Fibrosis bronchiolar

Bronchiolar fibrosis has been reported with chronically high exposures. However, chronic inhalation exposure at the low levels most exposed individuals are likely to experience, produces no changes in pulmonary function, or in other effects occasionally... 

Neuroendocrine cell h3fperplasia with bronchiolar fibrosis... 

Constrictive bronchiolitis is characterized by subepithehal acellular fibrosis in the walls of membranous and respiratory bronchioles causing concentric narrowing or complete obliteration of the airway lumen (Fig. 1) smooth muscle hyperplasia may also be present. Progressive concentric narrowing is associated with distortion of the lumen, mucostasis, and patchy chronic inflammation. Cicatritial bronchiolitis may be a very subtle lesion, the only clue present in the biopsy specimen being the reduction of the number of bronchioles compared with that of centrilobular arterial branches. A peculiar form of constrictive bronchiolitis, neuroendocrine cell hyperplasia with bronchiolar fibrosis has been reported by Aguayo et al. in 1992 (6). The mildest lesion consists of linear zones of neuroendocrine cell hyperplasia in the bronchiolar mucosa with focal sub-epithelial fibrosis. In more obvious lesions, plaque of eccentric fibrous tissue partially occludes the lumen. In most severe stage there is a total occlusion of the lumen by fibrous tissue with few visible neuroendocrine cells. 

G. Neuroendocrine Cell Hyperplasia with Bronchiolar Fibrosis... 

After intratracheal instillation of nickel chloride or nickel sulphate in rats, a modest inflammatory response with increased number of macrophages and polynuclear leucocytes was obtained, together with increased activities of lactate dehydrogenase and -glucuronidase in bronchoalveolar fluid [351]. More severe lesions were characterized by type II cell hyperplasia with epithelialization of alveoli, and in some animals, fibroplasia of the pulmonary interstitium. By inhalation in rats, the nickel salts produced chronic inflammation and degeneration of the bronchiolar epithelium [352, 353]. There was also atrophy of the olfactory epithelium and hyperplasia of the bronchial and mediastinal lymph nodes. Nickel sulphate also produced a low incidence of emphysema and fibrosis [353]. 

Male and female mice exposed at concentrations up to 4mg/m 6 hours/day for 104 weeks had clear evidence of carcinogenicity based on increased incidences of alveolar/bron-chiolar neoplasms. In rats similarly exposed at concentrations up to 2 mg/m there was some evidence of carcinogenicity in male rats and equivocal evidence in females based on the occurrence of alveolar/bronchiolar neoplasms. Exposure to vanadium pentoxide also caused a spectrum of nonneoplastic lesions in the respiratory tract including alveolar and bronchiolar epithelial hyperplasia, inflammation, fibrosis, and alveolar histocytosis of the lung. Elyper-plasia of the bronchial lymph node occurred in female mice, and an unusual squamous metaplasia of the lung occurred in rats. ... 

For similar routes and forms of mercury, the adverse health effects seen in children are similar to the effects seen in adults. For example, a young child who was intoxicated with mercury vapor, died of pulmonary edema and had a grayish, necrotic mucosa of the stomach and duodenum (Campbell 1948). These effects are similar to those seen in adult populations occupationally exposures to inhaled metallic mercury vapors. Respiratory effects in adults from inhalation of metallic mercury vapor include pulmonary edema, lobar pneumonia, fibrosis, desquamation of the bronchiolar epithelium, and death in severe cases due to respiratory failure (Gore and Harding 1987 Jaffe et al. 1983 Kanluen and Gottlieb 1991 Matthes et al. 1958 Taueg et al. 1992 Teng and Brennan 1959 Tennant et al. 1961). 

Chronic Inflammation is caused by prolonged exposure to airway irritants such as pollution and cigarette smoke. Bronchiolar inflammation results in narrowed airways, increased secretions, epithelial proliferation, loss of ciliated epithelium and fibrosis. Corticosteroids inhibit the inflammatory resjx)nse, but their use is at the expense of systemic side effects (Table 5.1B). 

Adesina AM, Vallyathan V, McQuiUen EN, et al. Bronchiolar inflammation and fibrosis associated with smoking. A morphologic cross-sectional population analysis. Am Rev Respir Dis 1991 143 144—149. 

A number of bronchiolar alterations have been described including proliferative bronchiolitis obhterans in FLD (82), peribronchiolar inflammation/ fibrosis with smooth muscle hypertrophy, and extrinsic narrowing of the small airways in pigeon breeder s disease (83), and less frequently, bronchiolitis obliterans organizing pneumonia (BOOP)-like lesions (84). 

The readership of the series of monographs Lung Biology in Health and Disease know that the series has attempted to address as many pulmonary disorders as possible, but never before has a volume focused on the rare and often puzzUng disorders of the interstitium and bronchiolar tissues. In 2004, the series introduced volume 185 titled Idiopathic Pulmonary Fibrosis edited by Dr. Joseph P. Lynch III to present diseases closely related to many of these diffuse disorders. However, this new volume rich with 35 chapters each addressing a different disorder presents in a comprehensive manner what we now know about Interstitial Pulmonary and Bronchiolar Disorders. Expert research scientists and clinicians from several countries shared their expertise and experience. Undoubtedly, the research community will be stimulated from reading this volume and the clinicians will be assisted in their search to provide the very best care to their patients. 

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