Extracorporeal life support in pediatric burn care: A systematic review.

A systematic review of the role of extracorporeal life support (ECLS) in pediatric patients with burn and smoke inhalation injury was undertaken. A systematic search of the literature according to a specific combination of keywords to ascertain the effectiveness of this treatment strategy was conducted. A total of 14 articles out of 266 were considered suitable for the analysis in pediatric patients. The PICOS approach and PRISMA flow chart were followed for the purpose of this review. Despite the limited number of studies on the subject, ECMO in burn and smoke inhalation injury provides an additional level of support in pediatric patients leading to positive outcomes. V-V ECMO demonstrated the best overall survival of all configurations, with similar outcomes to non-burned patients. Prolonged mechanical ventilation prior to ECMO decreases survival and increases mortality by 12% with each additional day off ECMO. Good outcomes have been described for scald burns, dressing changes, and pre-ECMO cardiac arrest.

Electric Cell-Substrate Impedance Sensing (ECIS) as a Platform for Evaluating Barrier-Function Susceptibility and Damage from Pulmonary Atelectrauma.

Biophysical insults that either reduce barrier function (COVID-19, smoke inhalation, aspiration, and inflammation) or increase mechanical stress (surfactant dysfunction) make the lung more susceptible to atelectrauma. We investigate the susceptibility and time-dependent disruption of barrier function associated with pulmonary atelectrauma of epithelial cells that occurs in acute respiratory distress syndrome (ARDS) and ventilator-induced lung injury (VILI). This in vitro study was performed using Electric Cell-substrate Impedance Sensing (ECIS) as a noninvasive evaluating technique for repetitive stress stimulus/response on monolayers of the human lung epithelial cell line NCI-H441. Atelectrauma was mimicked through recruitment/derecruitment (RD) of a semi-infinite air bubble to the fluid-occluded micro-channel. We show that a confluent monolayer with a high level of barrier function is nearly impervious to atelectrauma for hundreds of RD events. Nevertheless, barrier function is eventually diminished, and after a critical number of RD insults, the monolayer disintegrates exponentially. Confluent layers with lower initial barrier function are less resilient. These results indicate that the first line of defense from atelectrauma resides with intercellular binding. After disruption, the epithelial layer community protection is diminished and atelectrauma ensues. ECIS may provide a platform for identifying damaging stimuli, ventilation scenarios, or pharmaceuticals that can reduce susceptibility or enhance barrier-function recovery.

A Quantitative Analysis of Surgical Smoke Exposure as an Occupational Hazard.

OBJECTIVE: We hypothesized that OR airborne PM was different in quantity and mutagenic potential than office air and cigarette smoke. SUMMARY OF BACKGROUND DATA: Exposure to surgical smoke has been equated to cigarette smoking and thought to be hazardous to health care workers despite limited data. METHODS: PM was measured during 15 operations in ORs with 24.8 ±â€Š2.0 air changes/h, and in controls (cigarettes, office air with 1.9-2.9 air changes/h). Mutagenic potential was assessed by gamma Histone 2A family member X staining of DNA damage in small airway epithelial cells co-cultured with PM. RESULTS: Average PM concentration during surgery was 0.002 ±â€Š0.002 mg/m3 with maximum values at 1.08 ±â€Š1.30 mg/m3. Greater PM correlated with more diathermy (ρ = 0.69, P = 0.006). Values were most often near zero, resulting in OR average values similar to office air (0.002 ±â€Š0.001 mg/m3) (P = 0.32). Cigarette smoke average PM concentration was significantly higher, 4.8 ±â€Š5.6 mg/m3 (P < 0.001). PM collected from 14 days of OR air caused DNA damage to 1.6% ±â€Š2.7% of cultured cells, significantly less than that from office air (27.7% ±â€Š11.7%, P = 0.02), and cigarette smoke (61.3% ±â€Š14.3%, P < 0.001). CONCLUSIONS: The air we breathe during surgery has negligible quantities of PM and mutagenic potential, likely due to low frequency of diathermy use coupled with high airflow. This suggests that exposure to surgical smoke is associated with minimal occupational risk.

