Exploring First Responders' Use and Perceptions on Continuous Health and Environmental Monitoring.

First responders lose their lives in the line of duty each year, and many of these deaths result from strenuous physical exertion and exposure to harmful environmental agents. Continuous health monitoring may detect diseases and alert the first responder when vital signs are reaching critical levels. However, continuous monitoring must be acceptable to first responders. The purpose of this study was to discover first responders' current use of wearable technology, their perceptions of what health and environmental indicators should be monitored, and who should be permitted to monitor them. The survey was sent to 645 first responders employed by 24 local fire department stations. A total of 115 (17.8%) first responders answered the survey and 112 were used for analysis. Results found first responders perceived a need for health and environmental monitoring. The health and environmental indicators that respondents perceived as most important for monitoring in the field were heart rate (98.2%) and carbon monoxide (100%), respectively. Overall, using and wearing monitoring devices was not age-dependent and health and environmental concerns were important for first responders at any stage of their career. However, current wearable technology does not seem to be a viable solution for first responders due to device expense and durability issues.

Malondialdehyde-Acetaldehyde Adduct Formation Decreases Immunoglobulin A Transport across Airway Epithelium in Smokers Who Abuse Alcohol.

Alcohol misuse and smoking are risk factors for pneumonia, yet the impact of combined cigarette smoke and alcohol on pneumonia remains understudied. Smokers who misuse alcohol form lung malondialdehyde-acetaldehyde (MAA) protein adducts and have decreased levels of anti-MAA secretory IgA (sIgA). Transforming growth factor-ß (TGF-ß) down-regulates polymeric Ig receptor (pIgR) on mucosal epithelium, resulting in decreased sIgA transcytosis to the mucosa. It is hypothesized that MAA-adducted lung protein increases TGF-ß, preventing expression of epithelial cell pIgR and decreasing sIgA. Cigarette smoke and alcohol co-exposure on sIgA and TGF-ß in human bronchoalveolar lavage fluid and in mice instilled with MAA-adducted surfactant protein D (SPD-MAA) were studied herein. Human bronchial epithelial cells (HBECs) and mouse tracheal epithelial cells were treated with SPD-MAA and sIgA and TGF-ß was measured. Decreased sIgA and increased TGF-ß were observed in bronchoalveolar lavage from combined alcohol and smoking groups in humans and mice. CD204 (MAA receptor) knockout mice showed no changes in sIgA. SPD-MAA decreased pIgR in HBECs. Conversely, SPD-MAA stimulated TGF-ß release in both HBECs and mouse tracheal epithelial cells, but not in CD204 knockout mice. SPD-MAA stimulated TGF-ß in alveolar macrophage cells. These data show that MAA-adducted surfactant protein stimulates lung epithelial cell TGF-ß, down-regulates pIgR, and decreases sIgA transcytosis. These data provide a mechanism for the decreased levels of sIgA observed in smokers who misuse alcohol.