Health Impacts of Fire Smoke Inhalation

2008 ◽  
Vol 20 (8) ◽  
pp. 761-766 ◽  
Author(s):  
M. Stefanidou ◽  
S. Athanaselis ◽  
C. Spiliopoulou
2007 ◽  
Vol 27 (5) ◽  
pp. 525-526
Author(s):  
S. Gopu ◽  
H. Y. Wan Hussein ◽  
S. Ray

Atmosphere ◽  
2020 ◽  
Vol 11 (12) ◽  
pp. 1361
Author(s):  
Scott L. Goodrick

The Atmosphere Special Issue “Special Issue Air Quality and Smoke Management” explores our ability to simulate wildland fire smoke events and the potential to link such modeling to future studies of human health impacts [...]


2004 ◽  
Vol 287 (4) ◽  
pp. L859-L866 ◽  
Author(s):  
Simon S. Wong ◽  
Nina N. Sun ◽  
R. Clark Lantz ◽  
Mark L. Witten

To characterize the tachykininergic effects in fire smoke (FS)-induced acute respiratory distress syndrome (ARDS), we designed a series of studies in rats. Initially, 20 min of FS inhalation induced a significant increase of substance P (SP) in bronchoalveolar lavage fluid (BALF) at 1 h and persisted for 24 h after insult. Conversely, FS disrupted 51.4, 55.6, 46.3, and 43.0% enzymatic activity of neutral endopeptidase (NEP, a primary hydrolyzing enzyme for SP) 1, 6, 12, and 24 h after insult, respectively. Immunolabeling density of NEP in the airway epithelium largely disappeared 1 h after insult due to acute cell damage and shedding. These changes were also accompanied by extensive influx of albumin and granulocytes/lymphocytes in BALF. Furthermore, levels of BALF SP and tissue NEP activity dose dependently increased and decreased, respectively, following 0, low (10 min), and high (20 min) levels of FS inhalation. However, neither the time-course nor the dose-response study observed a significant change in the highest affinity neurokinin-1 receptor (NK-1R) for SP. Finally, treatment (10 mg/kg im) with SR-140333B, an NK-1R antagonist, significantly prevented 20-min FS-induced hypoxemia and pulmonary edema 24 h after insult. Further examination indicated that SR-140333B (1.0 or 10.0 mg/kg im) fully abolished early (1 h) plasma extravasation following FS. Collectively, these findings suggest that a combination of sustained SP and NEP inactivity induces an exaggerated neurogenic inflammation mediated by NK-1R, which may lead to an uncontrolled influx of protein-rich edema fluid and cells into the alveoli as a consequence of increased vascular permeability.


2013 ◽  
Vol 20 (1) ◽  
pp. 2-9 ◽  
Author(s):  
Kurt Anseeuw ◽  
Nicolas Delvau ◽  
Guillermo Burillo-Putze ◽  
Fabio De Iaco ◽  
Götz Geldner ◽  
...  

2021 ◽  
Vol 100 (11) ◽  
pp. 1224-1228
Author(s):  
Larisa M. Sosedova ◽  
Vera A. Vokina ◽  
Mikhail A. Novikov ◽  
Elizaveta S. Andreeva ◽  
Viktor S. Rukavishnikov

Introduction. The adverse negative effect of forest fire smoke on human health represents a unique interdisciplinary challenge to the scientific community. The influence of forest fire smoke on locomotor activity, cognitive indices, and brain bioelectrical activity parameters in exposed rats is presented. Materials and methods. Experimental studies were carried out on outbred white male rats. The animals of the experimental group were exposed to smoke inhalation forest fire for one day. Immediately after the end of the exposure, the animals were examined, including testing in an open field and Morris water maze, as well as an electroencephalographic examination. Results. At twenty-four-hour exposure to wildfire smoke in the model, conditions showed increasing motor and research activity of male rats against the backdrop of growing anxiety. Disorders of indicators of spatial memory and navigation learning were not revealed. On the encephalogram of the exposed animals, in comparison with the control group, the δ-rhythm range predominated, more pronounced in the leads of the right hemisphere. A decrease in the power spectrum and the average amplitude β1-rhythm, as well as a tendency to decrease the average amplitude of θ-rhythm, were revealed. The indices of the primary EEG rhythms did not have statistically significant differences when compared with the control group. Conclusion. The results showed that forest fire smoke leads to changes in the bioelectric activity of brain structures and dysregulation of individual behaviour in animals, all of which may indicate the formation of increased levels of stressing beyond physiological adaptation.


