Abstract
Increased respiratory disease and daily mortality rates are associated with higher levels of fine particulate air pollutants. We examined the possibility that deposition of even inert particles to previously injured lungs may accentuate pulmonary damage by investigating how the lung handles small carbon particles delivered during acute injury or during fibrotic repair. Mice received 2 mg carbon by intratracheal instillation into lungs already showing acute injury, 3 days after bleomycin (BL), or into lungs with fibrosis, 4 weeks after BL. At 3 days after BL, injury to the type I alveolar epithelium resulted in high protein levels in lavage fluid. Instilling carbon at this time induced a large increase in inflammatory cells, though many particles reached the interstitium, and a high proportion was retained up to 16 weeks later. However, fibrosis in these mice was equal to that found after BL alone. In the mice that received carbon 4 weeks after bleomycin, fibrotic repair had already occurred, and the epithelial surface was restored before particle instillation. After carbon, the subsequent inflammatory reaction cleared most particles, little reached the interstitium, and carbon retained at 16 weeks was not different from that in...Continue Reading
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