LAUSR

Cadmium exposure may result in a variety of pulmonary diseases. No studies have evaluated tracheal damage or even whether cadmium intake can damage the respiratory tract. We evaluated the possible injuries caused by cadmium poisoning via intake into the respiratory tract and the possible effects of water pH in their genesis. Ninety male Wistar rats were divided into six groups (n = 15): GC5—received CdCl2 (400 mg/l) in the drinking water at an acidic pH of 5; GC7 received CdCl2 (400 mg/l) in the drinking water at an acidic pH of 7.0; GC8—received CdCl2 (400 mg/l) in the drinking water at an acidic pH of 8.0; GW5—received water at an acidic pH of 5.0; GW7—received water at an acidic pH of 7.0; GW8—received water at an acidic pH of 8.0. Animals were euthanized after 6 months. Samples of the trachea and lung were removed for histopathologic analysis. The animals exposed to cadmium presented with goblet cells in the trachea at an average rate of 65.83 cells/6 high-power fields (HPF), whereas unexposed animals showed 85.16 cells/6HPF (p = 0.012). Further, pulmonary emphysema was demonstrated in 71.43 to 100% of exposed cases, whereas the unexposed animals presented emphysema in 6.66 to 15.38% of cases (p < 0.001). The respiratory tract is a target for cadmium-related injuries after intake; however, the pH of the water did not influence the development of these lesions.