Silicosis and silica exposure are associated with increased incidence of autoimmune disease. Yet the mechanism remains obscure with reports of both increased and decreased immunoglobulin levels; chemokine and cell-surface marker analysis has been similarly inconclusive. We report on a cross-sectional study of immune markers in a cohort of masons with the aim of identifying early markers of silica-related pathology for validation in a prospective study. Demographics, dust exposure history, symptoms, spirometry, exhaled nitric oxide and blood (for immunoglobulins, cytokines, cell counts and surface markers) were obtained from 15 cement masons and 24 electrician controls. Continuous variables were compared by student's t-test (electricians vs. masons) or by ANOVA (electricians vs. masons, subdivided by duration of employment). Compared to controls, masons had higher dust-hr-years (40.4 vs 8.4, p=0.0002), as well as serum ILl-B (12.5 vs 9.2 pg/ml, p=0.005), IL4 (176.9 vs 62.8 pg/ml, p=0.01), ILI0 (45.1 vs 20.9 pg/ml, p=0.0002), and IFN-gamma (142.4 vs 62.7, p=0.0003). By contrast, masons had a lower percentage of CD25-positive lymphocytes (12.4 vs 20.4, p=0.01). Results for dust-hr-years, IL10, and IFN-gamma retained significance following Bonferroni correction. The data suggest a proinflammatory state that may be simultaneously Immune-dysregulated, with reduced regulatory (suppressor) T-ceIls, amongst early-career masons. A larger, prospective study, based on the feasibility and results of the present pilot, may deepen insight into the mechanisms of immune disease amongst the silica-exposed.
Proceedings of the American Thoracic Society. 2005 ATS International Conference, May 20-25, 2005, San Diego, California