<p>Severe trauma induces systemic inflammatory responses that predispose the lung to secondary injury. Acute respiratory distress syndrome (ARDS) remains a major cause of morbidity and mortality following severe trauma, particularly in military and disaster settings where inhalation exposure to toxic combustion products frequently accompanies physical injury. Combustion-derived particles, irritant gases, and complex aerosols generated by explosions or fires may amplify trauma-induced pulmonary inflammation and accelerate alveolar–capillary barrier failure. This review highlights the interactions between hemorrhagic trauma and toxic inhalation that contribute to respiratory failure in combined injury settings. Hemorrhagic shock and tissue injury trigger systemic inflammation, endothelial dysfunction, and increased vascular permeability, while inhaled toxicants directly damage the pulmonary epithelium and endothelium. Together, these processes promote alveolar–capillary barrier disruption and progression toward ARDS. These mechanisms are particularly relevant in battlefield and disaster critical care settings where delayed evacuation, inhalation exposure, and limited respiratory support may aggravate progression toward severe respiratory failure. Current management remains largely supportive, but emerging therapeutic approaches aimed at preserving alveolar–capillary barrier integrity may offer future opportunities for respiratory protection. A better understanding of the interactions between trauma and toxic inhalation may help guide the development of respiratory countermeasures for trauma-associated ARDS.</p>