Airborne particulate matter modulates the production of reactive oxygen species in human polymorphonuclear granulocytes.

Abstract Causal relationships between airborne particles (especially particulate matter μ m in diameter) and increases in prevalences and symptoms of respiratory diseases have been postulated in many epidemiologic studies. Polymorphonuclear leukocytes (PMN) in the nasal or bronchial epithelium can be exposed to particulate matter (PM) and may upon exposure produce reactive oxygen species (ROS). Release of ROS can result in cellular and tissue damage and initiate or exacerbate inflammation. To elucidate the effect of PM on inflammatory reactions, we exposed human PMN to PM extracts. PM were collected with high volume samplers in two cities, Dusseldorf and Duisburg, in Germany and reflect sites with high traffic and industrial emissions respectively. The collected particles were extracted using water and then dichloromethane, resulting in an aqueous and an organic extract. The production of ROS was determined using luminol-enhanced chemiluminescence (LCL) of resting and zymosan-stimulated PMN. The present study shows that extracts of PM alone significantly stimulated the production and release of ROS in resting PMN. The effects of the PM extracts were inhibited by superoxide dismutase (SOD), catalase and sodium azide (NaN 3 ). Zymosan-induced LCL was, however, diminished by coincubation with PM extracts. The chemical composition is important when considering the effects of particles. Our study shows that only organic substances adsorbed to particles stimulate LCL. SOZ-induced LCL is inhibited by both types of extracts, but aqueous extracts have a stronger inhibitory effect. It is at present unclear which substances are responsible for these effects.