Air passage in higher animals, including man, is lined internally with small ciliated cells which are covered by a layer of watery, gelly-like substance – the mucus. Particles above 5 in diameter are trapped in the mucous lining, propelled up by co-ordinated movement of cilia to the throat from where they are coughed out or swallowed.
Within about twenty minutes of inhalation they are cleared from the respiratory track. However, in spite of such an efficient filtering mechanism some particles do reach alveolar chambers of lungs where actual gaseous exchange takes place. These particles are those which have a diameter usually less than 5 p.m.
Besides thin-walled cells which line the alveolar chambers, there are also present larger cells called alveolar macrophages which persistently work to keep the alveolar lumen free of all particulate material. Fine particles or aerosols which do reach the alveolor lumen are engulfed by these macrophages which are then passively transferred to the regional lymph nodes.
From nodes they are disposed of via upper respiratory track along with coarser particles, filtered earlier. Inert aerosols, such as particles of tin oxide, carborundum or diamond dust etc. may be retained in the lymph node or in the macrophage cytoplasm throughout the life of an individual without causing any harm.
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However, toxic particulate material like coal, mica, talc and some of crystalline forms of silica
may injure or kill alveolar macrophages. Elongate asbestos fibres which are less than 5 µm in era section may also reach the alveolar lumen. These fibres are many times longer than the actual diameter of the macrophage and hence are incompletely covered. In such cases a cytoplasmic sleeve forms covering the entire fibre and a number of macrophages may have to fuse together to engulf these fibres. Particles released from dead macrophages are engulfed again by newly formed macrophages.
As these macrophages tend to adhere to alveolar wall they are covered by newly formed epithelia cells. The cyclic engulfment of aerosols by macrophages, their release and epithelialization results in the formation of nodules which may grow large enough to block the alveolar lumen, making in Completely defunct. With aging of nodules collegen fibres are laid down and a fully develops nodule resembles a ball of wool.
The phenomenon is known as fibrosis. Since a large number of such nodules are formed simultaneously a considerably large respiratory area is lost. In order to compensate for the lost area the alveoli of other parts of lung get dilated – a feature which is known as compensate emphysema.
Thus aerosols which have a diameter less than 5 µm are dangerous while fibrous material with a cross-section less than 5 µm but lengths many times greater are much more risky to breathe in. This result in diseases like silicosis, asbestosis etc. and the individual is rendered susceptible to many types of infectious diseases. Tuberculosis is one of such diseases which are quite frequent in dirty, dusty and crowded cities in India.