Epidemiological and experimental evidence of environmental factor-related autoimmune thyroid disease: A systematic...

Environmental pollution is a significant contributor to the global burden of disease. However, its role in autoimmune thyroid disease (AITD) and associated functional disorders remains incompletely understood.

This study aims to systematically evaluate the impact of environmental factors on AITD risk and elucidate potential underlying mechanisms.

Following the PRISMA Statement, we conducted a systematic literature review by searching PubMed, Web of Science, Cochrane Library, and Embase databases to identify relevant population-based and experimental studies. Two researchers independently performed study screening, data extraction, and methodological quality assessment using the ROBINS-E tool. In cases of disagreement, a third researcher resolved discrepancies.

A total of 67 studies were included, comprising 18 addressing meteorological factors and 49 addressing environmental pollution. Overall, the evidence indicates that low temperatures, inadequate sunlight, and air pollutants (NO₂, SO₂, O₃, PM_2.5, PM₁₀, etc.) are strongly associated with elevated AITD risk. Chemical pollutants (e.g., polybrominated biphenyls and polycyclic aromatic hydrocarbons), heavy metals (lead, mercury, cadmium), and radiation exposure have been associated with increased thyroid autoantibody levels and thyroid dysfunction. Some studies indicate that vitamin D deficiency, viral infections, and smoking may mediate the relationship between environmental exposures and AITD. Mechanistically, inflammatory responses, oxidative stress, and immune cell infiltration are recognized as critical pathways.

Although current evidence suggests a correlation between diverse environmental factors and AITD occurrence, research remains limited. Modulating mitigating factors, such as reducing particulate matter emissions and supplementing vitamin D, may offer potential for prevention and adjuvant therapy. Environmental factors primarily influence the development and progression of AITD through modulation of inflammatory responses, oxidative stress, and immune cell infiltration, potentially revealing molecular mechanisms via regulation of genes such as BiP, S1PR, HIF-1, PERK, S1P, and PTP1B. Interventions targeting these molecular pathways may offer novel strategies for the prevention and treatment of environmentally associated AITD.