Long-term cadmium exposure induces chronic obstructive pulmonary disease-like lung lesions in a mouse model

Accumulating evidences demonstrate that long-term exposure to atmospheric fine particles and air pollutants elevates the risk of chronic obstructive pulmonary disease (COPD). Cadmium (Cd) is one of the important toxic substances in atmospheric fine particles and air pollutants. In this study, we aimed to establish a mouse model to evaluate whether respiratory Cd exposure induces COPD-like lung injury. Adult male C57BL/6 mice were exposed to CdCl2 (10 mg/L, 4 h per day) by inhaling aerosol for either 10 weeks (short-term) or 6 months (long-term). The mean serum Cd concen-tration was 6.26 mu g/L in Cd-exposed mice. Lung weight and coefficient were elevated in long-term Cd-exposed mice. Pathological scores and alveolar destructive indices were increased in long-term Cd-exposed mouse lungs. Mean linear intercept and airway wall thickness were accordingly elevated in Cd-exposed mice. Inflammatory cell infiltration was obvious and inflammatory cytokines, including TNF-alpha, IL-1 beta, IL-6, IL-8, IL-10 and TGF-beta, were up-regulated in Cd-exposed mouse lungs. alpha-SMA, N-cadherin and vimentin, epithelial-mesenchymal transition markers, and extracellular matrix collagen deposition around small airway, determined by Masson's trichrome staining, were shown in Cd-exposed mouse lungs. COPD-characteristic lung function decline was observed in long-term Cd-exposed mice. These outcomes show that long-term respiratory exposure to Cd induces COPD-like lung lesions for the first time.

Automated summary

Accumulating evidences show that long-term exposure to atmospheric fine particles and air pollutants increases the risk of COPD. Cadmium (Cd) is an important toxic substance in these pollutants. A mouse model was established to demonstrate that respiratory Cd exposure induces COPD-like lung injury.