Silica-associated Connective Tissue Disease: A Study of 24 Cases

Abstract

We prospectively studied all patients hospitalized for connective tissue disease (CTD) in our French rheumatology clinic from January 1979 to December 1989. Our aims were 1) to determine if CTDs associated with occupational exposure to silica (Si) are currently observed in a rheumatology clinic, and, if so, 2) to describe the major features of Si-associated CTD, and 3) to specify which individuals are affected by Si-associated CTD. Patients were divided into 2 groups based on their responses to a questionnaire: those who had been exposed to Si, and those who had no occupational exposure to Si. Among the 764 patients with CTD studied, 24 (3%) were patients with Si-associated CTD and 740 (97%) were patients with non-Si-associated CTD. The sex ratio between the 2 groups was significantly different with a high frequency of men and of immigrants in the Si-associated CTD group. Two thirds of the patients exposed to Si were male miners or sandblasters, but the other third had more unusual exposures to Si, which may involve members of all socio-economics sectors and both sexes, such as sculpture or exposure to abrasive powders. Progressive systemic sclerosis (PSS) was significantly more prevalent in the Si-associated CTD group. This group also consisted of patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), dermatomyositis (DM), and other autoimmune diseases. Si-associated CTD was characterized by the frequency of radiologic lung fibrosis, impaired pulmonary function tests, secondary Sjögren syndrome, and antinuclear antibodies. The number of mineral particles and crystalline Si content were raised in all the bronchoalveolar lavage specimens of Si-exposed patients but in none of those of nonexposed patients. In some cases of Si-associated CTD, the disease was reversible after early cessation of Si exposure. Epidemiologic studies are required to confirm our hypothesis that not only PSS and RA but also SLE and DM are associated with occupational exposure to Si. Pending such results, exposure to Si should be sought in the history of any patient with CTD, especially in a male patient with pulmonary signs, and if present, exposure should be stopped. In the meantime, steps should be taken to ensure that workers exposed to Si in all environments have adequate protection.

Evidence for the role of environmental agents in the initiation or progression of autoimmune conditions.

“…Systemic sclerosis (see "Organic Solvents") was most prevalent, but rheumatoid arthritis, SLE, and dermatomyositis also occurred. Frequency of lung fibrosis and the crystalline silica content of bronchoalveolar lavage specimens confirmed exposure to silica in these patients, and in some, cessation of exposure induced disease remission, strongly suggesting a cause-andeffect relationship (43). In a Scandinavian study, Brown et al (44) confirmed an increase in autoimmune disease among hospitalized silicotic patients, and others have specifically implicated the development of SLE in this patient group (45,46).…”

“…In a survey of over 3,000 gold miners, Steenland and Brown (42) showed that although silicosis and tuberculosis were associated, as expected, with silica exposure, risk was also increased for autoimmune diseases, including arthritis, SLE, and scleroderma. In the opposite manner, Koeger et al (43) reviewed 764 patients with autoimmune connective tissue disease and showed that in 3% of cases (n = 24), patients were exposed to silica chiefly through mining and sandblasting but also through less obvious routes such as sculpture work. Systemic sclerosis (see "Organic Solvents") was most prevalent, but rheumatoid arthritis, SLE, and dermatomyositis also occurred.…”

Environmentally induced autoimmune diseases: potential mechanisms.

“…Histone deacetylase inhibitors also reactivate retroviral expression (36). Reactivation of latent retroviruses has been proposed as a mechanism contributing to the development of autoimmunity (37) (58,59). It has been proposed that secretion of these cytokines and possibly other functions of silica-activated macrophages contribute to the fibrosis and possibly the induction of silica-induced autoimmunity.…”

A Rare Clinical Condition: Erasmus Syndrome

“…In addition, silicosis was also reported to be associated with pulmonary tuberculosis, lung cancer, rheumatoid arthritis, and systemic lupus erythematosus [4]. Although the pathogenesis of the relationship between silica powders and SS development has not been precisely explained yet, it is thought that silica particles are phagocytosed by macrophages, which ultimately leads to the release of lymphokine and chemokine by activating the fibroblasts.…”