Silica particles cause silicosis (SIL) and represent one of the most typical environmental and occupational substances that induce autoimmune disorders among the exposed population. Anti-nuclear antibody (ANA), anti-Sjögren’s-syndrome-related antigen A (SS-A), anti-centromere protein B (CENP)-B, and anti-scleroderma (Scl)-70 autoantibodies were examined in SIL and compared with those in healthy volunteers (HV) and patients with systemic sclerosis (SSc). Individuals with SIL were prone to autoimmune diseases and some autoantibodies seemed to be important as an estimation of this condition. Anti-Fas autoantibody found in SIL was functionally capable of inducing apoptosis in Fas-expressing cells, and this may cause a decrease of regulatory T cells (Tregs) expressing Fas in SIL. Moreover, responder T cells (Tresps) in SIL seemed to be activated chronically and protected from Fas-mediated apoptosis. Thus, an imbalance of Tresps (dominant) and Tregs (less) occurred in SIL. All of these causes of SIL are ready to further develop autoimmune diseases.

Many environmental and occupational substances such as vinyl chloride, epoxy resins, solvents, pesticides, paraffin/silicone and silica particles cause dysregulation of autoimmunity.

Silica-exposed patients suffer from silicosis  There are several typical pulmonary complications such as pulmonary tuberculosis, tuberculous pleurisy, pneumothorax, bronchiectasis and lung cancer.

In addition to these lung complications, it is well known that the condition of silicosis patients is often complicated with autoimmune diseases. The classical disease is known as Caplan’s syndrome, complicated with rheumatoid arthritis. Furthermore, other autoimmune diseases such as systemic sclerosis,systemic lupus erythematosus and anti-neutrophil cytoplasmic antibody (ANCA) positive vasculitis/nephritis have been reported in case reports and epidemiological investigations.