Persistent inflammation and impaired chemotaxis of alveolar macrophages on cessation of dust exposure.
Rats were exposed by inhalation to coal mine dust, titanium dioxide, or quartz. The magnitude of the consequent inflammatory response was assessed by counting numbers and types of leukocytes in the bronchoalveolar lavage fluid. The magnitude of the inflammatory response reflected the toxicity of the dusts, with quartz eliciting the greatest recruitment of inflammatory leukocytes, coal mine dust less than quartz, and titanium dioxide eliciting no inflammation. To assess the persistence of the inflammation, groups of rats were maintained in room air for 30 or 60 days after cessation of dust exposure and then numbers of leukocytes were assessed. Bronchoalveolar leukocytes in rats exposed to coal mine dust were reduced after exposure, but in the quartz-exposed rats the numbers increased with time after exposure. The chemotactic responses of bronchoalveolar leukocytes from rats inhaling coal mine dust and quartz were reduced and remained so after a 30-day recovery period. Their reduced ability to chemotact did not fully prevent macrophages from leaving the bronchoalveolar region of dust-exposed rats. However, it is likely that the delayed removal of inflammatory leukocytes with the potential to injure the lung tissue may contribute to septal damage and so contribute to the pathogenesis of pneumoconiosis.
Brown
G M
GM
Institute of Occupational Medicine, Edinburgh, Scotland.
Brown
D M
DM
Donaldson
K
K
D000818:Animals; D002634:Chemotaxis, Leukocyte / Q000502:physiology*; D003031:Coal / Q000009:adverse effects*; D007249:Inflammation / Q000473:pathology / Q000503:physiopathology; D016676:Macrophages, Alveolar / Q000473:pathology / Q000502:physiology*; D008297:Male; D011009:Pneumoconiosis / Q000209:etiology / Q000473:pathology*; D011791:Quartz / Q000009:adverse effects*; D051381:Rats; D014025:Titanium / Q000009:adverse effects*
D003031:Coal; D011791:Quartz; C009495:titanium dioxide; D014025:Titanium