Accidents at industrial facilities that use phosgene as a feedstock for the synthesis of chemical compounds can become a source of formation of a persistent focus of chemical contamination. Phosgene has an acylating effect on the macromolecules of the components of the aerogematic barrier, which leads to the development of toxic pulmonary edema. To date, it is not known which component of the aerogematic barrier (surfactant layer, alveolocytes or endotheliocytes) serves as the primary target for this toxicant. It has been found in vitro that the action of phosgene on the surfactant (Biosurf Ltd., Russian Federation) did not lead to a decrease in the content of main phospholipids (dipalmitoylphosphatidylcholine), but contributed to an increase in the content of compounds from the group of lysophosphatidylethanolamines (proinflammatory agents). In in vivo study with intraperitoneal administration of phosgene to laboratory animals (rats), there were no signs of an inflammatory reaction of the components of the mesentery of the small intestine. Pathological changes in the lungs and liver of animals that received phosgene intraperitoneal were also not detected. The results of the study indicate that endotheliocytes located in the aerogematic barrier do not play a leading role in the initiation of a proinflammatory cascade in lung tissues after inhaled exposure to phosgene. The primary sources of proinflammatory mediators that lead to the development of toxic pulmonary edema may be alveolocytes and/or surfactant components.