Here, we have overcome these challenges by developing sample-specific multidimensional libraries using the freely available software Skyline. Specifically, the human plasma library developed for this work contains over 500 unique, experimentally validated lipids, which is combined with adapted Skyline functions for highly confident lipid annotations such as indexed retention time (iRT) for retention time prediction and IMS drift time filtering for increased sensitivity and selectivity. For broad comparison with other lipidomic studies, this human plasma database was initially used to annotate LC-IMS-CID-MS data from a NIST SRM 1950 extract, giving comparable results to previous studies. This workflow was then utilized to assess matched plasma and bronchoalveolar lavage fluid (BALF) samples from patients with varying degrees of smoke inhalation injury to identify potential lipid-based patient prognostic and diagnostic markers.


Author(s):  
Kirk L. Cumpston ◽  
Viviana Rodriguez ◽  
Tammy Nguyen ◽  
Adam Maclasco ◽  
Carolyn Zin ◽  
...  
Keyword(s):  

2021 ◽  
Author(s):  
Ronald H. L. Li ◽  
Avalene W. K. Tan ◽  
Yu Ueda ◽  
Joshua A. Stern ◽  
Mehrab Hussain ◽  
...  

Abstract Wildfires pose a major health risk for humans, wildlife, and domestic animals. We previously discovered pathophysiologic parallels between domestic cats with naturally occurring smoke inhalation and thermal burn injuries and human beings with similar injuries; these were characterized by transient myocardial thickening, cardiac troponin I elevation and formation of intracardiac thrombosis. While the underlying mechanisms remain unclear, results from murine models suggest that platelet priming and activation may contribute to a global hypercoagulable state and thrombosis. Herein, we evaluated and compared the degree of platelet activation, platelet response to physiologic agonists and levels of platelet-derived microvesicles (PDMV) in 29 cats with naturally occurring wildfire thermal injuries, 21 clinically healthy cats with subclinical hypertrophic cardiomyopathy (HCM) and 11 healthy cats without HCM (CC). We also quantified and compared circulating PDMVs in WF cats to CC cats. In addition, we examined the association between thrombotic events, severity of burn injuries, myocardial changes, and the degree of platelet activation in cats exposed to wildfires. Flow cytometric detection of platelet surface P-selectin expression showed that cats in the wildfire group (WF) had increased platelet response to adenosine diphosphate (ADP) and thrombin compared to the 2 control groups indicating the presence of primed platelets in circulation. In addition, cats in the WF group had increased circulating levels of PDMV, characterized by increased phosphatidylserine on the external leaflet. Cats in the WF group with documented intracardiac thrombosis had elevated platelet activation and platelet priming in the presence of ADP or thrombin. While high dose arachidonic acid (AA) mostly resulted in platelet inhibition, persistent platelet activation in response to AA was noted among cats in the WF group with intracardiac thrombosis. Univariate and multiple logistic regression analyses demonstrated that increased platelet response to AA was independently associated with thrombotic events. This is the first study reporting the significant association between platelet priming and intracardiac thrombosis in domestic cats with naturally occurring wildfire-related injuries and smoke inhalation. Further studies are required to delineate additional mechanisms between inflammation and thrombosis, especially regarding platelet primers and the cyclooxygenase pathway.


2021 ◽  
Author(s):  
Jennifer Rusmaully ◽  
Nastassia Tvardik ◽  
Diane Martin ◽  
Régine Billmann ◽  
Sylvie Cénée ◽  
...  

Abstract BACKGROUND This study aims to provide new insights on the role of smoking patterns and cigarette dependence in female lung cancer, and to examine differences by histological subtype. METHODS We conducted a population-based case-control study in the great Paris area among women including 716 incident cases diagnosed between 2014 and 2017 and 757 age-matched controls. Detailed data on smoking history was collected during in-person interviews to assess intensity and duration of tobacco smoking, time since cessation, smoking habits (depth of smoke inhalation, use of filter, type of tobacco, and type of cigarettes) and Fagerström test for cigarette dependence. The comprehensive smoking index (CSI), a score modelling the combined effects of intensity, duration and time since quitting smoking was determined for each subject. Multivariable logistic regression models were fitted to calculate odds ratios (ORs) and their confidence intervals (95%CI) of lung cancer associated with smoking variables. RESULTS Lung cancer risk increased linearly with intensity and duration of tobacco smoking while it decreased with time since cessation, to reach the risk in never-smokers after 20 years of abstinence. The combined effect of intensity and duration of tobacco smoking was more than multiplicative (p-interaction 0.012). The OR in the highest vs the lowest quartile of CSI was 12.64 (95%CI 8.50; 18.80) (p-trend < 0.001). The risk of small cell or squamous cell carcinomas increased with the CSI more sharply than the risk of adenocarcinomas. Deep smoke inhalation, dark vs blond tobacco, conventional vs light cigarettes, and unfiltered vs filtered cigarettes, as well as having mixed smoking habits, were found to be independent risk factors. Having high cigarette addiction behaviours also increased the risk after adjusting for CSI. CONCLUSION This study provides additional insights on the effects of tobacco smoking patterns on lung cancer risk among women.


