Deposition of particles in the lower respiratory tract primarily occurs through inertial impaction at points of turbulent airflow, such as the nasopharynx, trachea, and bronchi. Additionally, deposition occurs at airway bifurcations due to the inability of particles to change direction rapidly. In areas where airflow is slower, smaller particles (0.2 to 2 µm) are deposited on surfaces through sedimentation caused by gravity. Particles with elongated shapes, like asbestos and silica, are deposited through interception when their distal tip comes into contact with cells or mucus layers. Smaller particles below 0.2 µm are deposited in the smaller airways and alveoli, mainly influenced by their diffusion coefficient and brownian motion. Unlike larger particles, the density of these smaller particles does not affect their diffusion, and their deposition is enhanced with decreased size. In the alveolar region where cilia and the mucociliary transport system are absent, these smaller particles are removed by the phagocytic activity of alveolar macrophages or absorption into the interstitium, followed by clearance through lymphatic drainage. Although most alveolar macrophages are located near the alveolar epithelium, some are found in the terminal airways and interstitial space.

Within the conducting airways, the mucociliary clearance system transports deposited particles from the terminal bronchioles to the major airways, where they can be coughed up and expectorated or swallowed. The removal of deposited particles can occur within minutes to hours. Particle clearance rate is faster in the trachea and main bronchi (5 to 20 µm/minute) compared to the bronchioles (0.5 to 1 µm/minute). Generally, the longer an inhaled material remains in the airways, the higher the likelihood of causing lung damage. The region between the terminal bronchioles and alveoli, which lacks ciliated cells, is considered the vulnerable area of an otherwise effective system. Particle clearance in this region, mediated by macrophages, is relatively slow, making it a common site for many occupational lung diseases.

In certain lung diseases, such as silicosis caused by inhalation of silica particles and pneumoconiosis (also known as "black lung" disease) caused by inhalation of coal dust particles, alveolar macrophages phagocytize the particles but are unable to destroy them. Consequently, the macrophages accumulate and concentrate the particles in the vulnerable area of the lung. These particles are not eliminated through mucociliary clearance and eventually enter the lung interstitium. The resulting inflammatory response leads to a granulomatous-like lesion with fibrosis, resulting in a restrictive lung disease. Silicosis and pneumoconiosis serve as classical examples of diseases originating from environmental workplace exposure. Increased awareness of the causes of these diseases and improved workplace environments have led to a reduction in their incidence.

The mucosal immune system comprises both adaptive and innate immunity.
are deposited in the lower respiratory tract predominantly by inertial impaction at points of turbulent airflow (i.e., nasopharynx, trachea, and bronchi) and at airway bifurcations because their tendency to move in a straight direction prevents them from changing directions rapidly. In more distal areas, where airflow is slower, smaller particles (0.2 to 2 µm) are deposited on the surface by sedimentation as a result of gravity. For substances with elongated shapes (i.e., asbestos, silica), the mechanism of deposition is interception. The elongated particle’s center of gravity is compatible with the flow of air; however, when the distal tip of the particulate comes in contact with a cell or mucus layer, deposition is facilitated. Particles smaller than 0.2 µm are deposited in the smaller airways and alveoli and are influenced mainly by their diffusion coefficient and brownian motion. Unlike the deposition of larger particles in the upper airways, particle density does not influence diffusion of these smaller particles, and deposition is enhanced with decreased size. These smaller particles come in contact with the alveolar epithelium, where cilia and the mucociliary transport system do not exist; thus they are removed by the phagocytic activity of alveolar macrophages or absorption into the interstitium with subsequent clearance by lymphatic drainage. Although most alveolar macrophages are adjacent to the epithelium of the alveolus, some are located in the terminal airways and interstitial space.
In the conducting airways, the mucociliary clearance system transports deposited particles from the terminal bronchioles to the major airways, where they are coughed up and either expectorated or swallowed. Deposited particles can be removed in a matter of minutes to hours. In the trachea and main bronchi, the rate of particle clearance is 5 to 20 µm/minute, but it is slower in the bronchioles (0.5 to 1 µm/minute). In general, the longer an inhaled material remains in the airways, the greater is the probability that the material will cause lung damage. The region from the terminal bronchioles to the alveoli is devoid of ciliated cells and is considered the “Achilles heel” in what is otherwise a highly effective system. The relatively slow rate of particle clearance in this area, which is mediated by macrophages, renders it the most common location for many occupational lung diseases.
Insomelungdiseases—forexample,thosecausedbyinhalationofsilicaparticles(silicosis) orcoaldustparticles(pneumoconiosis, the“blacklung”diseaseofcoalminers)—alveolarmacrophagesphagocytizetheparticlesbutareunabletodestroythem,andthemacrophageseventuallydie.Alveolarmacrophageshavelocalizedandconcentratedtheparticlesinthe“Achillesheel”regionofthelung.Theseparticlesarenotremovedviamucociliaryclearanceandeventuallyenterthelunginterstitium.Theensuinginflammatoryresponseleadstoagranulomatouslikelesionwithfibrosis,arestrictivelungdisease.Silicosisandpneumoconiosisareclassicalexamplesofdiseasesoriginatingthroughenvironmentalworkplaceexposure.Increasedawarenessofthecauseofthesediseasesandimprovedworkplaceenvironmentshaveledtoreductionintheincidenceofthesetypesoflungdiseases.
Mucosal Immune System: Adaptive and Innate Immunity