Lan Rui, Li Xue, Chen Xiangjun, Hu Jinbo, Luo Wenjin, Lv Liangjing, Shen Yan, Qin Yao, Mao Lina, Ye Hanwen, Li Qifu, Wang Zhihong
Department of Endocrinology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Tob Induc Dis. 2023 May 10;21:58. doi: 10.18332/tid/162607. eCollection 2023.
A large number of people around the world are exposed to the risks of passive smoking. This prospective study aimed to examine the association between secondhand smoke exposure, exposure time, and the incidence of chronic kidney disease (CKD) and determine whether this association was influenced by genetic susceptibility.
The study included 214244 participants of the UK Biobank who were initially free of CKD. Cox proportional hazards model was used to estimate the associations between secondhand smoke exposure time and the risks of CKD in people who have never smoked. The genetic risk score for CKD was calculated by a weighted method. The likelihood ratio test comparing models was used to examine the cross-product term between secondhand smoke exposure and genetic susceptibility to CKD outcomes.
During a median of 11.9 years of follow-up, 6583 incidents of CKD were documented. Secondhand smoke exposure increased the risk of CKD (HR=1.09; 95% CI: 1.03-1.16, p<0.01), and a dose-response relationship between CKD prevalence and secondhand smoke exposure time was found (p for trend<0.01). Secondhand smoke exposure increases the risk of CKD even in people who never smoke and have a low genetic risk (HR=1.13; 95% CI: 1.02-1.26, p=0.02). There was no statistically significant interaction between secondhand smoke exposure and genetic susceptibility to CKD (p for interaction=0.80).
Secondhand smoke exposure is associated with higher risk of CKD, even in people with low genetic risk, and the relationship is dose dependent. These findings change the belief that people with low genetic susceptibility and without direct participation in smoking activities are not prone to CKD, emphasizing the need to avoid the harm of secondhand smoke in public places.
全球大量人群面临被动吸烟风险。这项前瞻性研究旨在探讨二手烟暴露、暴露时间与慢性肾脏病(CKD)发病率之间的关联,并确定这种关联是否受遗传易感性影响。
该研究纳入了英国生物银行的214244名最初无CKD的参与者。采用Cox比例风险模型来估计从不吸烟人群中二手烟暴露时间与CKD风险之间的关联。通过加权法计算CKD的遗传风险评分。使用比较模型的似然比检验来研究二手烟暴露与CKD结局遗传易感性之间的交叉乘积项。
在中位随访11.9年期间,记录了6583例CKD事件。二手烟暴露增加了CKD风险(HR = 1.09;95% CI:1.03 - 1.16,p < 0.01),并且发现CKD患病率与二手烟暴露时间之间存在剂量反应关系(趋势p < 0.01)。即使在从不吸烟且遗传风险较低的人群中,二手烟暴露也会增加CKD风险(HR = 1.13;95% CI:1.02 - 1.26,p = 0.02)。二手烟暴露与CKD遗传易感性之间没有统计学上的显著交互作用(交互作用p = 0.80)。
二手烟暴露与较高的CKD风险相关,即使在遗传风险较低的人群中也是如此,并且这种关系是剂量依赖性的。这些发现改变了认为遗传易感性低且未直接参与吸烟活动的人不易患CKD的观念,强调了在公共场所避免二手烟危害的必要性。