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Pollard, Kenneth Michael. ?Environment, Autoantibodies, and Autoimmunity.? Frontiers in Immunology 6 (2015): 60. PMC. Web. 27 Mar. 2015. Introduction
Susceptibility to autoimmune disease is multifactorial and includes genetic predisposition, gender, ethnicity, age, and environment. While no single factor has been identified as preeminent, the role of the environment has garnered increasing interest. This reflects the ubiquitous nature of the environment, which encompasses everything around us including the air we breathe, the water we drink, the food we eat, synthetic and natural chemicals, microorganisms, industrial by-products, and physical factors such as radiation (1). The most convincing evidence for a role of exogenous factors in autoimmunity comes from studies implicating numerous medications in the induction of autoimmune disease, particularly the association of drug-induced systemic lupus erythematosus (SLE) with procainamide and hydralazine (2). Identification of the causal role of medications in the induction of autoimmune disease is due in large part to the fact that medications are taken under medical supervision where drug exposure and possible side effects can be closely monitored. This is not the case with non-therapeutic exposure to environmental factors where contact may include numerous exogenous factors at any particular time. Nonetheless, evidence for the association of (non-therapeutic) environmental exposure with autoimmunity has come from two well documented exposures...
... Conclusion
Strong evidence that environmental exposure can cause autoimmune disease comes from epidemiologic studies showing the association between a diversity of environmental exposures and an assortment of autoimmune diseases. This is further supported by the observation that gender ratios may differ from that of idiopathic autoimmune disease due to the occupational nature of exposure. Progress, however, in identifying and characterizing the presumably large number of environmental factors is hampered by the lack of accepted criteria for diagnosis and/or classification of environmentally associated autoimmunity. Postulated mechanisms suggest that specific types of exposures lead to specific outcomes in both humans and animal models. Environmental exposures can also commonly result in immune activation and autoimmunity without evidence of a defined autoimmune disease. The best example is exposure to mercury, which in humans and animal models, produces autoimmunity and tissue pathology that is mild in severity. Greater understanding of how different environmental exposures result in different disease phenotypes and varying degrees of severity will help identify the mechanisms and checkpoints that control development of autoimmunity and autoimmune disease...
Susceptibility to autoimmune disease is multifactorial and includes genetic predisposition, gender, ethnicity, age, and environment. While no single factor has been identified as preeminent, the role of the environment has garnered increasing interest. This reflects the ubiquitous nature of the environment, which encompasses everything around us including the air we breathe, the water we drink, the food we eat, synthetic and natural chemicals, microorganisms, industrial by-products, and physical factors such as radiation (1). The most convincing evidence for a role of exogenous factors in autoimmunity comes from studies implicating numerous medications in the induction of autoimmune disease, particularly the association of drug-induced systemic lupus erythematosus (SLE) with procainamide and hydralazine (2). Identification of the causal role of medications in the induction of autoimmune disease is due in large part to the fact that medications are taken under medical supervision where drug exposure and possible side effects can be closely monitored. This is not the case with non-therapeutic exposure to environmental factors where contact may include numerous exogenous factors at any particular time. Nonetheless, evidence for the association of (non-therapeutic) environmental exposure with autoimmunity has come from two well documented exposures...
... Conclusion
Strong evidence that environmental exposure can cause autoimmune disease comes from epidemiologic studies showing the association between a diversity of environmental exposures and an assortment of autoimmune diseases. This is further supported by the observation that gender ratios may differ from that of idiopathic autoimmune disease due to the occupational nature of exposure. Progress, however, in identifying and characterizing the presumably large number of environmental factors is hampered by the lack of accepted criteria for diagnosis and/or classification of environmentally associated autoimmunity. Postulated mechanisms suggest that specific types of exposures lead to specific outcomes in both humans and animal models. Environmental exposures can also commonly result in immune activation and autoimmunity without evidence of a defined autoimmune disease. The best example is exposure to mercury, which in humans and animal models, produces autoimmunity and tissue pathology that is mild in severity. Greater understanding of how different environmental exposures result in different disease phenotypes and varying degrees of severity will help identify the mechanisms and checkpoints that control development of autoimmunity and autoimmune disease...