Effect of smoking cessation on chronic waterpipe smoke inhalation-induced airway hyperresponsiveness, inflammation, and oxidative stress.

Waterpipe smoking (WPS) prevalence is increasing globally. Clinical and laboratory investigations reported that WPS triggers impairment of pulmonary function, inflammation, and oxidative stress. However, little is known if smoking cessation (SC) would reverse the adverse pulmonary effects induced by WPS. Therefore, we evaluated the impact of WPS inhalation for 3 mo followed by 3 mo of SC (air exposure) compared with those exposed for either 3 or 6 mo to WPS or air (control) in C57BL/6 mice. To this end, various physiological, biochemical, and histological endpoints were evaluated in the lung tissue. Exposure to WPS caused focal areas of dilated alveolar spaces and foci of widening of interalveolar spaces with peribronchiolar moderate mixed inflammatory cells consisting of lymphocytes, macrophages, and neutrophil polymorphs. The latter effects were mitigated by SC. Likewise, SC reversed the increase of airway resistance and reduced the increase in the levels of myeloperoxidase, matrix metalloproteinase 9, granulocyte-macrophage colony-stimulating factor, tumor necrosis factor-α, interleukin (IL)-6, and IL-1ß in lung tissue induced by WPS. In addition, SC attenuated the increase of oxidative stress markers including 8-isoprostane, glutathione, and catalase induced by WPS. Similarly, DNA damage, apoptosis, and the expression of NF-κB in the lung induced by WPS inhalation were alleviated by CS. In conclusion, our data demonstrated, for the first time, to our knowledge, that SC-mitigated WPS inhalation induced an increase in airway resistance, inflammation, oxidative stress, DNA injury, and apoptosis, illustrating the benefits of SC on lung physiology.

Does High-Frequency Chest Wall Oscillation Have an Impact on Improving Pulmonary Function in Patients With Smoke Inhalation Injury?

Smoke inhalation results in bronchospasm of the trachea, increasing secretion of mucus, casts formation, and improvement of blood flow of the airway. High frequency chest wall oscillation is a common modality used for clearing mucus secretion in patients suffering from hypersecretion of thick mucus and used also to help cough clearance. This study aimed to detect the effect of high frequency chest wall oscillation in improving pulmonary function in burn patients suffering from smoke inhalation. Sixty smoke inhalation injury patients were randomly distributed into two groups of equal size. Group A: received high frequency chest wall oscillation and conventional chest physical therapy (breathing exercises, early ambulation, and cough training) thrice per week for 8 weeks. Group B: received traditional chest physical therapy (breathing exercises, early ambulation, and cough training) thrice per week for 8 weeks. Pulmonary function test (forced vital capacity, forced expiratory volume in the first second and peak expiratory flow rate) was measured at enrollment and after 8 weeks by using spirometer. Pulmonary function increased significantly posttreatment when compared with that pretreatment in groups A and B (P > .001). Also, they increased significantly in group A compared with that of group B posttreatment (P > .05). High-frequency chest wall oscillation have an impact on improving pulmonary function and should be handled to be a part of the pulmonary rehabilitation plan for smoke inhalation injury patients.

Working in Smoke:: Wildfire Impacts on the Health of Firefighters and Outdoor Workers and Mitigation Strategies.

Wildland firefighters work on wildfire incidents all over the United States and perform arduous work under extreme work conditions, including exposure to smoke. Wildland fire smoke is a mixture of hazardous air pollutants. For assessing wildland firefighter exposure to smoke, most studies measured carbon monoixde (CO) and particulate matter and reported changes in lung health by measured lung function, airway responsiveness, and respiratory symptoms across individual work shifts and single fire seasons. All fire personnel should understand the hazards of smoke and develop ways to mitigate exposure to smoke.

Association of low FVC spirometric pattern with WTC occupational exposures.

