Current perspectives on particulate induced XXXX .

@entity1 @entity137 @entity5 @entity1544 @entity2543 @entity3440 @entity6701 @entity35
1. Chronic exposure to insoluble particulates can lead to the development of @entity5 . These have been classified as broncho-alveolar or squamous/epidermoid according to their histopathological characteristics and have been reported in inhalation studies in @entity35 of materials ranging from diesel exhaust and @entity3440 to @entity6701 . 2. The sequence of changes within the @entity35 lung leading to @entity5 has been characterised. It is apparent that one prerequisite is that the lung load of the particulate matter must exceed the normal clearance capacity, either by overloading the normal alveolar macrophage mediated mechanism or by induction of @entity137 with materials such as @entity3440 . This results in inflammatory responses, including, or resulting in, @entity2543 and @entity1544 . The persistence of these tissue responses over chronic time periods can lead to tumorigenesis. 3. Research into the mechanisms involved in the initiation and progression of both the inflammatory response and subsequent tumorigenic response to lung particulate loading is in progress. Impairment of macrophage function and mobility by inert particles constitutes one route by which this can arise, as does @entity137 to this cell type by biologically reactive particles. At the molecular level, the role of inflammatory mediators, especially the cytokines, has received much attention. 4. Particulate induced @entity5 are perceived to be a phenomenon specific to the @entity35 and their relevance to @entity1 is questionable.
