Xu Hongli, Chen Weiwei, Sun Jinjun
Department of Tuberculosis, Affiliated Hospital of Shaoxing University, Zhejiang, China.
Front Public Health. 2025 Apr 4;13:1548401. doi: 10.3389/fpubh.2025.1548401. eCollection 2025.
This study aims to shed light on the connection of urinary exposures with risk of chronic obstructive pulmonary disease (COPD) among smokers, thereby providing scientific evidence for the prevention and intervention of COPD.
Data of the National Health and Nutrition Examination Survey (NHANES) 2007-2016 were utilized, including 3,973 smokers aged 20 or older. We employed the weighted multivariate logistic and weighted quantile sum (WQS) regression models to delve into the link of urinary concentrations of exposures to COPD risk. Additionally, restricted cubic spline regression was utilized to examine the dose-response relationship between biomarker concentrations and COPD risk. The stability of the associations across different participant characteristics was evaluated through subgroup and mediation analyses.
Our study encompassed a total of 3,973 participants, of whom 472 were diagnosed with COPD. Regression analyses revealed the inverse association between urinary concentrations of benzophenone-3 (BP-3) and propyl paraben (PrP) and COPD risk. Higher quartiles of BP-3 and PrP exhibited lower COPD incidence [BP-3: odds ratio (OR) = 0.64, 95% confidence interval (95%CI) (0.47, 0.89), = 0.007; PrP: OR = 0.56, 95%CI (0.36, 0.86), = 0.008]. Significant synergistic interactions among urinary exposures were observed [WQS: 0.75, 95%CI (0.65, 0.88), = 0.026], with BP-3 and PrP contributing 40.31 and 40.01% to the weighted analysis, respectively. Mediation analysis proved that inflammatory markers, such as white blood cell (WBC) count and neutrophil-to-lymphocyte ratio (NLR), significantly mediated the association between BP-3, PrP, and COPD risk (all -values <0.05).
BP-3 and PrP in environmental exposure in smokers have an inverse correlation with COPD risk, with WBC and NLR partially mediating this association.
本研究旨在揭示吸烟者尿液暴露与慢性阻塞性肺疾病(COPD)风险之间的联系,从而为COPD的预防和干预提供科学依据。
利用2007 - 2016年国家健康与营养检查调查(NHANES)的数据,其中包括3973名20岁及以上的吸烟者。我们采用加权多元逻辑回归和加权分位数和(WQS)回归模型来探究尿液中暴露物质浓度与COPD风险之间的联系。此外,使用受限立方样条回归来检验生物标志物浓度与COPD风险之间的剂量反应关系。通过亚组分析和中介分析评估不同参与者特征之间关联的稳定性。
我们的研究共纳入3973名参与者,其中472人被诊断为COPD。回归分析显示,尿液中二苯甲酮 - 3(BP - 3)和对羟基苯甲酸丙酯(PrP)的浓度与COPD风险呈负相关。BP - 3和PrP的较高四分位数显示出较低的COPD发病率[BP - 3:优势比(OR)= 0.64,95%置信区间(95%CI)(0.47,0.89),P = 0.007;PrP:OR = 0.56,95%CI(0.36,0.86),P = 0.008]。观察到尿液暴露之间存在显著的协同相互作用[WQS:0.75,95%CI(0.65,0.88),P = 0.026],BP - 3和PrP在加权分析中分别贡献40.31%和40.01%。中介分析证明,炎症标志物,如白细胞(WBC)计数和中性粒细胞与淋巴细胞比值(NLR),显著介导了BP - 3、PrP与COPD风险之间的关联(所有P值<0.05)。
吸烟者环境暴露中的BP - 3和PrP与COPD风险呈负相关,白细胞和中性粒细胞与淋巴细胞比值部分介导了这种关联。