BACKGROUND: A reduced forced vital capacity without obstruction (low FVC) is the predominant spirometric abnormality reported in workers and volunteers exposed to dust, gases, and fumes at the World Trade Center (WTC) disaster site in 2001-2002. While low FVC has been associated with obesity and metabolic syndrome, its association with WTC occupational exposures has not been demonstrated. We estimated the prevalence of this abnormality and examined its association with WTC exposure level. METHODS: Longitudinal study of the relation between arrival at the WTC site within 48 h and FVC below the lower limit of normal (FVC < LLN, with normal FEV1/FVC ratio) at any time in 10,284 workers with at least two spirometries between 2002 and 2018. Logistic regression and linear mixed models were used for the multivariable analyses. RESULTS: The prevalence of low FVC increased from 17.0% (95% CI 15.4%, 18.5%) in June 2003, to 26.4% (95% CI 24.8%, 28.1%) in June 2018, and exceeded at both times that of obstruction. The rate of FVC decline was -43.7 ml/year during the study period. In a multivariable analysis adjusting for obesity, metabolic syndrome indicators, and other factors, early arrival at the WTC disaster site was significantly associated with low FVC, but only among men (ORadj = 1.29, 95% CI 1.17, 1.43). Longitudinal FVC rate of decline did not differ by WTC site arrival time. CONCLUSIONS: Among WTC workers, the prevalence of low FVC increased over a 16-year period. Early arrival to the WTC disaster site was significantly associated with low FVC in males.

Ion transport mechanisms for smoke inhalation-injured airway epithelial barrier.

Smoke inhalation injury is the leading cause of death in firefighters and victims. Inhaled hot air and toxic smoke are the predominant hazards to the respiratory epithelium. We aimed to analyze the effects of thermal stress and smoke aldehyde on the permeability of the airway epithelial barrier. Transepithelial resistance (RTE) and short-circuit current (ISC) of mouse tracheal epithelial monolayers were digitized by an Ussing chamber setup. Zonula occludens-1 tight junctions were visualized under confocal microscopy. A cell viability test and fluorescein isothiocyanate-dextran assay were performed. Thermal stress (40 °C) decreased RTE in a two-phase manner. Meanwhile, thermal stress increased ISC followed by its decline. Na+ depletion, amiloride (an inhibitor for epithelial Na+ channels [ENaCs]), ouabain (a blocker for Na+/K+-ATPase), and CFTRinh-172 (a blocker of cystic fibrosis transmembrane regulator [CFTR]) altered the responses of RTE and ISC to thermal stress. Steady-state 40 °C increased activity of ENaCs, Na+/K+-ATPase, and CFTR. Acrolein, one of the main oxidative unsaturated aldehydes in fire smoke, eliminated RTE and ISC. Na+ depletion, amiloride, ouabain, and CFTRinh-172 suppressed acrolein-sensitive ISC, but showed activating effects on acrolein-sensitive RTE. Thermal stress or acrolein disrupted zonula occludens-1 tight junctions, increased fluorescein isothiocyanate-dextran permeability but did not cause cell death or detachment. The synergistic effects of thermal stress and acrolein exacerbated the damage to monolayers. In conclusion, the paracellular pathway mediated by the tight junctions and the transcellular pathway mediated by active and passive ion transport pathways contribute to impairment of the airway epithelial barrier caused by thermal stress and acrolein. Graphical abstract Thermal stress and acrolein are two essential determinants for smoke inhalation injury, impairing airway epithelial barrier. Transcellular ion transport pathways via the ENaC, CFTR, and Na/K-ATPase are interrupted by both thermal stress and acrolein, one of the most potent smoke toxins. Heat and acrolein damage the integrity of the airway epithelium through suppressing and relocating the tight junctions.

Chronic cigarette smoke exposure triggers a vicious cycle of leukocyte and endothelial-mediated oxidant stress that results in vascular dysfunction.

