Focal emphysema

Hamster Inhalation 650 4 h/d 5 d/wk 19-74 d Dilated bronchi and alveolar ducts small scattered areas of focal emphysema. LOAEL 650 Goldring ct al. 1970... 

Chronic bronchitis, pneumoconiosis, obstructive lung disease, focal emphysema, progressive massive fibrosis (PMF), coal workers pneumoconiosis (CWP), siUcosis Acute bronchospasm, pneumonitis, chronic exposure leads to Itmg fibrosis, progressive massive fibrosis (PMF), coal workers pneumoconiosis (CWP), silicosis Ocular and upper airway irritation, bronchospasm in severe exposure, contact dermatitis... 

In animal studies, the lowest oral LD50 for acrolein is 7 mg kg in rabbits. An animal inhalation exposure study at 10 ppm for 3.5 h resulted in respiratory irritation in cats. Another inhalation study on rats exposed to 8 ppm for 4 h resulted in the death of one animal while all the animals died at 16 ppm. A subchronic inhalation study with rats exposed to 4 ppm, 6hday, for 60 days resulted in 32/57 animal deaths due to bronchiolar necrosis and focal emphysema. The dermal LD50 has been reported to range from 160 to 1000 mg kg body weight in... 

Focal haemorrhage and pulmonary oedema are typical of the acute toxic effects, but there does not appear to be extensive permanent damage from non-fatal doses. However, residual focal emphysema and interstitial fibrosis remaining after the initial lesions have cleared are possible long term results of the injury [1794,2235]. 

Churg 1998), a form of pneumoconiosis that was believed to produce major functional impairment. For this reason, dusts producing only macules were originally considered to be inert. However, more recent studies have shown that, although macules may initially have little associated fibrosis, with time and/or continued dust accumulation, considerable fibrosis may occur and that, with sufficient exposure, no dust is truly inert. Many dusts that produce macules can also cause fibrosis of the walls of the small airways, presumably as a reaction to the dust accumulating in and around the airways, and the airways may become so distorted and fibrotic as to be almost unrecognizable (Fig. 2.1.2). In addition, enlarged airspaces frequently develop around the fibrotic small airways (Fig. 2.1.2), a process termed focal emphysema. 

Fig. 2.1.2. Fibrotic macule from the lung of a hematite (iron-ore) miner. In contrast to figure 2.1.1, there is both marked fibrosis and focal emphysema (arrows). Lesions of this type may cause airflow obstruction...

Fig. 2.1.5. Gough (1-mm paper) section of a lung with simple coal worker s pneumoconiosis. Note the black macules and focal emphysema in the centers of the lobules...

Fig. 2.1.6. Microscopic image of a coal dust macule from a case of simple coal worker s pneumoconiosis. Although the macule represents a fibrotic and distorted respiratory bronchiole, it is impossible to see the underlying airway in this advanced lesion. Focal emphysema is also present (arrows)...

Fig.6.9a,b. Coal worker s pneumoconiosis computed tomography scan showing with more severe micronodular lung, subpleural and peribronchovascular involvement, a, b Axial views with slice thickness of 1 mm. Multiple micronodules are seen in both lungs. The distribution of the micronodules is diffuse, and, except for the left upper lobe (b), where micronodules can be seen in the interlobular septa (black arrows) and centrilobular, the relationship between the micronodules and the secondary pulmonary lobule is difficult to appreciate. Notice also the peribronchovascular (white arrowheads) and the subpleural micronodules, as well as focal emphysema surrounding some of the micronodules (white arrows)... 

Focal emphysema is the form most commonly associated with coal mining, which constitutes a 1-2 mm zone of tissue destruction around the coal-dust macula. Focal emphysema differs from centrilobu-lar emphysema only through its association with the macula and in its often limited extent (Attfield and Wagner 1996) (Fig. 6.9). 

Occupational exposures to silica and asbestos are associated with lung injury in humans. This can include an irritant bronchitis, bronchiolitis, focal emphysema, pneumoconioses, an increased incidence of tuberculosis, bronchogenic carcinoma, pleural effusions and plaques, and mesothelioma. Industrialization greatly increased both the number of workers with a significant exposure to these mineral oxides and the incidence of disease after their exposure. Lung injury after silica and asbestos continues to result in a significant human morbidity and mortality, despite predictions of its pending elimination. 

Intratracheal administration to guinea pigs of 100 mg of tantalum oxide produced transient bronchitis, interstitial pneumonitis, and hyperemia, but it was not flbrogenic. There were some slight residual sequelae in the form of focal hypertrophic emphysema and organizing pneumonitis around metallic deposits, and there was slight epithelial hyperplasia in the... 

Rats exposed 6 hours/day for 5 days to 50mg/m and examined at various intervals after exposure showed no pulmonary response to titanium dioxide as determined by bronchoalveolar lavage fluid parameters or histopathology. Repeated exposure of rats to concentrations of 10-328mppcf of air for as long as 13 months caused small focal areas of emphysema, which were attributed to large deposits of dust. There was no evidence of any specific lesion being produced by titanium dioxide. ... 

In guinea pigs 120mg zinc/m as zinc chloride 1 hour/day 5 days/week for up to 3 weeks was lethal focal alveolitis, consolidation, emphysema, infiltration with macrophages, and fibrosis were observed at necropsy. Mice and rats exposed to 122 mg zinc/m as zinc chloride for 1 hour/day, 5 days/week, survived 20 weeks of exposure but showed increased macrophages in lungs when euthanized 13 months after exposure. ... 

Structural changes such as atrophy, focal squamous metaplasia and ciliary abnormalities in the epithelium in the central airways have been described. The major cellular component is the CD8-1- T-lym-phocytes in both the central and peripheral airways (O Shaughnessy et al. 1997). Besides CD8+ T lymphocyte infiltration in the peripheral airways, increased smooth muscle thickness occurs. The main morphological form and degree of emphysema can be demonstrated, but the techniques are time consuming, and CT scan pictures seem to be a better way to demonstrate changes in vivo (Gould et al. 1988). 

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