A study was made on the effect of Cd²⁺ on respiration and adenosinetriphosphatase activity of pulmonary alveolar macrophage (PAM) cells. Approximately 5 mm Cd²⁺ inhibited endogenous respiration in PAM cells and 0.5 mm Cd²⁺ inhibited respiration in mitochondria of PAM cells. Tetramethyl-p-phenylenediamine, an artificial electron carrier, restored the Cd²⁺-inhibited respiration in both cells and mitochondria, indicating that Cd²⁺ presumably bound certain respiratory chain components. Cadmium ion also inhibited the Na⁺K⁺, Mg²⁺ ATPase system of PAM cells and cellular membranes. The interaction of this metal ion with the vital processes of respiration and energy transfer in PAM cells might relate to pulmonary pathology arising from occupational and environmental exposure to cadmium. It is hypothesized that the biochemical alterations of pulmonary cells may be more sensitive and easily discernible parameters of the manifestations of noxious inhalants than the conventional pathophysiological parameters.