Inhalation Injury: Update on Pathogenesis, Emerging Hazards, and Management

Inhalation injury, the pulmonary and systemic damage caused by a single or brief exposure to toxic gases, vapors, aerosols, or particulate matter, encompasses exposure categories ranging from structural-fire smoke and industrial chemical releases to wildfire smoke, earthquake-generated dust, and novel consumer products. Relevant exposures differ markedly in timescale, and four entities are distinguished: acute inhalation injury; subacute toxic pneumonitis, which follows repeated exposure peaks or sustained exposure over weeks to months; chronic inhalational disease; and population-level environmental exposure, which indicates the scale of exposure rather than the incidence of acute injury. Mass-casualty disasters of the twentieth century, from urban smog and industrial chemical releases to fires and warfare, shaped early understanding of the field, and several contemporary exposure categories have emerged in recent years. Injury involves three potentially interacting processes: thermal damage to the upper airway, chemical irritation and inflammatory injury throughout the lower airways and alveoli, and systemic toxicity from absorbed asphyxiants. The site of injury is determined by the water solubility of inhaled gases and the aerodynamic diameter of inhaled particles, and both chemicals and ultrafine particles can translocate across the alveolar-capillary membrane into the systemic circulation. Underrecognized categories include chloramines generated by mixing household cleaning agents, fumigants used in ships, freight containers, and greenhouses, fluorine-based agents from waterproofing sprays and polymer pyrolysis, and pesticides that injure the lung by inhalation or systemic absorption. Management has relied largely on observational data, small case series, and expert opinion; international guidelines for acute respiratory distress syndrome now provide a firmer evidence base for ventilatory support, whereas adjunctive therapies, including nebulized anticoagulants, hyperbaric oxygen, and corticosteroids, remain uncertain. Most survivors recover, but a clinically important minority develop reactive airways dysfunction syndrome, bronchiolitis obliterans, organizing pneumonia, bronchiectasis, or accelerated decline in lung function, and long-term data for emerging exposure categories are sparse. Sequelae are not confined to the lung: structural airway lesions, sinonasal and ocular damage, late neurological effects, and psychosocial and medicolegal consequences all contribute to the burden and are systematically underrecorded. This review is organized around mechanism rather than setting, bringing together the pathogenesis of injury, the widening spectrum of environmental.