Aug 2026· Journal of Autoimmunity· Vol 163, pp.
103606
· 0 citations· 51 references
Medicine
TL;DR
UHI exposure may be a modifiable environmental risk factor for RA and provide new insights into the biological mechanisms underlying this association, with proteomic analyses suggested that this association may involve not only canonical immune-inflammatory pathways, but also hypoxia response and protein transport.
Abstract
Background
Urban heat island (UHI) exposure is an increasingly common consequence of urbanization and climate warming, but its association with rheumatoid arthritis (RA) risk remains unclear.
Objective
To investigate the association between UHI exposure and incident RA, and to further assess the roles of genetic susceptibility and plasma proteomic profiles in this association.
Methods
This study included 400,628 urban residents with UHI exposure data and free of RA at baseline. Cox proportional hazards models were used to evaluate the association between UHI exposure and incident RA. Polygenic risk scores were used to assess effect modification by genetic susceptibility. Proteomic analyses identified candidate proteins and enriched pathways underlying the association. Mendelian randomization, colocalization, and mediation analyses assessed causal relevance and mediation.
Results
Over a median follow-up of 14.05 years, 5397 incident RA cases were documented. Each standard-deviation increase in UHI exposure was associated with a 17% higher risk of RA. This association was more pronounced among older adults and individuals with lower socioeconomic status. An additive interaction was observed between UHI exposure and genetic risk for RA. Proteomic analyses suggested that this association may involve not only canonical immune-inflammatory pathways, but also hypoxia response and protein transport, with CD40, VCAM1, and SUGP1 emerging as potential molecular mediators.
Conclusions
UHI exposure may be a modifiable environmental risk factor for RA and provide new insights into the biological mechanisms underlying this association.
Findings underscore the crucial role of residential environmental factors in the risk of arthritis development and have important implications for public health policies aimed at reducing the prevalence of arthritis.
Xiangbin Jia, Xin Xiong, Zi-Chao Jiang et al.· Journal of Global Health· 0 citations
It is suggested that a moderate reduction in risk factor exposure achieved a preventive impact comparable to total eradication, supporting the potential for efficient public health strategies.
It is demonstrated that genomic susceptibility is organised into biologically distinct profiles defined by coordinated variant, gene, pathway, and cumulative risk signals, which provides a practical basis for risk stratification and supports the application of genomics in personalised medicine.
Bana Sarahbibi Mohmedsalim, Subhabrata Sarkar, Sukanta Bandyopadhyay et al.· Genetics and Molecular Resea...· 0 citations
It is suggested that long-term air pollution exposure is associated with incident RA risk and that systemic metabolic perturbations may represent potential biological pathways underlying this association.
Yang-Chang Zhang, Tian Liang, Yang Pu et al.· Frontiers in Public Health· 0 citations
Available evidence suggests that genetic variants are involved in the association between air pollution exposure and CV adverse events, which could provide further knowledge of the etiology of CVD, offering new tools for targeted prevention and treatment of more susceptible subjects from a more personalized medicine po...
M. Gaggini, C. Vassalle· International Journal of Mol...· 0 citations
Long-term exposure to air pollutants, particularly NO2 and PM10, is associated with an increased risk of microvascular complications among individuals with diabetes, and the observed risk appears to be persistent and may begin at relatively low exposure levels, underscoring the need for preventive strategies targeting...