Narrative review examines silicate pneumoconiosis mechanisms and epidemiological links to tuberculosis.

This narrative review synthesizes current knowledge regarding silicate pneumoconiosis and silicosis across human and animal populations globally. The scope encompasses exposure to silicate particles, including quartz, cristobalite, and tridymite, as well as environmental sources like Saharan dust clouds, volcanic activity, and soil-derived particulates. The authors do not report a specific sample size or follow-up duration, characterizing the evidence through qualitative synthesis rather than pooled effect sizes or statistical comparisons.

Key findings focus on mechanistic insights where macrophage-mediated uptake of silica triggers oxidative stress, lysosomal disruption, and cyclical cell death, ultimately promoting chronic inflammation and fibrosis. The review notes heightened toxicity associated with freshly fractured silica due to reactive surface radicals. Additionally, synergistic interactions with iron and other minerals are described as amplifying oxidative damage within the lung tissue.

Epidemiologically, the text links silica exposure to autoimmune disorders, cardiovascular disease, and increased susceptibility to tuberculosis and pulmonary mycoses. Observations include pulmonary crystalline deposits in Caribbean animal populations. The authors acknowledge limitations regarding the lack of reported safety data, including adverse events and tolerability. The review covers human and animal populations without detailing specific cohorts.

Practice relevance emphasizes the need for integrated diagnostic, preventive, and regulatory approaches to address these exposures. The review does not establish causality or report specific p-values or confidence intervals. Clinicians should interpret these findings as descriptive associations requiring further investigation to confirm clinical implications and safety profiles.