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Evidence for the Role of Environmental Agents in the
Initiation or Progression of Autoimmune Conditions
Jonathan J. Powell, Judy Van de Water, and M. Eric
Gershwin
Division of Rheumatology/Allergy and Clinical
Immunology, University of California at Davis School of Medicine, Davis,
California USA
http://ehpnet1.niehs.nih.gov/docs/1999/suppl-5/667-672powell/abstract.html
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. Key
words: autoimmunity, environmental agents, MHC, pollution, self-antigen,
xenobiotic -- Environ Health Perspect 107(suppl 5):667-672 (1999).
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