intercellular adhesion molecule-1 ( icam-1 ) is expressed on a variety of cells including endothelial cells , alveolar epithelial cells , and alveolar macrophages . 
 endothelial / epithelial cell icam-1 participates in the migration of leukocytes out of the blood in response to pulmonary inflammation , whereas alveolar macrophage icam-1 may represent cell activation . 
 our previous studies have shown that there is increased expression of icam-1 in lung tissue during acute inflammation following intratracheal injection with silica particles ( 2 mg / mouse ) . 
 this increased expression was shown to play a role , in part , in the migration of neutrophils from the circulation into the tissue parenchyma . 
 the aim of the current work is to localize expression of icam-1 during acute inflammation in lungs of mice exposed to either silica or the nuisance dust , titanium dioxide . in silica - exposed mice , 
 a significant increase in icam-1 was detected on day-1 and localized by immunohistochemistry to aggregates of pulmonary macrophages and to type ii epithelial cells . 
 areas of the lung with increased icam-1 expression also showed increased tumor necrosis factor alpha expression . 
 immunocytochemical staining of bronchoalveolar lavage ( bal ) cells demonstrated increased icam-1 expression associated with alveolar macrophages 3 , 5 , and 7 days following silica exposure . finally , soluble icam-1 levels in the bal fluid were significantly increased in mice exposed to silica on the same days . 
 titanium dioxide exposure elicited a minimal increase in expression of icam-1 in the lungs . 
 these data demonstrate that exposure to the toxic particle silica specifically increases icam-1 expression localized to pulmonary macrophages and type ii epithelial cells.imagesfigure 2 . 
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