Cytotoxicity and induction of proinflammatory cytokines from human monocytes exposed to fine (PM2.5) and coarse particles (PM10-2.5) in outdoor and indoor air

Increased incidence of mortality and morbidity due to cardiopulmonary compl ications has been found to associate with elevated levels of particulate ai r pollution (particulate matter with an aerodynamic diameter < 10 mu m, PM1 0 and <2.5 mu m, PM2.5). Lung injury and an imbalance of inflammatory media tors are proposed causative mechanisms, while the toxic constituents may be acidity, transition metals, organic, and biogenic materials. To compare th e ability of inhalable fine particles (PM2.5), and coarse particles (PM10-2 .5) to cause cell injury and cytokine production in monocytes, dichotomous Andersen samplers were used to collect size-fractionated PM10 for in vitro testing of the particle extracts, Particles from both outdoor and indoor ai r were collected onto Teflon filters, on nine separate occasions, Each filt er was water extracted and each extract assessed for ability to cause cell death, as well as interleukin (IL)-6 and IL-8 production in human monocytes , Significant toxicity and cytokine production was induced by outdoor PM10- 2.5, but not by outdoor PM2.5 or the particles collected indoors. Outdoor P M10-2.5 induced 20 times the amounts of IL-6 and IL-8 than the fine particl es. Cytotoxicity was inhibited by deferoxamine, a chelator of transition me tals, while cytokine production was not, On the other hand, lipopolysacchar ide binding protein (LBP) completely inhibited cytokine induction by PM10-2 .5, suggesting that gram-negative bacteria and/or endotoxins are components of PM10-2.5. The effective proinflammatory effects of endotoxin on macroph ages may upset lung homeostasis while metals-induced cytotoxicity/necrosis may set up inflammation independent of macrophage-derived cytokines. (C) 19 99 Academic Press.