The pulmonary alveolar macrophages possess metabolic pathways operative predominantly in the aerobic environment. These cells consume 0.15 to 0.2μmolar O2/mg protein/sec in vitro. Mitochondria from these cells manifest a respiratory rate of 0.5 to 0.6μmolar O2/mg protein/sec for succinate as a substrate. Mitochondrial oxidation is coupled to phosphorylation; adenosine diphosphate (ADP):oxygen (0) ratios are approximately 2 for flavin-linked and 3 for pyridine nucleotide-linked substrates. Cadmium ion adversely affects respiration of alveolar macrophages. It completely inhibits macrophage mitochondrial oxygen uptake at 50μmolar concentrations and uncouples oxidative phosphorylation at 5μmolar concentrations. This and several other divalent cations, like Cu++, Hg++, Sn++ and Zn++, also inhibit adenosine triphosphatase (ATPase) activity of alveolar macrophages. Since metal fumes and oxides are common air pollutants, a study of this sort might provide information on mechanisms at the biochemical level as to how toxic inhalants initiate pulmonary pathology.