Environmental factors in polymyalgia rheumatica and giant cell arteritis

Introduction.Polymyalgia rheumatica (PMR) and giant cell arteritis (GCA) are closely inter-related inflammatory conditions predominantly affecting individuals over 50 years of age.A significant geographic and demographic variability, with higher incidence rates in Caucasian patients of Northern European ancestry has been reported for both.Genetic predisposition, epigenetic alterations, immune system senescence, age-related changes of hypothalamic-pituitary-adrenal axis function, and environmental factors are theorised to influence disease susceptibility in PMR and GCA.Methods.This narrative review synthesises the current evidence regarding environmental factors implicated in the pathogenesis of PMR and GCA.Relevant keywords, including "polymyalgia rheumatica", "giant cell arteritis", "environment", "gene-environment interaction", "precipitating factors" were used to search PubMed and Scopus databases.Results.Immunogenic bacterial and viral infections with respiratory and neurotropic affinity, ultraviolet (UV) radiation, vitamin D deficiency, air pollution and cigarette smoking have been considered as trigger factors of PMR/GCA although with mixed results.Seasonal variations have been inconsistently linked to disease onset, with hypotheses ranging from infectious outbreaks in winter to UV-induced vascular inflammation in summer.Air pollution, particularly particulate matter (PM10), has been associated with increased GCA incidence, potentially through inflammatory amplification in predisposed individuals.Recent emerging evidence also implicates vaccines and immune checkpoint inhibi-tors as triggers for PMR and GCA-like syndromes, potentially through mechanisms of heightened immune activation.Conclusions.The interplay between genetic and environmental factors, including possible epigenetic effects, highlights the complex immune pathophysiology of PMR and GCA.While some progress has been made in identifying triggers, many mechanisms remain unclear.Further research is necessary to elucidate causative pathways and early steps potentially informing preventive strategies.