A patient with long-term sandblasting exposure develops pneumonia-like symptoms without fever or sputum. Which cell type is most responsible for the pathogenesis of this disease?

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Inhaled silica dust from long-term sandblasting triggers silicosis, where alveolar macrophages are the main drivers. These macrophages attempt to engulf silica particles, but silica is toxic to them, leading to macrophage injury and death and the release of inflammatory cytokines like TNF-α and IL-1. This inflammatory environment stimulates fibroblasts to produce collagen, forming nodular fibrotic lesions and progressive lung fibrosis. The resulting dry cough and dyspnea without fever or sputum reflect this chronic fibrotic process driven by macrophage-mediated inflammation and repair. Macrophages orchestrate this response, whereas eosinophils, mast cells, and neutrophils are more characteristic of allergic reactions or acute bacterial processes, not the fibrotic pneumoconiosis seen here.