ZnCl₂ smoke-induced acute lung injury: mechanism and prevention

Zinc chloride (ZnCl₂) smoke, a byproduct of smoke bombs widely used in military and firefighting training, poses significant risks to respiratory health and environmental safety. Inhalation of excessive ZnCl₂ smoke can cause acute lung injury (ALI), but the underlying mechanisms are unknown. This study investigated the pulmonary toxicity of ZnCl₂ smoke in mice, focusing on its pathogenic mechanisms and potential preventive treatments. ZnCl₂ smoke exposure resulted in severe lung damage, including alveolar collapse, air-blood barrier disruption, oxidative stress, and apoptosis. Pulmonary surfactant vesicles (PSVs), prepared using natural bovine pulmonary surfactants, were intratracheally administered to the lung prior to exposure. Budesonide (BUD), a standard inhaled corticosteroid with anti-inflammatory and immunomodulatory effects, was used as a positive control to evaluate the comparative efficacy of PSVs. PSV treatment significantly mitigated inflammation, oxidative damage, and apoptosis by modulating key molecular markers, such as downregulating TNF-α, IL-6, IL-1β, MPO, and MDA, while upregulating Bcl-2 and SOD. Additionally, PSVs preserved air-blood barrier integrity, reduced pulmonary edema, and improved lung function and exercise capacity. These findings provide the mechanistic evidence of ZnCl₂ smoke-induced ALI and demonstrate the potential of PSVs as an effective therapeutic strategy for mitigating respiratory toxicity.