asbestos--amosite and Acute-Disease

We report a sentinel case of acute eosinophilic pneumonia in a firefighter exposed to high concentrations of World Trade Center dust during the rescue effort from September 11 to 24. The firefighter presented with a Pa(O2) of 53 mm Hg and responded to oxygen and corticosteroids. Computed tomography scan showed patchy ground glass density, thickened bronchial walls, and bilateral pleural effusions. Bronchoalveolar lavage recovered 70% eosinophils, with only 1% eosinophils in peripheral blood. Eosinophils were not degranulated and increased levels of interleukin-5 were measured in bronchoalveolar lavage and serum. Mineralogic analysis counted 305 commercial asbestos fibers/10(6) macrophages including those with high aspect ratios, and significant quantities of fly ash and degraded fibrous glass. Acute eosinophilic pneumonia is a rare consequence of acute high dust exposure. World Trade Center dust consists of large particle-size silicates, but fly ash and asbestos fibers may be found in bronchoalveolar lavage cells.

Topics: Acute Disease; Administration, Oral; Adrenal Cortex Hormones; Adult; Anti-Inflammatory Agents; Asbestos, Amosite; Bronchoalveolar Lavage Fluid; Dust; Eosinophils; Fires; Follow-Up Studies; Glass; Humans; Male; Microscopy, Electron; New York City; Occupational Diseases; Occupations; Prednisone; Pulmonary Eosinophilia; Radiography, Thoracic; Rescue Work; Smoke Inhalation Injury; Terrorism; Time Factors; Tomography, X-Ray Computed; Treatment Outcome

The early response of the lung to a single exposure of amosite asbestos was examined via scanning electron microscopy and correlated light microscopy in the guinea pig model. At 2 h post-exposure, lesions consisted of discrete areas of atelectasis with influx of neutrophils and macrophages. Free asbestos fibres were evident in affected areas. By 4 h post exposure, affected regions were more extensive with phagocytic cell numbers increased both in reactive sites and in adjacent tissue. By 1 day post-exposure, the inflammatory response was well developed and encompassed wide areas of the lung. Activated phagocytes were congregated in atelectatic regions and on blood vessel walls. Numerous macrophages were present even in alveoli distant to reactive loci. The 6 day and 12 day time frames marked a subsiding of the inflammatory response in which macrophages outnumbered PMNs in the comparably fewer reactive areas. There was a notable decrease both in marginated leucocytes and in accumulations of phagocytes in tissue adjacent to affected regions.

Topics: Acute Disease; Animals; Asbestos; Asbestos, Amosite; Asbestosis; Bronchi; Disease Models, Animal; Female; Guinea Pigs; Leukocytes; Lung; Male; Microscopy, Electron, Scanning; Phagocytosis; Pulmonary Alveoli; Sodium Chloride; Time Factors

The acute morphological response to amosite asbestos in the guinea pig was studied by light microscopy and by transmission, scanning, and scanning transmission electron microscopy. Fiber identification was carried out by energy dispersive X-ray analysis. Animals were studied at postinjection intervals of 2, 4, and 12 hr and 1-7 days. Three groups of test animals were studied for each time interval. These consisted of a vascularly perfused parenchymal group and a free cell lavaged group. The information obtained was compared with saline-injected and normal control animals. The acute tissue response was characterized by intraalveolar, not interstitial, events. The early phagocytic response was shared between polymorphs and macrophages, while in the longer intervals, the macrophages were the phagocytic cell type. Packaging differences within the two types of phagocytes were seen. Endothelial stability was noted, while some edematous type I pneumocytes were observed. Fibrotic involvement was limited to some intraalveolar fibrin deposits. It is suggested that the term "free asbestos fibers" refers to an extracellular event, while intracellular fibers are coated with either a membranous sheath, a siderosome, or a classical ferruginous coating.

Topics: Acute Disease; Animals; Asbestos; Asbestos, Amosite; Asbestosis; Guinea Pigs; Histocytochemistry; Iron; Lung; Macrophages; Phagocytosis