Qian Jing, Zhu Jiahao, Wang Yifan, Dai Ruoqi, Miao Jingyou, Yang Ye, Zhao Wenxia, Wang Jing, Ding Lilu, Zhou Dan, Yu Min, Li Yingjun
Department of Epidemiology and Health Statistics, School of Public Health, Hangzhou Medical College, Hangzhou, China.
Department of Psychology, University of Toronto Scarborough, Toronto, Canada.
Ecotoxicol Environ Saf. 2025 Jan 15;290:117770. doi: 10.1016/j.ecoenv.2025.117770. Epub 2025 Jan 22.
The influence of air pollution on osteoarthritis (OA) remains underexplored.
We conducted a prospective cohort study in the UK Biobank, estimating exposure levels of particulate matter (PM, PM, PM) nitrogen oxides (NO, NO), and air pollutants exposure score (APES). Cox models assessed associations between air pollution exposure and OA incidence, joint replacement, and survival. Additionally, using genome-wide association statistics, we examined the potential causal associations between air pollution-related DNA methylation (DNAm) and OA risk. Gene-environment interaction analyses were conducted to explore the potential modification effect of DNA methylation-related genetic variants on the impact of air pollution on OA risk.
Individual exposure to each air pollutant was associated with an increased risk of developing OA, but not with progression from OA to joint replacement. For APES, the hazard ratio for incident OA was 1.09 (95 % CI = 1.04-1.13), and the hazard ratio of progression from OA to death was 1.16 (95 % CI = 1.00-1.35) in the highest quartile group compared to the lowest quartile group. Moreover, genetically predicted methylation at the PM-related CpG site cg04027612 near the GDF5 gene was associated with a lower risk of OA. A potential epigenetic modification effect of cg04027612 near GDF5 on OA risk was observed.
Long-term exposure to air pollution was associated with an increased risk of OA in the population and poorer survival outcomes for OA patients, with epigenetic changes in GDF5 potentially playing a role in the underlying mechanisms.
空气污染对骨关节炎(OA)的影响仍未得到充分研究。
我们在英国生物银行进行了一项前瞻性队列研究,估计了颗粒物(PM、PM、PM)、氮氧化物(NO、NO)的暴露水平以及空气污染暴露评分(APES)。Cox模型评估了空气污染暴露与OA发病率、关节置换和生存率之间的关联。此外,我们使用全基因组关联统计数据,研究了空气污染相关的DNA甲基化(DNAm)与OA风险之间的潜在因果关联。进行了基因-环境相互作用分析,以探讨DNA甲基化相关基因变异对空气污染对OA风险影响的潜在修饰作用。
个体接触每种空气污染物都与患OA的风险增加相关,但与OA进展为关节置换无关。对于APES,在最高四分位数组与最低四分位数组相比,新发OA的风险比为1.09(95%CI = 1.04-1.13),从OA进展到死亡的风险比为1.16(95%CI = 1.00-1.35)。此外,在GDF5基因附近与PM相关的CpG位点cg04027612处的基因预测甲基化与较低的OA风险相关。观察到GDF5附近的cg04027612对OA风险有潜在的表观遗传修饰作用。
长期暴露于空气污染与人群中OA风险增加以及OA患者较差的生存结果相关,GDF5的表观遗传变化可能在潜在机制中起作用。