A significant proportion of early childhood wheezing appears not to be due to atopy-induced pulmonary inflammation, and mediator studies in atopic adults and older children may not be relevant to this age group. The usefulness of inflammatory markers in young children is related to 1) whether atopic and nonatopic wheezing are associated with different patterns of pulmonary inflammation, and 2) whether indirect measurements truly reflect the inflammatory milieu within the lung. Both assumptions remain unproved. Bronchoalveolar lavage (BAL) directly samples the alveolar milieu and is a potential tool for defining both the pulmonary mediator profile, and to validate plasma mediator concentrations. BAL fluid (BALF) eosinophil cationic protein (ECP) concentrations accurately reflect pulmonary eosinophil activation, and the BALF interleukin-2 to interleukin-4 ratio may be helpful in defining those children with established pulmonary sensitization to allergen. Of the mediators that have been measured in the plasma, ECP eosinophil protein X (EPX) and major basic protein (MBP) correlate well with atopy-induced wheezing. However atopic activation in other sites may also increase the plasma concentrations of eosinophil-specific mediators. The profile of adhesion molecules in the plasma (e.g. soluble intercellular adhesion molecule-1, soluble vascular cell adhesion molecule-1 and E-selection) reflects transmigration of specific types of leucocytes across the pulmonary endothelium. To date, the potential of this group of soluble markers to define the nature of pulmonary inflammation is unclear. More information is therefore required on pulmonary inflammation in early childhood to guide the future use of plasma markers.