Human alveolar macrophages: a lesion in arachidonic acid metabolism in cigarette smokers.

Human pulmonary macrophages (PAM) recovered from young cigarette smokers and from age- and sex-matched subjects who had never smoked were used to investigate arachidonic acid metabolism. The uptake of radiolabeled arachidonic acid by PAM obtained from smokers and nonsmokers was not significantly different. The phagocytic indexes of the smoker and nonsmoker macrophages were 17.4 X 3.9% and 18.5 +/- 5.0%, respectively. Both smoker and nonsmoker macrophages produced prostaglandin E2 (PGE2), thromboxane B2 (TXB2) and prostaglandin F2 alpha (PGF2 alpha). A significant decrease in PGE2 and TXB2 synthesis but not in PGF2 alpha synthesis by the smoker PAM compared PAM compared with the nonsmoker PAM was observed using 2 different assays to measure prostaglandin production. Nonsmoker macrophages produced 644 +/- 128,239 +/- 53, and 29 +/- 12 ng/1.5 X 10(6) cells of PGE2, TXB2, and PGF2 alpha, respectively, whereas smoker macrophages synthesized 168 +/- 20, 41 +/- 3, and 17 +/- 1 ng/1.5 X 10(6) cells, as measured by radioimmunoassay. Similar differences were observed using isotopic assays. A cigarette-smoke-induced lesion in phospholipid hydrolysis or the mechanism regulating phospholipid hydrolysis seem most consistent with these findings.