Although there is a strong association between cigarette smoking exposure (CSE) and vascular endothelial dysfunction (VED), the underlying mechanisms by which CSE triggers VED remain unclear. Therefore, studies were performed to define these mechanisms using a chronic mouse model of cigarette smoking (CS)-induced cardiovascular disease mirroring that in humans. C57BL/6 male mice were subjected to CSE for up to 48 wk. CSE impaired acetylcholine (ACh)-induced relaxation of aortic and mesenteric segments and triggered hypertension, with mean arterial blood pressure at 32 and 48 wk of exposure of 122 ± 6 and 135 ± 5 mmHg compared with 99 ± 4 and 102 ± 6 mmHg, respectively, in air-exposed mice. CSE led to monocyte activation with superoxide generation in blood exiting the pulmonary circulation. Macrophage infiltration with concomitant increase in NADPH oxidase subunits p22phox and gp91phox was seen in aortas of CS-exposed mice at 16 wk, with further increase out to 48 wk. Associated with this, increased superoxide production was detected that decreased with Nox inhibition. Tetrahydrobiopterin was progressively depleted in CS-exposed mice but not in air-exposed controls, resulting in endothelial nitric oxide synthase (eNOS) uncoupling and secondary superoxide generation. CSE led to a time-dependent decrease in eNOS and Akt expression and phosphorylation. Overall, CSE induces vascular monocyte infiltration with increased NADPH oxidase-mediated reactive oxygen species generation and depletes the eNOS cofactor tetrahydrobiopterin, uncoupling eNOS and triggering a vicious cycle of oxidative stress with VED and hypertension. Our study provides important insights toward understanding the process by which smoking contributes to the genesis of cardiovascular disease and identifies biomarkers predictive of disease.NEW & NOTEWORTHY In a chronic model of smoking-induced cardiovascular disease, we define underlying mechanisms of smoking-induced vascular endothelial dysfunction (VED). Smoking exposure triggered VED and hypertension and led to vascular macrophage infiltration with concomitant increase in superoxide and NADPH oxidase levels as early as 16 wk of exposure. This oxidative stress was accompanied by tetrahydrobiopterin depletion, resulting in endothelial nitric oxide synthase uncoupling with further superoxide generation triggering a vicious cycle of oxidative stress and VED.

Smoke inhalation injury in a 2-year-old domestic fire victim.

Smoke inhalation injury is common in victims of domestic fires, among whom children are the most vulnerable. Cyanide poisoning may occur in addition to carbon monoxide poisoning and is challenging to diagnose. In France, the recommended antidotes are hydroxocobalamin for cyanide and hyperbaric oxygen for carbon monoxide. We managed a 26-month-old girl who sustained smoke inhalation injury with both carbon monoxide and cyanide poisoning during a house fire. Despite hydroxocobalamin and sodium thiosulfate therapy combined with hyperbaric oxygen, she had residual neurological impairments 3 months after the injury. The treatment challenges and detailed neurological follow-up data are described.

Association of Obesity with Quantitative Chest CT Measured Airway Wall Thickness in WTC Workers with Lower Airway Disease.

BACKGROUND: We previously reported that wall area percent (WAP), a quantitative CT (QCT) indicator of airway wall thickness and, presumably, inflammation, is associated with adverse longitudinal expiratory flow trajectories in WTC workers, but that obesity and weight gain also seemed to be independently predictive of the latter. Previous studies have reported no association between WAP and obesity, so we investigated that association in nonsmoking WTC-exposed individuals and healthy unexposed controls. METHODS: We assessed WAP using the Chest Imaging Platform QCT system in a segmental bronchus in 118 former WTC workers, and 89 COPDGene® WTC-unexposed and asymptomatic subjects. We used multiple regression to model WAP vs. body mass index (BMI) in the two groups, adjusting for important subject and CT image characteristics. RESULTS: Unadjusted analyses revealed significant differences between the two groups with regards to WAP, age, gender, scan pixel spacing and slice interval, but not BMI or total lung capacity. In adjusted analysis, there was a significant interaction between BMI and WTC exposure on WAP. BMI was significantly and positively associated with WAP in the WTC group, but not in the COPDGene® group, but stratified analyses revealed that the effect was significant in WTC subjects with clinical evidence of lower airway disease (LAD). DISCUSSION: Unlike non-diseased subjects, BMI was significantly associated with WAP in WTC workers and, in stratified analyses, the association was significant only among those with LAD. Our findings suggest that this adverse effect of obesity on airway structure and inflammation may be confined to already diseased individuals.

