title: Particles causing lung disease.
abstract: The lung has a limited number of patterns of reaction to inhaled particles. The disease observed depends upon the location: conducting airways, terminal bronchioles and alveoli, and upon the nature of inflammation induced: acute, subacute or chronic. Many different agents cause narrowing of conducting airways (asthma) and some of these cause permanent distortion or obliteration of airways as well. Terminal bronchioles appear to be particularly susceptible to particles which cause goblet cell metaplasia, mucous plugging and ultimately peribronchiolar fibrosis. Cancer is the last outcome at the bronchial level and appears to depend upon continuous exposure to or retention of an agent in the airway and failure of the affected cells to be exfoliated which may be due to squamous metaplasia. Alveoli are populated by endothelial cells, Type I or pavement epithelial cells and metabolically active cuboidal Type II cells that produce the lungs specific surfactant, dipalmytol lecithin. Disturbances of surfactant lead to edema in distal lung while laryngeal edema due to anaphylaxis or fumes may produce asphyxia. Physical retention of indigestible particles or retention by immune memory responses may provoke hyaline membranes, stimulate alveolar lipoproteinosis and finally fibrosis. This later exuberant deposition of connective tissue has been best studied in the occupational pneumoconioses especially silicosis and asbestosis. In contrast emphysema a catabolic response, appears frequently to result from leakage or release of lysosomal proteases into the lung during processing of cigarette smoke particles. The insidious and probably most important human lung disease due to particles is bronchiolar obstruction and obliteration, producing progressive impairment of air flow. The responsible particle is the complex combination of poorly digestive lipids and complex carbohydrates with active chemicals which we call cigarette smoke. More research is needed to perfect, correct and quantify our preliminary picture of the pathogenesis of lung disease by particles, but a useful start has been made.
mesh_terms: D000818:Animals; D001980:Bronchi / Q000033:anatomy & histology / Q000166:cytology / Q000187:drug effects; D006801:Humans; D008064:Lipidoses / Q000503:physiopathology; D008074:Lipoproteins / Q000097:blood; D008171:Lung Diseases / Q000209:etiology*; D010316:Particle Size; D011650:Pulmonary Alveoli / Q000502:physiology; D011654:Pulmonary Edema / Q000209:etiology / Q000503:physiopathology; D011656:Pulmonary Emphysema / Q000209:etiology / Q000503:physiopathology; D011658:Pulmonary Fibrosis / Q000209:etiology / Q000503:physiopathology; D012907:Smoking
chemical_list: D008074:Lipoproteins