Asbestos is a well-known hazardous substance that causes occupational and environmental diseases including asbestosis (lung fibrosis). Silica exposure which causes silicosis (another type of lung fibrosis) has long been linked to the development of autoimmune diseases; however, there are few studies on the relationship between asbestos exposure and autoimmune diseases.
A total of 54 individuals who had worked in a former asbestos textile factory underwent autoantibody-related blood tests, chest X-ray imaging, and pulmonary function tests. Based on the job exposure matrix (JEM), the estimated asbestos exposure concentrations were determined, and the presence of asbestosis was determined by chest radiography.
Scleroderma (Scl-70) and ribonucleoprotein (RNP) antibodies were significantly lowered in the pleural plaque present group than in the absent group. Additionally, Scl-70, RNP, and Sjögren's syndrome type B (SS-B) antibodies were significantly lowered in the asbestosis present group. When stratifying variables with or without asbestosis, Scl-70, Smith, SS-B, and RNP antibodies decreased in female, crocidolite handling group, and higher estimated asbestos exposure level group.
Contrary to our expectations that autoantibody titers would be higher in groups with high asbestos exposure or in the asbestosis group, those with asbestosis showed lower titers. But as our research has some methodological limitations, the lowered titer of autoimmune antibody in our asbestos exposed subjects could not be simply interpreted as a lowered risk of autoimmune diseases. So careful interpreting should be taken when examine autoantibodies to screening or diagnose autoimmune diseases in people with asbestos exposure. In addition, it is necessary to establish relevance of asbestosis and autoantibodies through further studies of larger scale and higher confidence levels.
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The International Agency for Research on Cancer classifies asbestos as belonging to Carcinogen Group 2A for gastric cancer. We herein report a case of gastric cancer associated with asbestosis and describe the work-related and risk assessments of asbestos exposure for gastric cancer.
The 66-year-old male patient in our case worked in asbestos spinning factories. His level of cumulated asbestos fiber exposure was estimated to be 38.0–71.0 f-yr/cc. Thus, the Excess Life Cancer Risk for lung cancer associated with asbestos exposure was 9,648×10−5, almost 9,600 times the value recommended by the United States of America Environmental Protection Agency (1 × 10−5). The relative risk of developing lung cancer for this patient was more than 25 f-yr/cc, a well-known criterion for doubling the risk of lung cancer.
The patient’s exposure to high-dose asbestos was sufficient to increase his risk of gastric cancer because as the risk of lung cancer increased, the risk of gastric cancer was due to increase as well. Therefore, occupational asbestos fiber exposure might be associated with gastric cancer in this case.
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