Alveolar persistence

Decrease in lung capacity, alveolar volume, and diffusing capacity for carbon monoxide values remained depressed for at least 72 h after last exposure. Persistent inflammation of proximal portion of alveolar ducts and adjacent alveoli. 

Paraquat tends to rapidly localize in selected tissues of injected mice, including melanin, alveolar type cells of the lung, choroid plexus, muscle, proximal tubules of the kidney, liver, gallbladder, and intestinal contents (Waddell and Marlowe 1980). Half-time persistence of paraquat in rat tissues ranged from 20 to 30 min in plasma to about 5 days in muscle (Sharp et al. 1972). 

Because of the complexity of the actual structures, the emphasis in modeling has been on obtaining an average representation, and the variability among individuals tends to be neglected. There are two experimental studies of variability of airway dimensions in living humans as revealed by aerosol-deposition studies. Lapp et al. assessed the size of alveolar spaces in terms of half-life of aerosol persistence during breath-... 

In rats, inhalation of massive levels of y-alumina with an average particle size of 0.0005-0.04p for up to 285 days caused heavy desquamation of alveolar cells and secondary inflammation, but only slight evidence of fibrosis. The dust concentration in the exposure chamber was described as so high that visibility was reduced a few breaths of the atmosphere by the investigators caused bronchial irritation and persistent cough. 

A 68-year-old woman, with a history of alcohol abuse and a leiomyoma of the stomach, aspirated barium sulfate and became dyspneic and developed hypoxia (Pa02 46mmHg). At bronchoscopy the bronchial mucosa was coated with barium and a chest X-ray showed heavy alveolar deposition of barium sulfate distributed over the entire lung, with some predominance in the lower zones. The patient developed a fever (39°C) and a leukocytosis (12 x 10 /I) the day after aspiration. She was given cefotiam 2000 mg and metronidazole 500 mg intravenously every 8 hours. The fever resolved within 2 days and Staphylococcus aureus was cultured from the bronchial fluid. She was discharged 2 days later, but the chest X-ray continued to show persistent alveolar deposition of the barium sulfate with only a slight improvement compared with the initial X-ray. 

M. tuberculosis bacteria persist in the harsh environment of the host s alveolar macrophages. These bacteria are able to survive by downregulating the host s immune response. Specifically, M. tuberculosis prevents activation of the infected macrophages. Macrophage activation would lead to production of pro-inflammatory cytokines, such as IL-12, IL-18 and tumor necrosis factor a (TNF-a), and to production of interferon-y producing T cells, allowing the host to combat the infection [303]. Both the LAMs and the mycolic acids of M. tuberculosis are able to modulate the host s immune response. 

Radiographic features tend to be quite variable hilar adenopathy with alveolar infiltrates, tissue excavation of an infiltrate (resulting in a thin-walled cavity), or small pleural effusions are all seen commonly. With chronic persistent pneumonia, chest radiographs usually demonstrate apical fibronodular lesions or slowly progressive cavitation. 

Asbestos induces NF-kB and AP-1 transcription-factor activation, possibly through ROS-mediated hpid peroxidation and arachidonic acid metabolism. In macrophages, asbestos caused increased release of arachidonic acid and the formation of prostaglandins E2 and F2a In alveolar macrophages, asbestos induced the releases of arachidonic acid metabolites as early as 1 h post-in vitro exposure. Persistent release of arachidonic acid metabolites at sites of asbestos deposition are implicated in the constitutive activation of NF-kB. ... 

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