2021 ◽  
Vol 12 ◽  
Author(s):  
Zhonghua Fu ◽  
Zhengying Jiang ◽  
Guanghua Guo ◽  
Xincheng Liao ◽  
Mingzhuo Liu ◽  
...  

Smoke inhalation injury is an acute pathological change caused by thermal stimulation or toxic substance absorption through respiratory epithelial cells. This study aims to probe the protective effect and mechanism of recombinant human keratinocyte growth factor 2 (rhKGF-2) against smoke inhalation-induced lung injury (SILI) in rats. The SILI was induced in rats using a smoke exposure model, which were then treated with rhKGF-2. The rat blood was collected for blood-gas analysis, and the levels of inflammatory factors and oxidative stress markers in the plasma were measured. The rat lung tissues were collected. The pathological changes and cell apoptosis were determined by hematoxylin-eosin (HE) staining and TdT-mediated dUTP nick end labeling (TUNEL) assay, and the PI3K/Akt/Nrf2/HO-1/NQO1, and FoxO1-NLRP3 inflammasome expression were verified by western blot (WB). Both of the human alveolar epithelial cell (HPAEpiC) and primary rat alveolar epithelial cell were exposed to lipopolysaccharide (LPS) for making in-vitro alveolar epithelial cell injury model. After treatment with rhKGF-2, GSK2126458 (PI3K inhibitor) and AS1842856 (FoxO1 inhibitor), the cell viability, apoptosis, inflammation, oxidative stress, reactive oxygen species (ROS), PI3K/Akt/Nrf2, HO-1/NQO1, and FoxO1-NLRP3 in HPAEpiC and primary rat alveolar epithelial cell were examined. The data suggested that rhKGF-2 reduced LPS-induced HPAEpiC cell and primary rat alveolar epithelial cell apoptosis and the expression of inflammatory factors and oxidative stress factors. Moreover, rhKGF-2 improved the blood gas and alleviated SILI-induced lung histopathological injury in vivo via repressing inflammation, NLRP3 inflammasome activation and oxidative stress. Mechanistically, rhKGF-2 activated PI3K/Akt pathway, enhanced Nrf2/HO-1/NQO1 expression, and attenuated FoxO1-NLRP3 inflammasome both in vitro and in vivo. However, pharmaceutical inhibition of PI3K/Akt pathway attenuated rhKGF-2-mediated protective effects against SILI, while suppressing FoxO1 promoted rhKGF-2-mediated protective effects. Taken together, this study demonstrated that rhKGF-2 mitigated SILI by regulating the PI3K/Akt/Nrf2 pathway and the FoxO1-NLRP3 axis, which provides new reference in treating SILI.


2021 ◽  
Vol 12 ◽  
Author(s):  
Samaneh Sadat Alavi ◽  
Siyavash Joukar ◽  
Farzaneh Rostamzadeh ◽  
Hamid Najafipour ◽  
Fatemeh Darvishzadeh-mahani ◽  
...  

Despite its negative effect on the cardiovascular system, waterpipe smoking (WPS) is currently popular worldwide, especially among youth. This study investigated the effects of moderate endurance exercise on heart function of rats exposed to WPS and its possible mechanism. The animals were randomly divided into four groups: control group (CTL), the exercise group (Ex) which trained for 8 weeks, the waterpipe tobacco smoking group (S) exposed to smoke inhalation (30 min per day, 5 days each week, for 8 weeks), and the group that did exercise training and received waterpipe tobacco smoke inhalation together (Ex + S). One day after the last session of Ex and WPS, cardiac pressures and functional indices were recorded and calculated. The levels of SIRT1, SIRT3, Klotho, Bax, and Bcl-2 in the serum and heart, the expression of phosphorylated GSK3β of heart tissue, and cardiac histopathological changes were assessed. WPS reduced systolic pressure, +dP/dt max, -dP/dt max, and heart contractility indices (P &lt; 0.001 vs. CTL) and increased cardiac tissue lesions (P &lt; 0.05 vs. CTL) and end diastolic pressure and Tau index (P &lt; 0.001 vs. CTL) of the left ventricle. Exercise training normalized the left ventricular end diastolic pressure, +dP/dt max, and contractility index. Also, exercise improved the levels of SIRT1, SIRT3, Klotho, and Bcl-2 and reduced Bax level in the heart. The findings showed that WPS causes left ventricular dysfunction. Moderate exercise prevented WPS-induced heart dysfunction partly through its anti-apoptotic features and activation of the sirtuins and Klotho pathways.


Sign in / Sign up

Export Citation Format

Share Document