Circulating cell-free DNA as a potential marker in smoke inhalation injury.

Failure in evaluation of smoke inhalation injury (SII) is related to increased morbidity and mortality. Prognostic biomarkers that reflect the injury are undoubtedly needed. Cell-free DNA (CFD) concentrations are associated to the extent of tissue damage and inflammation in various pathologies. We have developed a simple assay for CFD quantification and previously found it prognostic in various pathologies including burns, lung disease, and sepsis. The aim of this study was to evaluate admission CFD as an injury severity marker in patients with SII.In a prospective study, we measured admission CFD levels in 18 SII patients and matched control subjects. Daily CFD levels were also performed in 4 hospitalized patients. Serum CFD levels were measured by our direct rapid fluorometric assay.Admission CFD levels of SII patients were significantly higher than those of healthy controls, 879 (236-3220) ng/mL vs. 339 (150-570) ng/mL, [median (range)], P < .0001. Admission CFD levels of hospitalized patients were significantly higher than those of nonhospitalized patients, 1517 (655-3220) ng/mL vs. 675 (236-1581) ng/mL, P < .05. Admission CFD positively correlated with hospitalization time (Rho = 0.578, P < .05) and was in linear correlation with CO poisoning (carboxyhemoglobin (COHb) levels, R = 0.621, P < .0001). Additionally, along with the recovery of hospitalized patients, we observed a matched reduction of CFD levels.CFD appears to be a potentially valuable marker for severity and follow-up of SII. We believe this rapid assay can help introduce the routine use of CFD measurement into daily practice.

Respiratory Management in Smoke Inhalation Injury.

Smoke inhalation injury (SII) is a major morbidity and cause of mortality in patients with burns. Damage caused by inhalation of thermal or chemical irritants, including toxic fumes and chemicals, leads to respiratory cilia and epithelial cell injuries, which turn to severe bronchospasm and alveolar damage and results in acute respiratory distress syndrome. Respiratory management plays a vital role in the treatment of SII. In this review, we provide an overview of SII with emphasis on respiratory management, including aerosol therapy, bronchial hygiene therapy, advanced ventilation modes, and heated humidified high-flow nasal cannula. In summary, the information may be helpful for further improvements in outcomes.

Exposure to cigarette smoke via respiratory system may induce abnormal alterations of reproductive organs in female diabetic rats.

Cigarette smoke (CS) has harmful effects on human fertility, reproduction, and development as well as on patients suffering from metabolic diseases such as diabetes than on healthy individuals. This study was conducted to investigate the relationship between CS exposure and histological alterations of reproductive organs in female diabetic rats. We evaluated the histology of uteruses and ovaries obtained from female rats exposed to smoke from standard cigarettes for 4 weeks (28 hours a week). After CS exposure, tissue slides were made from uterine and ovarian samples and examined after hematoxylin and eosin staining. Immunohistochemistry was used for detection of matrix metallopeptidase 9 (MMP9), C-X-C chemokine receptor type 4 (CXCR4), and estrogen receptor (ER)α in the uterus and ovary. MMP9 is an inflammatory biomarker that increases during progression to endometriosis. As a chemokine receptor, CXCR4 is involved in development of the inner wall of the uterus and cell adhesion. In the uterus, the occurrence of MMP9, CXCR4, and ERα and the number of endometrial glands were increased by CS exposure, while in the ovary, occurrence of MMP9, CXCR4, ERα, proliferating cell nuclear antigen and the number of corpus lutea or cyst follicles were increased by CS exposure. Collectively, this study indicates that CS induced abnormal development of the uterus and ovary under induced diabetes, leading to adverse effects on normal function of reproductive organs in female rats. HIGHLIGHTS: Cigarette smoke (CS) exposure adversely affected reproductive organs of diabetic female rats. In the uterus, expression of matrix metallopeptidase 9 (MMP9), C-X-C chemokine receptor type 4 (CXCR4), estrogen receptor (ER)α, and the number of endometrial glands were increased by CS exposure, In the ovary, the expression of MMP9, CXCR4, ERα, and proliferating cell nuclear antigen and the number of corpus lutea or cyst follicles were increased by CS exposure. Exposure to CS via the respiratory system exerted a harmful impact on the uterus and ovary in female rats with diabetes.

