PLATE NO. IX Ulceration of trachea by mustard gas. The characteristic feature is the sloughing of the tracheal mucous membrane. The reddening of the base of the tongue and of the pharynx, with a sharp delimitation where the oesophagus has refused ingress to the toxic vapour, is seen also with chlorine and other irritant gasses. But the pharyngeal inflammation with mustard gas may proceed further to a local ulceration that will cause dysphagia for many days. The mucous membrane of the trachea and bronchi is affected by di-chlor-ethyl-sulphide in much the same way as is the skin. It reacts with an intense inflammation, and death of the surface layers soon results. The mass of necrotic tissue, exuded fibrin, and pus cells may form a yellowish-grey slough in which all manner of organisms flourish. Subsequently this false membrane comes away in patches or in entire casts from the raw surface of the bronchial wall. Meantime the infected débris and secretions tend to accumulate in the bronchial ramifications at the bases of the lungs, and infection may spread from them into the lung tissues and alveoli. Septic broncho-pneumonia, localised abscesses, superficial pleurisy, and even empyema or pyopneumothorax then develop and cause death. The drawing is of a trachea at the twelfth day after gassing. The base of the tongue and the pharynx show characteristic inflammation. Yellow necrotic sloughs lie on the larynx and at the bifurcation of the trachea. Between these the trachea is red and glistening, because it is now completely denuded of both mucous membrane and of slough. The dotted line points to a little group of ulcers on the posterior wall from which bleeding has occurred. The trachea and bronchi contained an abundance of thin yellow pus. [Illustration: PLATE IX.] PLATE NO. X Microscopic section of human lung from mustard gas poisoning, with death at end of second day (40 hours). The bronchiole is filled with fibrin and pus cells, and its lining epithelium has been completely destroyed. The inflammation has caused a characteristic ring of haemorrhage in the tissues around the bronchial tube, and infection is beginning to appear in the alveoli nearest to these inflamed tissues. But there is no generalised pulmonary oedema and no disruptive emphysema. Di-chlor-ethyl-sulphide may cause some catarrhal desquamation of the pulmonary endothelial cells, but it rarely excites an outpouring of oedema fluid from the pulmonary vessels. The pathological changes in the bronchioles and in the alveoli are therefore in the sharpest contrast with those caused by phosgene (see Plate No. I). As infection spreads into the lung tissues, patches of septic broncho-pneumonia and small abscesses develop, and these often excite an inflammatory oedema around them.