Cell markers, cytokines, and immune parameters in cement mason apprentices

Abstract

Objective. Cement masons are known to have significant silica exposure, and silica exposure and silicosis are thought to increase risk of autoimmune disease. Because the mechanisms remain obscure, with inconclusive reports of systemic immune effects following silica exposure, our goal was to identify potential early markers of silica-related immunologic and respiratory effects. Methods. We conducted a cross-sectional study of cement mason apprentices and electrician (control) apprentices. Demographics, dust exposure history, symptoms, spirometry, exhaled nitric oxide, and blood (for immunoglobulins, cytokines, cell counts, and surface markers) were obtained from 11 cement mason apprentices and a comparison group of 21 electrician apprentices. Results. Masons had significantly higher (P < 0.05) masonry dust exposure (42 versus 9 dust-hour-years), serum interleukin-1␤ (IL-1␤; 12 versus 9 pg/ml), IL-2 (20 versus 8 pg/ml), IL-4 (193 versus 67 pg/ml), IL-10 (44 versus 21 pg/ml), and interferon-␥ (139 versus 65 pg/ml) compared with electricians. In contrast, masons had significantly lower percentages of CD25؉ (12% versus 20%) and CD69؉ (4% versus 9%) lymphocytes. Conclusion. Mason apprentices had higher levels of serum proinflammatory cytokines and lower percentages of CD25؉ and CD69؉ lymphocytes than did electrician apprentices. These preliminary findings suggest that mason apprentices may be at greater risk of a systemic proinflammatory state that is potentially linked to immune dysregulation. Although distinct limitations of this preliminary data are recognized, this is consistent with early biologic effects leading to increased incidence of autoimmune disease among silica-exposed workers. Prospective studies are needed to validate these initial findings and clarify the temporal sequence of observed relationships.

Treatment of silicosis with hepatocyte growth factor-modified autologous bone marrow stromal cells: a non-randomized study with follow-up

“…Recent studies have demonstrated that silicosis is an immune-associated disease as pulmonary silicosis is usually accompanied by abnormalities of immune parameters, and the patients with silicosis have a tendency to suffer from autoimmune diseases (Valletta et al, 1992;Cooper et al, 2002;Carlsten et al, 2007;Sauni et al, 2012). In this study, we found that IgG levels were elevated in patients with silicosis, and that this elevation could be downregulated by MSC therapy.…”

The effect of cement dust exposure on haematological and liver function parameters of cement factory workers in Sokoto, Nigeria

“…In addition, occupational exposure to silica, the major component of cement, may increase the risk of autoimmune disease. Carlsten et al, (2007) recently showed that cement masons had higher levels of proinflammatory cytokines and lower percentages of CD25+ and CD69+ lymphocytes compared to control. This led them to suggest that cement masons may be at a greater risk of a systemic proinflammatory state which could be linked to immune dysregulation (Carlsten et al, 2007).…”

“…Carlsten et al, (2007) recently showed that cement masons had higher levels of proinflammatory cytokines and lower percentages of CD25+ and CD69+ lymphocytes compared to control. This led them to suggest that cement masons may be at a greater risk of a systemic proinflammatory state which could be linked to immune dysregulation (Carlsten et al, 2007). It is conceivable that such a proinflammatory state and the accompanying autoimmune disease process may occur in the haemopoietic system thereby accounting for the results of the present study.…”

Increased alveolar nitric oxide and systemic inflammation markers in silica-exposed workers

“…The inflammatory effects of silica in the peripheral lung, which may eventually lead to the development of silicosis, might be seen as increased levels of alveolar NO. The effect of silica exposure on exhaled NO has been reported in only one previous study, which found no effect 11. However, the study measured exhaled NO at a single exhalation flow rate, using an off-line method, which is not sensitive to increased alveolar NO concentrations.…”