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

Abstract

The concordance of autoimmune disease among identical twins is virtually always less than 50% and often in the 25-40% range. This observation, as well as epidemic clustering of some autoimmune diseases following xenobiotic exposure, reinforces the thesis that autoimmune disease is secondary to both genetic and environmental factors. Because nonliving agents do not have genomes, disease characteristics involving nonliving xenobiotics are primarily secondary to host phenotype and function. In addition, because of individual genetic susceptibilities based not only on major histocompatibility complex differences but also on differences in toxin metabolism, lifestyles, and exposure rates, individuals will react differently to the same chemicals. With these comments in mind it is important to note that there have been associations of a number of xenobiotics with human autoimmune disease, including mercury, iodine, vinyl chloride, canavanine, organic solvents, silica, l-tryptophan, particulates, ultraviolet radiation, and ozone. In addition, there is discussion in the literature that raises the possibility that xenobiotics may also exacerbate an existing autoimmune disease. In this article we discuss these issues and, in particular, the evidence for the role of environmental agents in the initiation or progression of autoimmune conditions. With the worldwide deterioration of the environment, this is a particularly important subject for human health.

Occupational exposures at a polyvinyl chloride production facility are associated with significant changes to the plasma metabolome

“…VC exposure has been linked to several pathologies including a variety of cancers (Makk et al, 1974; Mastrangelo et al, 2004; Ruckart et al, 2015), liver disease (Cave et al, 2010), and autoimmune diseases (Powell et al, 1999). In the present study, we performed metabolomics analyses of plasma samples to obtain a comprehensive view of the alterations of metabolism in individuals who were exposed to VC and other chemicals, without developing cancer.…”

Drugs and autoimmunity – A contemporary review and mechanistic approach

“…It was shown, using a mouse strain that is deficient for the FcRg-chain or FcgRIII, that Fc-receptors can be important in the determining activation or inhibition of immune responses [78]. Others substances associated with autoimmunity include iodine [79,80], vinyl chloride [81], canavanine [82], organic solvents [83], L-tryptophan [79], anilides [84], vaccines, microbials, and a variety of pollutants including particulate silica [85], airborne particulate pollution, ozone [86], and ultraviolet radiation [87,88]. The current swine flu pandemic has renewed interest in the role of vaccine induced autoimmunity [89], as we recollect the high association between the influenza vaccine used in the last swine flu epidemic and Gullain Barre syndrome [90].…”

Autoimmunity and environmental factors in the pathogenesis of primary biliary cirrhosis

“…For example, some metals can induce autoimmune reactions by creating new high af®nity sites for MHC determinants on selfepitopes (56). The chronic presence of the self-protein serves to perpetuate the immune response initiated by the xenobiotic-induced adduct and leads to autoimmunity (59,60). For example, in murine models, SLE can be elicited with an isoaspartyl-modi®ed form of self-antigen (61).…”