The effects of urban air and diesel particles on inflammatory pulmonary cytokine gene expression were studied in-vitro. Alveolar macrophages isolated from 3 month old Fischer-344-rats were incubated with 0 to 400 micrograms per milliliter (microg/ml) urban air particulate samples collected at St. Louis, Missouri (A1648 particles) or diesel particle samples collected from the exhausts of diesel forklifts (D1651 particles) for 18 hours (hr). The extent of secretion of tumor-necrosis-factor-alpha (TNFa) was determined. A1648 particles caused a significant dose related induction of TNFa release. Maximum release occurred following treatment with 200microg/ml A1648 particles. D1651 particles did not induce secretion of TNFa. Rat alveolar macrophages were incubated with 0 to 200microg/ml A1648 or 100microg/ml D1651 particles or 100microg/ml bacterial lipopolysaccharide (LPS) for 2hr. The RNA was then extracted and the effects on expression of TNFa, interleukin-1alpha (IL1a), interleukin-1beta (IL1b), interleukin-6 (IL6), and macrophage-inflammatory-protein-2 (MIP-2) mRNA were determined. A1648 particles significantly increased expression of TNFa, IL1a, IL1b, IL6, and MIP-2 mRNA. D1651 particles did not induce expression of any of the cytokine mRNAs. LPS significantly induced expression of the five cytokine mRNAs. Expression of TNFa mRNA by A1648 particles was examined in more detail by treating rat alveolar macrophages with 100microg/ml A1648 particles in the presence or absence of catalase, dimethyl-sulfoxide (DMSO), or 1,1,3,3-tetramethyl-2-thiourea (TMTU) or in cultures that had been pretreated with polymyxin-B. Neither catalase, DMSO, nor TMTU had any effect on induction of TNFa by A1648 particles, indicating that reactive oxidant species were not involved in the process. Polymyxin-B prevented the A1648 particulate induced increase in TNFa secretion, suggesting that endotoxin might play a role in the induction of TNFa by A1648 particles. Rat alveolar macrophages were incubated with 0 to 400microg/ml A1648 or D1651 particles. The cultures were analyzed for increases in endotoxin content. A1648, but not D1651, particles significantly increased the endotoxin concentrations in the cultures. The authors conclude that urban air A1648 particles, but not D1651 particles, stimulate inflammatory cytokine expression in rat alveolar macrophages. This effect may be due to the presence of endotoxin on the A1648 particles.