Environmental factors and rheumatic diseases.

Abstract

The pathogenesis and pathophysiology of rheumatic diseases is complex and relies on the interaction of different factors. The common view is that the pathological autoimmunity develops in genetically predisposed individuals upon exposure to an environmental trigger. This highlights the importance of recognizing and deconstructing the effects of environmental agents in rheumatic diseases. Several factors have been identified in the last decades, with detrimental or protective effects, impacting not only on disease onset, but also on its natural history. Cigarette smoking has been identified as one of the strongest environmental risk factors, being associated with disease development and severity for several rheumatic diseases, including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and spondyloarthropathies. Moreover, other airborne pollutants, such as silica, solvents, asbestos and metals are recognized risk factors for rheumatic diseases. The effect of some other agents is however not straightforward, of which a remarkable example is alcohol consumption. Alcohol has been associated with both pro- and anti-inflammatory effects, exerting a variable effect on rheumatic diseases depending on quantity and frequency of consumption, as well as sex and ethnicity. Similarly, ultraviolet light exposure has been associated with a higher risk of SLE but lower risk of RA. The relationship between microbial exposure and autoimmunity is also complex: while some infectious agents increase the risk of rheumatic diseases, it is widely accepted that less exposure to microbial agents, particularly during immune system development, increases the risk of autoimmunity. Furthermore, in recent years the spotlight has switched to the human microbiome, as alterations in organ-specific microbiome composition are anticipated to be early participants in the onset of immune-mediated illnesses. The aim of this review is to highlight the most relevant environmental factors and their role in Rheumatology, with a specific focus on proposed pathophysiological effect and correlation with clinical outcomes.