Jj. Powell et al., Evidence for the role of environmental agents in the initiation or progression of autoimmune conditions, ENVIR H PER, 107, 1999, pp. 667-672
The concordance of autoimmune disease among identical twins is virtually al
ways less than 50% and often in the 25-40% range. This observation, as well
as epidemic clustering of some autoimmune diseases following xenobiotic ex
posure, reinforces the thesis that autoimmune disease is secondary to both
genetic and environmental factors. Because nonliving agents do not have gen
omes, disease characteristics involving nonliving xenobiotics are primarily
secondary to host phenotype and function. In addition, because of individu
al genetic susceptibilities based not only on major histocompatibility comp
lex differences but also on differences in toxin metabolism, lifestyles, an
d exposure rates, individuals will react differently to the same chemicals.
With these comments in mind it is important to note that there have been a
ssociations of a number of xenobiotics with human autoimmune disease, inclu
ding 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 xen
obiotics may also exacerbate an existing autoimmune disease. In this articl
e we discuss these issues and, in particular, the evidence for the role of
environmental agents in the initiation or progression of autoimmune conditi
ons. With the worldwide deterioration of the environment, this is a particu
larly important subject for human health.