[Treatment of patients with different degree of acute respiratory distress syndrome caused by inhalation of white smoke].

Objective: To summarize the treatment experience of patients with different degree of acute respiratory distress syndrome (ARDS) caused by inhalation of white smoke from burning smoke bomb. Methods: A batch of 13 patients with different degree of ARDS caused by inhalation of white smoke from burning smoke bomb, including 2 patients complicated by pulmonary fibrosis at the late stage, were admitted to our unit in February 2016. Patients were divided into mild (9 cases), moderate (2 cases), and serious (2 cases) degree according to the ARDS Berlin diagnostic criteria. Patients with mild and moderate ARDS were conventionally treated with glucocorticoid. Patients with severe ARDS were sequentially treated with glucocorticoid and pirfenidone, and ventilator-assisted breathing, etc. were applied. The vital signs, arterial oxygenation index, changes of lung imaging, pulmonary ventilation function, general condition, and the other important organs/systems function were timely monitored according to the condition of patients. The above indexes were also monitored during the follow-up time of 10-15 months post injury. Data were processed with SPSS 18.0 statistical software. Results: (1) The symptoms of respiratory system of patients with mild and moderate ARDS almost disappeared after 3 days' treatment. Their arterial oxygenation index was decreased from post injury day 1 to 4, which almost recovered on post injury day 7 and completely recovered one month post injury. The symptoms of respiratory system of patients with severe ARDS almost disappeared at tranquillization condition 1-3 month (s) post injury. Their arterial oxygenation index was decreased from post injury day 3 to 21, which gradually recovered 1-3 month (s) post injury and was normal 15 months post injury. (2) Within 24 hours post injury, there was no obvious abnormality or only a little texture enlargement of lung in image of chest CT or X-rays of patients with mild and moderate ARDS. One patient with moderate ARDS had diffuse patchy and ground-glass like increased density shadow (pulmonary exudation for short) at post injury hour 96. Chest iconography of all patients with mild and moderate ARDS showed no abnormalities 10 months post injury. Both lungs of each of the two patients with severe ARDS showed obvious pulmonary exudation at post injury hours 45 and 75, respectively. One patient with severe ARDS showed no abnormality in chest image 10 months post injury, but there was still a small mesh-like increased density shadow in double lobes with slight adhesion of pleura in the other patient with severe ARDS 15 months post injury. (3) All patients showed severe restrictive hypoventilation when admitted to hospital. Pulmonary ventilation function of patients with mild and moderate ARDS recovered to normal one month post injury, and they could do exercises like running, etc. Pulmonary ventilation function of one patient with severe ARDS recovered to normal 6 months post injury, and the patient could do exercises like running, etc. The other patient with severe ARDS showed mild restrictive hypoventilation 15 months post injury and could do exercises like rapid walking, etc. (4) The condition of all mild and one moderate ARDS patients was better on post injury day 3, and they were transferred to the local hospital for subsequent treatment and left hospital on post injury day 21. One patient with moderate ARDS healed and left hospital on post injury day 29. Patients with severe ARDS healed and left hospital on post injury day 81. During the follow-up time of 10-15 months post injury, the other important organs/systems of all patients showed no abnormality, and there was no adverse reaction of glucocorticoid like osteoporosis, femoral head necrosis, or metabolic disorder. Two patients with severe ARDS did not have any adverse reaction of pirfenidone like liver function damage, photosensitivity, anorexia, or lethargy. Conclusions: Early enough and uninterrupted application of glucocorticoid can significantly reduce the ARDS of patients caused by inhalation of white smoke from burning smoke bomb. Sequential application of glucocorticoid and pirfenidone can effectively treat pulmonary fibrosis at the late stage.

