Autoimmune Disease
Autoimmune disease is not an exaggerated response to foreign matter.
This syndrome occurs when foreign chemicals modify tissues or immune cells, affecting the regulation of immune response such as the production of antibodies and inflammatory response.
The result is an immune response against our own tissues, tissue damage and disease.
The mechanisms which allow this to occur in the body are complex, but there are genetic and environmental factors which affect an individuals susceptibility to autoimmune disease.
Exposure to sulfa, penicillin, vinyl chloride, gold salts, silica, mercury, methyl dopa, and other compounds can induce this response by the immune system. Systemic lupus and rheumatoid arthritis are two autoimmune diseases.
It should be noted that viral, hormonal, and emotional factors can also contribute to the development of autoimmune disease.
Silica
Although the most common health effect of silica exposure are the lung diseases occupational exposure to respirable crystalline silica is also associated with a number of other diseases, including systemic autoimmune diseases, such as rheumatoid arthritis, scleroderma, systemic lupus erythematosus (SLE), and some of the small vessel vasculitides and with renal diseases i.e. rapid progressive glomerulonephritis, nephrotic syndrome, and end stage renal disease.
Scleroderma is an uncommon disease that results in hard, thickened areas of skin and
sometimes problems with internal organs and blood vessels.
There's no cure, but most people can lead a full, productive life. Scleroderma is an autoimmune condition, which means the body attacks its own tissues.
The high attributable risk of silica dust exposure for scleroderma has become apparent. Scottish stonemasons were probably the first occupational group with scleroderma to be described.
Bramwell B: Diffuse scleroderma: its frequency and occurrence in stonemasons; its treatment by fibrinolysisin: elevations of temperature due to fibrinolysin injections. Edinburg Med J 1914, 12:387.
In a survey done in East Germany between 1981 and 1988, we found that 93 of 120 male scleroderma patients had long-term exposure to silica dust.
The silicosis is the pneumoconiosis more frequent, resulting from the inhalation of silica or silicates containing mineral dust, mainly characterized by irreversible lung fibrosis. It is associated with the development of other diseases, including pulmonary tuberculosis, lung cancer and autoimmune diseases. The connective tissue disease after exposure to silica occurs usually after 15 years of initial exposure. The Erasmus syndrome describes the association of systemic sclerosis following exposure to silica with or without silicosis.
Caplan's syndrome or Caplan disease or rheumatoid pneumoconiosis is a combination of rheumatoid arthritis (RA) and pneumoconiosis that manifests as intrapulmonary nodules, which appear homogenous and well-defined on chest X-ray
Caplan syndrome occurs only in patients with both RA and pneumoconiosis related to mining dust (coal, asbestos, silica). The condition occurs in miners (especially those working in anthracite coal-mines), asbestosis, silicosis and other pneumoconioses.
Vasculitis means inflammation of the blood vessels. It can affect any of the body’s blood vessels, causing a variety of symptoms and potential complications. Inflammation causes swelling of the blood vessel walls, reducing or even blocking the flow of blood to tissues and organs. The amount of damage vasculitis causes depends on which part of the body is affected.
The larger the affected blood vessels, the more damage there may be. And the more important the affected body tissue, the more serious the damage will be.
The walls of affected blood vessels can swell and bulge (this is called an aneurysm) and may even burst, causing bleeding inside your body.
Apart from the damage to the blood vessel itself, this can lead to damage in the tissues or organs that are supplied by the blood vessel.
Vasculitis can occur on its own (primary vasculitis) or with other conditions (secondary vasculitis) including rheumatoid arthritis, lupus or Sjögren's syndrome.
Silica exposure is a notorious risk factor for developing AAV, which is potentially lethal when not identified.
When we see a silicosis patient with new‐onset prolonged fever and generalized fatigue, AAV should be taken into consideration.
In conclusion, with respect to work‐related disease and potential compensation, it is essential to recognize silica exposure as a risk factor for developing AAV such as MPA.
We describe a case of pulmonary silicosis complicated by microscopic polyangiitis.
We report a case of pulmonary silicosis with P-ANCA associated microscopic polyangiitis.
Our case is unique in that both diagnoses are definitively proven histologically.
Exposure to silica should be considered in the history of patients with autoimmune diseases.
Furthermore patients with pulmonary silicosis may develop ANCA-associated vasculitis in extrapulmonary sites.
Evidence in recent years indicates that silica causes lung cancer, and probably renal disease, in addition to its well‐known relationship to silicosis.
There is also suggestive evidence that silica can cause arthritis and other auto‐immune diseases.
Silica has, therefore, joined a handful of other toxic exposures such as tobacco smoke, dioxin, and asbestos which cause multiple serious diseases.
One agent, many diseases: Exposure‐response data and comparative risks of different outcomes following silica exposure
This article collects the evidence that shows that the biological reactions to Silica are due to the stimulation of the Immune System. Both Innate and Adaptive Immunity are involved.
The following sets of events take place sequentially:
(1) Silica is recognized as a PAMP (pathogen-associated molecular pattern) by the Receptors of Innate Immunity;
(2) This causes the stimulation first and then the death of the key cells of Innate Immunity (the macrophages);
(3) While stimulated, macrophages produce cytokines (IL-1 and TNF) that stimulate fibroblasts;
(4) The same and possibly other cytokines produced by silica- activated macrophages induce the maturation of dendritic cells, which are the connecting elements between the Innate and the Adaptive (lymphoid) Immune Systems;
(5) It follows a polyclonal activation of the Adaptive Immunity;
(6) The end result is the formation of fibro-hyaline tissue.
In view of the double involvement of the Innate and the Adaptive Immune Systems and their cooperation in the stimulation of fibrosis, Silicosis can be considered as a "Collagen" Disease, related to other diseases of that group like Rheumatoid Arthritis, Lupus erythematosus and Scleroderma.
Not surprisingly the incidence of these Diseases has been shown to be significantly increased in human exposed to Silica.