Alveolar-interstitial region

In the alveolar-interstitial region, human lung clearance has been measured. The ICRP model uses two half-times to represent clearance about 30% of the particles have a 30-day half-time, and the remaining 70% are assigned a half-time of several hundred days. Over time, AI particle transport falls, and some compounds have been found in lungs 10-50 years after exposure. 

FIG. 3. Respiratory tract regions defined in the new ICRP model [19], The extrathoracic (ET) airways are divided into Ef, the anterior nasal passage, and ET2, which consists of the posterior nasal and oral passages, the pharynx and larynx. The thoracic regions are bronchial (BB trachea, and main bronchi), bronchiolar (bb bronchioles) and alveolar-interstitial (AT the gas exchange region). Lymphatic tissue is associated with the extrathoracic and thoracic airways (LN j and LNj.jj respectively). 

Capillary endothelial cells comprise 30-42% of cells in the alveolar region and comprise the walls of the extensive network of blood capillaries in the lung parenchyma. The endothelium forms a continuous, attenuated cell layer that transports respiratory gases, water, and solutes. However, it also forms a barrier to the leakage of excess water and macromolecules into the pulmonary interstitial space. Pulmonary endothelial cells, like type I cells, are vulnerable to injury from inhaled substances and substances in the systemic circulation. Injury to the endothelium results in fluid and protein leakage into the pulmonary interstitium and alveolar spaces, resulting in pulmonary edema. 

McGavran PD, Butterick CJ, Brody AR. 1989. Tritiated thymidine incorporation and the development of an interstitial lesion in the bronchiolar-alveolar regions of the lungs of normal and complement deficient mice after inhalation of chrysotile asbestos. JEPTO 9 377-391. 

Morphologically, emphysema is associated with a destruction of the alveolar septum, which results in a dilation and consequent enlargement of the alveolar spaces (Fig. 19). This is apparently caused by a breakdown of the interstitial connective tissue proteins (primarily elastin) that provide the major structural framework of the lung parenchyma. Two types of emphysema have been defined on the basis of the types of destruction of the alveolar septa observed and the type of dilation of the terminal respiratory unit (the acini) that is observed. A typical acinus branches from a terminal bronchiole and consists of the respiratory bronchioles that have alveolated walls and lead to the alveolar ducts and ultimately to the alveolar sacs (see Fig. 3). In centrilobular (or centriacinar) emphysema, the sites of degradation and dilation are limited to the region of the terminal and respiratory bronchioles. In panlobular (or panacinar) emphysema, the entire acinus (including the alveolar ducts and sacs) is more uniformly affected. 

Brody AR, Overby LH. Incorporation of tritiated thymidine by epithelial and interstitial cells in bronchiolar-alveolar regions of asbestos-exposed rats. Am J Pathol 1989 134(1) 133-140. 

With prolonged exposure to particulate matter at sufficiently high concentrations, the particulate matter continuously deposited in the alveolar spaces can trigger a sustained inflammatory reaction. The inflammation can alter particle clearance, initially increase the rate of clearance, and then later canse inhibition of clearance. This, in turn, intensifies the inflammatory reaction, which further impairs clearance and enhances the rate of particle accumulation in the alveolar region. Some of these particles are found in the interstitial areas and others in the alveolar spaces, where aggregates of macrophages, particles, and proteinaceous material may be observed. Adjacent epithelial cells become hypertrophic, hyperplastic, and occasionally, metaplastic. Freqnently, bronchiolar epithelium may appear to be extending down into the alveoli. This pattern of particle-indnced overload disease has been described in detail in rats chronically exposed to diesel exhaust or carbon black particles (39,40). The extent to which similar lesions are produced in humans exposed to similar levels of diesel soot or carbon black is not well understood. 

Immunologically sensitized cells are present both in the bronchial mucosa and in the alveolar regions of the lungs. The interstitial location (42) of many of these cells begs the question of how the inhaled allergen accesses these cells. Recently, data (43) have presented that indicate that the epithelium in persons with asthma, when compared with that of controls, lacks the ability to deactivate... 

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