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Human bronchoalveolar macrophages were separated from other free lung cells by density sedimentation on Percoll gradients. They were then tested for cytotoxicity against the human lung adenocarcinoma cell line A549, using a Selenomethionine-75 post-labelling assay. The cytotoxicity of the macrophages increased as the effector:target cell ratio was increased, approaching 100% at 20:1. There was no significant difference in the cytotoxicity of macrophages isolated from the lungs of bronchial-carcinoma or non-carcinoma patients. The highly cytotoxic nature of the macrophages was not due to selection of a more potent cytotoxic subpopulation of macrophages on the Percoll gradient, nor to a generally elevated activation of the macrophages due to the pathological conditions in the patients' lungs. An attempt to determine whether low concentrations of macrophages could potentiate target-cell growth proved negative. Cytotoxicity of macrophages for cultured lung target cells was not restricted to A549 cells and is not in accordance with the view that defective bronchoalveolar macrophage cytotoxicity contributes to the emergence of bronchial neoplasia.

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Previously reported differences between the cytostatic activity of human peripheral blood monocytes (PBM) and bronchoalveolar macrophages (BAM) for cultured human lung tumor cells have been further investigated. The differences are both quantitative and qualitative and are shown not to be due to the respective methods of purification. There was a varying contribution of cytolysis to the cytostasis detected by the 75selenomethionine post-labeling assay used. Bronchoalveolar macrophages were cytolytic when tested at both low and high E:T ratios but PBM were only cytolytic at the low E:T ratio. A variable dependence upon soluble cytostatic factor(s) was suggested, and there was evidence of heterogeneity in the factors released by the two populations. Cytostatic factor production by both populations appeared to be under similar regulatory constraints. In vitro maturation of PBM altered their cytostatic dose-response curve to one resembling that previously reported for BAM. It was also shown that sera from poor-prognosis lung tumor patients, which suppressed the in vitro maturation of PBM, also suppressed the in vitro cytostatic activity of PBM for cultured human lung tumor cells.

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