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Published on: May 2, 2018
Potential occupational and environmental factors in SSc onset
Irena Walecka1, Marek Roszkiewicz2, Aleksandra Malewska2
1Dermatology Department, Central Clinical Hospital of the Ministry of the Interior and Administration, Warsaw, Poland. irena.walecka@cskmswia.pl.
Systemic sclerosis (SSc) is a fibrotic connective tissue disease. Environmental and occupational exposures, like silica and solvents, are linked to SSc onset, though more research is needed for other factors.
Area of Science:
- Rheumatology
- Environmental Medicine
- Occupational Health
Background:
- Systemic sclerosis (SSc), or scleroderma, is a rare connective tissue disease characterized by chronic, progressive fibrosis affecting multiple organ systems.
- SSc presents in subsets including diffuse SSc (dSSc), limited SSc (lSSc), and scleroderma without sclerosis (SSSC).
- The exact pathogenesis of SSc remains incompletely understood.
Purpose of the Study:
- To review and summarize current data on environmental and occupational factors implicated in the onset of Systemic Sclerosis.
Main Methods:
- This review synthesizes existing literature on known and potential environmental and occupational triggers for SSc.
- Data on factors with established correlations and those requiring further investigation were analyzed.
Main Results:
- A strong correlation exists between SSc onset and exposure to crystalline silica and various organic solvents (e.g., white spirit, aromatic solvents, chlorinated solvents, ketones, welding fumes).
- The role of other potential factors such as asbestos, air pollution, certain chemicals, silicone breast implants, smoking, drug reactions, diet, and heavy metals requires additional research.
Conclusions:
- While the complete pathogenesis of SSc is not fully elucidated, significant evidence links the disease's development to specific environmental and occupational exposures.
- Further studies are warranted to clarify the contribution of numerous other suspected environmental and occupational factors to SSc etiology.
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