The effect of endotoxin LPS (5,000 nanograms) is compared on airway inflammation and methacholine response and lung function in normals and asthmatics; the effect of LPS (500 nanograms) is compared on allergen-induced reactivity and inflammatory cell influx following LPS exposure (5,000 nanograms) in asthmatics, likely as a result of decreasing baseline inflammation. To examine potential cellular mediation of the effect of LPS in asthma, cytokine secretion of mononuclear cells to LPS of subjects responding to LPS (or those in whom LPS enhance response to allergen) is compared to those who did not respond. In vitro monocyte and in vivo airway responses of asthmatics who are responsive and non-responsive is compared to baseline sputum and nasal lavage fluid IL-8 and ECP to determine if either in vitro monocyte responses or IL-8 and ECP in readily obtained airway fluids may serve as biomarkers of LPS responsiveness and might be used as a marker for a LPS-response phenotype in humans for future mechanistic and intervention studies. Finally, practical data on the effect of LPS in asthmatics (at levels found in typical work settings) and the ability of standard anti-inflammatory therapy to protect asthmatic workers unavoidable exposed to LPS will be obtained.