Burns ◽  
2009 ◽  
Vol 35 ◽  
pp. S14
Author(s):  
J.L. Fortin ◽  
T. Desmettre ◽  
V. Peureux ◽  
C. Manzon ◽  
G. Capellier

2013 ◽  
Vol 29 (11) ◽  
pp. 1234-1240 ◽  
Author(s):  
Santiago Mintegi ◽  
Nuria Clerigue ◽  
Vincenzo Tipo ◽  
Eduardo Ponticiello ◽  
Davide Lonati ◽  
...  

2017 ◽  
Vol 51 (12) ◽  
pp. 6674-6682 ◽  
Author(s):  
Ana G. Rappold ◽  
Jeanette Reyes ◽  
George Pouliot ◽  
Wayne E. Cascio ◽  
David Diaz-Sanchez

Author(s):  
Yufei Zou ◽  
Susan M. O’Neill ◽  
Narasimhan K. Larkin ◽  
Ernesto C. Alvarado ◽  
Robert Solomon ◽  
...  

Large wildfires are an increasing threat to the western U.S. In the 2017 fire season, extensive wildfires occurred across the Pacific Northwest (PNW). To evaluate public health impacts of wildfire smoke, we integrated numerical simulations and observations for regional fire events during August-September of 2017. A one-way coupled Weather Research and Forecasting and Community Multiscale Air Quality modeling system was used to simulate fire smoke transport and dispersion. To reduce modeling bias in fine particulate matter (PM2.5) and to optimize smoke exposure estimates, we integrated modeling results with the high-resolution Multi-Angle Implementation of Atmospheric Correction satellite aerosol optical depth and the U.S. Environmental Protection Agency AirNow ground-level monitoring PM2.5 concentrations. Three machine learning-based data fusion algorithms were applied: An ordinary multi-linear regression method, a generalized boosting method, and a random forest (RF) method. 10-Fold cross-validation found improved surface PM2.5 estimation after data integration and bias correction, especially with the RF method. Lastly, to assess transient health effects of fire smoke, we applied the optimized high-resolution PM2.5 exposure estimate in a short-term exposure-response function. Total estimated regional mortality attributable to PM2.5 exposure during the smoke episode was 183 (95% confidence interval: 0, 432), with 85% of the PM2.5 pollution and 95% of the consequent multiple-cause mortality contributed by fire emissions. This application demonstrates both the profound health impacts of fire smoke over the PNW and the need for a high-performance fire smoke forecasting and reanalysis system to reduce public health risks of smoke hazards in fire-prone regions.


2006 ◽  
Vol 21 (S2) ◽  
pp. s49-s55 ◽  
Author(s):  
Marc Eckstein ◽  
Paul M. Maniscalco

AbstractThe contribution of smoke inhalation to cyanide-attributed morbidity and mortality arguably surpasses all other sources of acute cyanide poisoning. Research establishes that cyanide exposure is: (1) to be expected in those exposed to smoke in closed-space fires; (2) cyanide poisoning is an important cause of incapacitation and death in smoke-inhalation victims; and (3) that cyanide can act independently of, and perhaps synergistically with, carbon monoxide to cause morbidity and mortality. Effective prehospital management of smoke inhalation-associated cyanide poisoning is inhibited by: (1) a lack of awareness of fire smoke as an important cause of cyanide toxicity; (2) the absence of a rapidly returnable diagnostic test to facilitate its recognition; and (3) in the United States, the current unavailability of a cyanide antidote that can be used empirically with confidence outside of hospitals. Addressing the challenges of the prehospital management of smoke inhalation-associated cyanide poisoning entails: (1) enhancing the awareness of the problem among prehospital responders; (2) improving the ability to recognize cyanide poisoning on the basis of signs and symptoms; and (3) expanding the treatment options that are useful in the prehospital setting.


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