Scientific medicine has reached that evolutionary period where, in addition to the specific infecting microorganism, associated etiological factors find an important place in the interpretation of a disease. More and more attention is being directed toward the latter factors and the rôle they play in respiratory infections. Many different factors open the pulmonary portal for organisms and, in this way, terminate by a serious respiratory inflammatory complication what otherwise might have been a relatively mild disease. In the past two years this has been demonstrated for measles. For the above reasons, not only the immediate action but the complications and sequelæ, too, of the inhalation of irritating gases by normal healthy animals, emphasize themselves as a framework for a more comprehensive interpretation of respiratory disease in general. B. THE PRIMARY INJURY With few exceptions, the gases studied have their most marked effect upon the respiratory tract. They differ, however, in the localization of the lesions and in the extent of the damage. For instance, mustard gas, in high concentrations, has a necrotizing effect upon the entire respiratory tract even to the pulmonary parenchyma itself. Inhaled in a more dilute form it involves the larynx and the trachea and has spent itself before the lung is reached. With phosgene, the opposite is true. The upper respiratory tract is only slightly involved. The outspoken lesions involve the bronchioles, the ducti alveolares, and extend to the alveolar walls of the lung. Chlorine, while it produces a less severe lesion of the upper respiratory tract, extends more often through all of the ramifications of the tracheal tree to the lung. With vital stains (trypan blue), it may be readily demonstrated that these gases kill the epithelium of the respiratory tract and extend through this superficial cellular coat to the deeper tissues of the bronchiolar wall and to the lung tissue, killing it entirely, just as a corrosive chemical destroys the wall of the stomach.