Silicate pneumoconiosis—a literature review

Silicate pneumoconiosis is a chronic lung condition resulting from inhalation and retention of silicate particles, including crystalline forms such as quartz, cristobalite, and tridymite. While occupational exposure remains the most recognized source, emerging evidence highlights significant environmental contributions from Saharan dust clouds, volcanic activity, and soil-derived particulates. This review synthesizes historical and contemporary literature on the classification, sources, and pathogenicity of silicate pneumoconiosis, emphasizing its fibrotic and non-fibrotic forms. Mechanistic insights reveal that macrophage-mediated uptake of silica triggers oxidative stress, lysosomal disruption, and cyclical cell death, ultimately promoting chronic inflammation and fibrosis. Experimental studies demonstrate that freshly fractured silica exhibits heightened toxicity due to reactive surface radicals, while synergistic interactions with iron and other minerals amplify oxidative damage. Epidemiological data link silica exposure not only to silicosis but also to autoimmune disorders, cardiovascular disease, and increased susceptibility to tuberculosis and pulmonary mycoses. Recent findings from Caribbean animal populations underscore the prevalence of pulmonary crystalline deposits, supporting their role as sentinel species for environmental monitoring. These observations challenge traditional definitions that disregard early lesions and advocate for expanded surveillance strategies. By consolidating multidisciplinary evidence, this review underscores the global health implications of silicate exposure and highlights the need for integrated diagnostic, preventive, and regulatory approaches to mitigate its impact on human and animal health.