Introduction
Environmental factors combined with genetic susceptibility are largely believed to be essential working partners in the development of autoimmune disease [1–4]. The term ‘environmental factors’ or ‘environmental agents’ in the discussion of the pathogenesis of autoimmune disease, is a blanket term to address environmental components such as microbial agents, vaccines, diet, drug exposure, heavy metals, ultraviolet radiation and smoking, among many others [3–9]. Monozygotic concordance rates below 50% are indicative that environment as well as genetics are involved [10–13]. As well, studies on genetically similar populations living under different conditions have demonstrated different incidence rates of autoimmune disease. The induction of autoimmune disease by these exposures may be through various mechanisms such as the alteration of autoantigen structure, altered expression of antigens, stimulatory effects on the immune system, T-cell dysregulation, apoptosis-mediated autoimmunity, molecular mimicry and immunological cross-reactivity [5, 14–18].
Cigarette smoking is one example of non-infectious agents which have been studied in rheumatoid arthritis (RA), autoimmune thyroiditis, inflammatory bowel disease, and primary biliary cirrhosis (PBC) [19–22]. Cigarette smoke has been shown to increase the production of pro-inflammatory cytokines, and reduce the levels of anti-inflammatory cytokines. Free radicals contained in cigarette smoke can provoke cellular destruction and release of intracellular autoantigens. Various toxins found within cigarette smoke may cause DNA damage and genetic mutations, as well as stimulate autoreactive T cells [21]. An alteration in oestrogen metabolism, which has been indicated as a feature in autoimmune disease, has also been found to occur in active smokers [23, 24]. However, the effect of tobacco smoke in the loss of self-tolerance may be more complicated, as it appears that smoking abstinence exacerbates gastrointestinal symptoms in patients with ulcerative colitis (UC). Such an effect has not been noted in patients with Crohn’s disease, the other major inflammatory bowel disease.
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Silica exposure has also been investigated as a factor involved in autoimmune disease [12, 25, 26]. Silica has been linked with scleroderma, RA, vasculitis and systemic lupus erythematosus (SLE) [12, 25, 26]. Silica acts as an immune stimulant, increasing pro-inflammatory cytokine production, as well as inducing apoptosis and necrosis [12, 25, 26]. Interestingly, silica has also been shown to increase autoantibody production [27] and immune complex formation in animal models. Animals exposed to silica have demonstrated increases in B and CD4 T cell counts, as well as altering T helper and T regulatory cell ratios [28]. Apart from silica, exposure to solvents such as trichloroethylene, mineral spirits, and petroleum based products have been linked to scleroderma and other undifferentiated connective tissue diseases [29].
Primary biliary cirrhosis is one autoimmune disease in which multiple environmental factors have been implicated. Hair dyes have been added to this list, but very few studies address these compounds. Hair dyes have been previously explored in relation to SLE, both epidemiologically and immunologically. This review will examine the literature surrounding the use of hair dyes in SLE in relation to PBC. As PBC and SLE very rarely co-occur in an affected individual, the effect of hair dyes in either disease may help us understand the complex role of these compounds as environmental triggers of autoimmunity.
