nitrogen-dioxide and Pulmonary-Alveolar-Proteinosis

Various inhaled or administered compounds have adverse effects on the surfactant system. In experimental animals quartz inhalation induces alveolar proteinosis. This condition may also be induced by amphiphilic drugs or through increases in surfactant apoproteins. In one experimental model, damage to Clara cells by a methyl-furan derivative led to an increase in extracellular surfactant levels without a change in whole lung pool size. A comparative study of the effects of nitrogen dioxide in the rat and hamster demonstrated differing effects on Clara cells, type II and surfactant levels. These and other studies demonstrate that the effects of chemicals and drugs on cells involved in surfactant synthesis, secretion and catabolism provide a sensitive indicator of incipient toxic effects in the lung.

Topics: Animals; Furans; Humans; Lung; Nitrogen Dioxide; Pulmonary Alveolar Proteinosis; Pulmonary Alveoli; Pulmonary Surfactants; Quartz; Silicon Dioxide; Toxins, Biological

The highly pulmonary concentration of 1,2-dipalmitoyl-sn-glycerol-3-phosphorylcholine (dipalmitoyllecithin) and its implication as an important component of lung surfactant have promoted investigation of phospholipid metabolism in the lung. This review will set the contents including recent informations for better understanding of phospholipid metabolism of the lung in normal state (physiological significances of lung phospholipids, characteristics of phospholipids in lung tissue and alveolar washing, biosynthetic pathways of dipalmitoyllecithin, etc.) as well as in toxic states (pulmonary oxygen toxicity, etc.) and in diseased states (idiopathic respiratory distress syndrome, pulmonary alveolar proteinosis, etc.) Since our main concern has been to clarify the most important route for supplying dipalmitoyllecithin, this review will be focused upon the various biosynthetic pathways leading to the formation of different molecular species of lecithin and their potential significance in the normal, toxic, and diseased lungs.

Topics: Fetus; Humans; Lung; Lung Diseases; Nitrogen Dioxide; Oxygen; Ozone; Phosphatidylcholines; Phospholipids; Pulmonary Alveolar Proteinosis; Pulmonary Surfactants; Respiratory Distress Syndrome

Pulmonary alveolar proteinosis was diagnosed via bronchoscopy in a patient. There was no previous history of inhalation dust exposure. NO2 has been implicated in pulmonary alveolar proteinosis development in animal models. In this case, the diffusion capacity was a sensitive indicator of the disease process.

Topics: Adult; Humans; Male; Nitrogen Dioxide; Occupational Diseases; Pulmonary Alveolar Proteinosis