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. 2014 Aug 15;15(8):14269–14297. doi: 10.3390/ijms150814269

Table 2.

Panel findings studies of animal models in the role of environmental factors and development of autoimmune disease.

We Are Confident of the Following We Consider the Following Likely, but Requiring Confirmation Broad Themes to Be Pursued in Future Investigations
Forms of inorganic mercury (HgCl2, vapor, amalgam) induce systemic autoimmune disease in rats (transient) and mice, and exacerbates systemic autoimmune disease in lupus-prone mice;
Several mineral oil components and certain other hydrocarbons can induced an acute inflammatory arthritis in some rat strains;
The mineral oil component 2,6,10,14-tetramethylpentadecane (TMPD or pristane) induces lupus-like disease and inflammatory arthritis in several strains of mice;
For a limited number of pathogens there is a clear association with development of autoimmune diseases;
Excess iodine increases the incidence of autoimmune thyroiditis in genetically predisposed animal models.
Gold causes (transient) nephropathy in rats. Gold and silver cause autoimmune responses, but not autoimmune disease, in mice; but the ability of silver and gold to exacerbate spontaneous autoimmune disease requires study;
Silica exacerbates autoimmune disease but more studies are needed using more species/strains and a wider range of doses and exposure routes;
Trichloroethylene (TCE) exacerbates systemic autoimmunity although responses are often limited and transient. Studies of autoimmune liver disease are needed with additional species/strains and in developmental studies;
TCDD exposure during fetal or early neonatal development may promote autoimmunity;
Organochlorine pesticides may enhance lupus-like disease in a predisposed mouse strain;
Sunlight/ultraviolet (UV) light exposure exacerbates lupus in genetically prone mice.
Studies should be “shaped by what is observed in humans, not by what is possible in mice” [53];
Studies should not be restricted to a “gold standard” animal model. Multiple models should be investigated to reflect human genetic heterogeneity;
When using spontaneous disease models it is important to consider whether environmental exposures directly impacts idiopathic autoimmunity, or reflects environmental factor-specific autoimmunity;
More studies on the effects of environmental factor exposure on expression of autoimmunity during different stages of life (gestational to adulthood) are needed.