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To the Editors: Autoimmune diseases can be defined as clinical syndromes caused by the activation of T-cells or B-cells, or both, in the absence of an ongoing infection or other discernible cause 1. These cells recognise specific foreign antigens but even in healthy individuals they possess a low-level of autoreactivity towards own antigens. Autoreactivity is increased in autoimmune diseases either systemically (as in rheumatoid arthritis) or organ-specifically (Graves’ disease and type 1 diabetes mellitus). These diseases are diagnosed by clinical symptoms and by specific types of autoantibodies. The prevalence of autoimmune diseases ranges from 5–10% of the population in Western countries, including common diseases, such as rheumatoid arthritis and autoimmune thyroiditis, and many rare ones 2. Epidemiological studies have demonstrated that genetic factors are crucial determinants of susceptibility to autoimmune disease 1. For many of these diseases a familial clustering is reported. However, even in a genetically predisposed person, some trigger, an environmental exposure or a change in the internal environment, is usually required to precipitate autoreactivity 3. Smoking is an environmental risk factor for some autoimmune diseases, including rheumatoid arthritis, systemic lupus erythematosus, Graves’ disease and primary biliary cirrhosis, but for many other autoimmune diseases data on smoking are either lacking or controversial. Chronic obstructive pulmonary disease (COPD) is a slowly progressive disease characterised by irreversible airflow limitation, which is caused by chronic inflammatory immune response to inhaled gases and particles 4. It may affect up to 10% of the population. In the early phase, the inflammatory process is located in central airways but in progressive disease the distal airspaces are enlarged because of …
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Hemminki et al. (2011) studied this question.
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