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.