Prognostic value of serum zinc levels in patients with acute HC/zinc chloride smoke inhalation.

Hexachloroethane (HC)/zinc chloride (ZnCl, smoke bomb) exposure in the military setting results in lung injury which is uncommon and has been rarely described in previous studies. The aim of this study is to investigate the correlation between the serum zinc in patients with HC/ZnCl smoke inhalation lung injury and disease severity. A total of 15 patients with HC/ZnCl-related conditions were recruited in this study. The serum zinc level and the pulmonary function tests and liver function tests including total lung capacity (TLC), forced vital capacity (FVC), forced expiratory pressure in 1 second (FEV1), alanine aminotransferase (ALT), and aspartate transaminase (AST) were analyzed. Eleven cases had mild clinical manifestations. Four cases rapidly developed features typical of severe adult respiratory distress syndrome. The level of serum zinc was increased, but FVC, FEV1, and TLC was decreased significantly in the moderate and severe cases. In addition, the serum zinc level correlated well with the TLC, FVC, and FEV1 (r = -0.587, -0.626, -0.617, respectively; P = .027, .017, .019, respectively). The 4 cases in moderate and severe group had delayed impairment of liver functions after the accident. This study suggested that the serum zinc level may be associated with the severity of lung and liver injuries after HC/ZnCl smoke inhalation.

Who Among the Elderly Is Most Vulnerable to Exposure to and Health Risks of Fine Particulate Matter From Wildfire Smoke?

Wildfires burn more than 7 million acres in the United States annually, according to the US Forest Service. Little is known about which subpopulations are more vulnerable to health risks from wildfire smoke, including those associated with fine particulate matter. We estimated exposure to fine particles specifically from wildfires, as well as the associations between the presence of wildfire-specific fine particles and the amount of hospital admissions for respiratory causes among subpopulations older than 65 years of age in the western United States (2004-2009). Compared with other populations, higher fractions of persons who were black, lived in urban counties, and lived in California were exposed to more than 1 smoke wave (high-pollution episodes from wildfire smoke). The risks of respiratory admissions on smoke-wave days compared with non-smoke-wave days increased 10.4% (95% confidence interval: 1.9, 19.6) for women and 21.7% (95% confidence interval: 0.4, 47.3) for blacks. Our findings suggest that increased risks of respiratory admissions from wildfire smoke was significantly higher for women than for men (10.4% vs. 3.7%), blacks than whites (21.7% vs. 6.9%), and, although associations were not statistically different, people in lower-education counties than higher-educated counties (12.7% vs. 6.1%). Our study raised important environmental justice issues that can inform public health programs and wildfire management. As climate change increases the frequency and intensity of wildfires, evidence on vulnerable subpopulations can inform disaster preparedness and the understanding of climate change consequences.

A Coordinated Emergency Response: A Color Dust Explosion at a 2015 Concert in Taiwan.

In June 2015, nearly 500 concert attendees suffered injuries from smoke inhalation and severe burns following a color-dust explosion at a waterpark in Taiwan. We report on the progressions of the incident and government responses, share cross-departmental mobilization and case management lessons, and reflect on clinical and complex policy issues emerged. The timely and coordinated emergency responses, a high-quality universal health care system, and dedicated clinicians voluntarily working overtime resulted in an unprecedented 2.4% mortality rate (international statistics predicted 26.8%).