Xiao Xueqi, Yang Yuting, Zhang Binghua, Chi Kaiyi, He Huijuan, Guo Liyu, Pan Long, Deng Yingyu, Wang Peipei, Lin Xin, Wei Kepeng, Liang Jianpeng, Jiang Wenjuan, Jiao Meiting, Zhong Wangye, Tu Peinan, Huang Linxuan, Guan Tianwang, Wu Gaobo
The Second Clinical Medical College, Southern Medical University, Guangzhou, Guangdong, China.
The 10th Affiliated Hospital of Southern Medical University (Dongguan People's Hospital), Southern Medical University, Guangdong Provincial Key Laboratory of Cardiac Function and Microcirculation, Dongguan, Guangdong, China.
Clin Cardiol. 2025 Dec;48(12):e70235. doi: 10.1002/clc.70235.
Previous studies have not fully explored the association between air pollutants and heart failure (HF) incidence in cancer participants, nor the role of genetic susceptibility. We aimed to assess air pollutants' impact on HF risk and their joint contribution with genetic susceptibility to incident HF in this group.
This study utilized data from the UK Biobank and included 50 923 cancer participants. The relationship between air pollutants and the onset of HF was examined using a Cox proportional hazards model. Furthermore, a polygenic risk score was constructed to evaluate the comprehensive impact of air pollutant exposure, genetic susceptibility, and their interactions on the risk of HF among cancer participants.
The research results show that when comparing individuals in the lowest exposure quartile with those in the highest exposure quartile, the multivariate-adjusted HRs were 1.22 (1.07, 1.38) for PM, 1.16 (1.03, 1.32) for PM, 1.20 (1.06, 1.36) for NO, and 1.26 (1.11, 1.43) for NO. For the joint associations, cancer participants with both high genetic risk and elevated air pollutant exposure exhibited the highest risk of HF events. The risk estimates for the incidence of HF were 2.06 (1.52, 2.78) for PM 1.70 (1.27, 2.27) for PM 1.77 (1.32, 2.37) for NO, and 1.61 (1.21, 2.13) for NO.
Our findings indicate that long-term combined exposure to multiple air pollutants, including PM, PM, NO, and NO, is associated with an elevated risk of new-onset HF in cancer patients, particularly among individuals with a high genetic predisposition to the disease.
以往研究尚未充分探讨空气污染物与癌症患者心力衰竭（HF）发病率之间的关联，也未涉及遗传易感性的作用。我们旨在评估空气污染物对该组患者HF风险的影响及其与遗传易感性对HF发病的联合作用。
本研究利用英国生物银行的数据，纳入了50923名癌症患者。使用Cox比例风险模型检验空气污染物与HF发病之间的关系。此外，构建了多基因风险评分，以评估空气污染物暴露、遗传易感性及其相互作用对癌症患者HF风险的综合影响。
研究结果显示，将暴露于最低四分位数的个体与最高四分位数的个体进行比较时，PM的多变量调整后风险比（HR）为1.22（1.07，1.38），PM为1.16（1.03，1.32），NO为1.20（1.06，1.36），NO为1.26（1.11，1.43）。对于联合关联，遗传风险高且空气污染物暴露升高的癌症患者发生HF事件的风险最高。HF发病率的风险估计值，PM为2.06（1.52，2.78），PM为1.70（1.27，2.27），NO为1.77（1.32，2.37），NO为1.61（1.21，2.13）。
我们的研究结果表明，长期联合暴露于多种空气污染物，包括PM、PM、NO和NO，与癌症患者新发HF风险升高相关，尤其是在对该疾病具有高遗传易感性的个体中。
