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Combustion emissions from diesel engines emit particulate matter which deposits within the lungs. Alveolar macrophages (AMs) encounter the particles and attempt to engulf the particles. Emissions particles from diesel combustion engines have been found to contain diverse biologically active components including metals and polyaromatic hydrocarbons which cause adverse health effects. However little is known about AM response to particles from the incorporation of biodiesel. The objective of this study was to examine the toxicity in Wistar Kyoto rat AM of biodiesel blend (B20) and low sulfur petroleum diesel (PDEP) exhaust particles. Particles were independently suspended in media at a range of 1-500 mu g mL(-1). Results indicated B20 and PDEP initiated a dose dependent increase of inflammatory signals from AM after exposure. After 24 h exposure to B20 and PDEP gene expression of cyclooxygenase-2 (COX-2) and macrophage inflammatory protein 2 (MIP-2) increased. B20 exposure resulted in elevated prostaglandin E-2 (PGE(2)) release at lower particle concentrations compared to PDEP. B20 and PDEP demonstrated similar affinity for sequestration of PGE(2) at high concentrations, suggesting detection is not impaired. Our data suggests PGE(2) release from AM is dependent on the chemical composition of the particles. Particle analysis including measurements of metals and ions indicate B20 contains more of select metals than PDEP. Other particle components generally reduced by 20% with 20% incorporation of biodiesel into original diesel. This study shows AM exposure to B20 results in increased production of PGE(2) in vitro relative to diesel. Published by Elsevier Ltd.