Environmental Risk Factors for Acute Respiratory Distress Syndrome

Acute respiratory distress syndrome (ARDS) remains a major cause of morbidity and mortality in critically ill patients. Over the past several decades, alcohol abuse and cigarette smoke exposure have been identified as risk factors for the development of ARDS. The mechanisms underlying these relationships are complex and remain under investigation but are thought to involve pulmonary immune impairment and alveolar epithelial and endothelial dysfunction. This review summarizes the epidemiologic data supporting links between these exposures and ARDS susceptibility and outcomes and highlights key mechanistic investigations that provide insight into the pathways by which each exposure is linked to ARDS

Clearing the Air. Smoking and Incident Asthma in Adults

Quai des hommes, looking northeast from the pedestrian path, rest pavilion at left, vertical "dock" at right; The cultural section of the project (Station des Quais), gathers four contemporary gardens inspired by the mood of the river; the Quai des brumes, the Quai des flots, the Quai des hommes and the Quai des vents. At Quai des hommes (Man Dock) a long narrow boardwalk recalls the deep bond between man and the river. The end of the boardwalk it becomes a tall vertical freestanding wall with a window cutout to frame the landscape of the opposite shore. There are also stone steps down to the shore. "Restoring the river to Quebec" is the mandate that was given to the National Capital Commission Quebec for the realization of the Promenade Samuel-De Champlain. This was once one of the most degraded shoreline areas. Source: Commission de la Capitale Nationale Quebec; http://www.capitale.gouv.qc.ca/ (accessed 7/27/2014

Glucose Phosphorylation and Mitochondrial Binding Are Required for the Protective Effects of Hexokinases I and II▿ †

Alterations in glucose metabolism have been demonstrated for diverse disorders ranging from heart disease to cancer. The first step in glucose metabolism is carried out by the hexokinase (HK) family of enzymes. HKI and II can bind to mitochondria through their N-terminal hydrophobic regions, and their overexpression in tissue culture protects against cell death. In order to determine the relative contributions of mitochondrial binding and glucose-phosphorylating activities of HKs to their overall protective effects, we expressed full-length HKI and HKII, their truncated proteins lacking the mitochondrial binding domains, and catalytically inactive proteins in tissue culture. The overexpression of full-length proteins resulted in protection against cell death, decreased levels of reactive oxygen species, and possibly inhibited mitochondrial permeability transition in response to H2O2. However, the truncated and mutant proteins exerted only partial effects. Similar results were obtained with primary neonatal rat cardiomyocytes. The HK proteins also resulted in an increase in the phosphorylation of voltage-dependent anion channel (VDAC) through a protein kinase Cɛ (PKCɛ)-dependent pathway. These results suggest that both glucose phosphorylation and mitochondrial binding contribute to the protective effects of HKI and HKII, possibly through VDAC phosphorylation by PKCɛ

Cigarette Smoking and ARDS After Blunt Trauma: The Influence of Changing Smoking Patterns and Resuscitation Practices.

BackgroundCigarette smoking is associated with an increased risk of developing ARDS. However, whether changes in smoking patterns or processes of care impact this relationship is unclear.Research questionAre changes in smoking and resuscitation patterns associated with changes in the relationship between smoking and ARDS?Study design and methodsWe conducted a prospective cohort study of critically injured adults with blunt trauma from 2005 to 2015. Plasma cotinine, a tobacco biomarker, was measured to categorize patients by smoking status. We used regression to assess the relationship between smoking, resuscitation practices, and ARDS over time.ResultsIn the overall cohort, active (OR, 1.9; 95% CI, 1.0-3.5; P = .046) and passive (OR, 2.6; 95% CI, 1.4-4.8; P = .002) smoking were associated with an increased risk of developing ARDS in multivariate analyses. In contrast to the dose-response relationship in patients enrolled from 2005 to 2008, passive cigarette smoke exposure was associated with the highest risk of developing ARDS in patients enrolled from 2009 to 2015, suggesting a threshold effect. Packed RBC (pRBC) and fresh frozen plasma (FFP) transfusions were associated with an increased risk of developing ARDS, particularly in active smokers (pRBC: OR, 5.6; P < .001; FFP: OR, 4.5; P < .001) compared with passive smokers or nonsmokers. Blood product transfusion and smoking patterns changed over time.InterpretationDespite changes in resuscitation and smoking patterns, cigarette smoking remains associated with an increased risk of developing ARDS. However, this relationship changed over time, with passive smokers at particularly increased risk of developing ARDS in later years, which may be related to changes in smoking patterns or transfusion practices over time. These findings highlight the need for additional mechanistic and epidemiologic studies of the effects of low levels of cigarette smoke exposure on lung health