Clinical studies show that elevated levels of C3a and C5a occur in bronchoalveolar lavage (BAL) fluids of individuals with asthma and ARDS when compared to healthy individuals (Wills-Karp 2007) . Elevated levels of C3a and C5a may also be found in the serum of ARDS patients. Similarly, in septic patients, elevated levels of the MAC complex precede the development of ARDS (Langlois and Gawryl 1988). There is substantial evidence suggesting that varied environmental factors trigger complement activation at the airway interface, leading to recruitment of cells that release inflammatory mediators resulting in further exacerbation of the inflammatory process in asthma and ARDS (Wills-Karp 2007) . For example, TNFα and IL-1 generated from inflammatory cells induce up-regulation of adhesion molecules (ICAM-1 and E-selectin) on vascular endothelial cells and in pulmonary epithelial cells, which results in tethering of neutrophils to these surfaces. Neutrophils can exert further tissue damage by releasing myeloperoxidase, elastase, etc. Examples of environmental triggers that activate complement are seen in elevated BAL C3 levels in humans exposed to ozone, and elevated serum C3 levels in children with chronic exposure to cigarette smoke. It has been suggested that proteases released from infiltrating cells into the airways can directly cleave C3 and C5, thereby generating C3a and C5a. Alternatively, antibodycontaining immune complexes as well as carbohydrate moieties and macromolecular structures present on pathogens and allergens can activate all three complement pathways. It is likely that complement gets activated by a number of different pathways in asthma and ARDS, although the exact mechanisms are not fully understood.