In this period inflammation served as a unifying mechanism linking environmental, occupational, and parenchymal lung diseases, with research spanning airway reactivity, hypersensitivity pneumonitis, and interstitial fibrosis. Researchers integrated physiology, pathology, and exposure science, adopting quantitative approaches to relate gas exchange and diffusion properties to clinical status. A defining pattern emerged: tissue inflammation and subsequent fibrosis largely determine prognosis in interstitial lung disease, while pollutant exposures reveal the environmental and immune drivers of disease initiation and progression.