Lin Baihao, Liu Wanlu, Wang Hank-Han, Qian Haixia, Zhu Xinyu, Xu Mengya, Zheng Yuyu, Alhazmi Nada, Bai Yansen
School of Public Health, Guangzhou Medical University, Xinzao, Panyu District, Guangzhou, China.
Departments of Biochemistry, Case Western Reserve University School of Medicine, Cleveland, OH, USA.
Ecotoxicol Environ Saf. 2025 Jan 1;289:117496. doi: 10.1016/j.ecoenv.2024.117496. Epub 2024 Dec 9.
Preserved ratio impaired spirometry (PRISm) and airflow obstruction are recognized as critical early signs of chronic obstructive pulmonary disease (COPD). While these conditions arise from concurrent exposure to toxicants and essential nutrients, how vitamin D modifies the pulmonary toxicity induced by polycyclic aromatic hydrocarbons (PAHs) and the metabolic mechanisms involved is still unclear.
Based on the National Health and Nutrition Examination Survey (NHANES) 2007-2012, data on urinary PAH metabolites (ΣOH-PAHs), serum vitamin D metabolite levels [Σ25(OH)D], and pulmonary function tests [forced expiratory volume in one second (FEV1), forced vital capacity (FVC) and FEV1/FVC] from 2189 participants, including 369 subjects with early lung dysfunction, defined as PRISm or airflow obstruction. Multiple metabolic disorder indicators were calculated using biochemical markers. The interaction effects between vitamin D and PAHs were evaluated using multiple linear and logistic regression models. Causal mediation analyses and structural equation modeling were employed to investigate the mediating roles of metabolic indicators.
PAHs and vitamin D had opposite effects on lung function parameters [FEV1: β (95 CIs) = -0.01 (-0.02, -0.01) vs. 0.01 (0.01, 0.04); FVC: β (95 CIs) = -0.01 (-0.02, 0.01) vs. 0.04 (0.01, 0.06)] and risk of early lung dysfunction [OR (95 CIs) = 1.22 (1.06, 1.40) vs. 0.52 (0.37, 0.73)]. Decreased associations of ΣOH-PAHs with FEV1, FVC, and early lung dysfunction, as well as with metabolic score-visceral adiposity index (MSV) were visualized with increased Σ25(OH)D among subjects with body mass index (BMI) < 28 kg/m. Furthermore, 2.18 %, 18.20 %, 5.70 %, and 4.70 % of the associations of co-exposure to ΣOH-PAHs and Σ25(OH)D with FEV1, FVC, FEV1/FVC, and early lung dysfunction disease were mediated by MSV.
Our findings indicated that vitamin D antagonizes the hazardous effects of PAHs on early lung dysfunction by metabolic alteration, providing new insight into the identification of the underlying high-risk populations and accessible prevention and intervention measures for attenuating PAH-induced lung dysfunction.
肺功能测定比率降低（PRISm）和气流阻塞被认为是慢性阻塞性肺疾病（COPD）的关键早期迹象。虽然这些情况是由于同时接触有毒物质和必需营养素引起的，但维生素D如何改变多环芳烃（PAHs）诱导的肺毒性以及其中涉及的代谢机制仍不清楚。
基于2007 - 2012年美国国家健康与营养检查调查（NHANES），收集了2189名参与者的尿多环芳烃代谢物（ΣOH - PAHs）、血清维生素D代谢物水平[Σ25(OH)D]以及肺功能测试数据[一秒用力呼气量（FEV1）、用力肺活量（FVC）和FEV1/FVC]，其中包括369名早期肺功能障碍患者，定义为PRISm或气流阻塞。使用生化标志物计算多种代谢紊乱指标。使用多元线性和逻辑回归模型评估维生素D和多环芳烃之间的相互作用。采用因果中介分析和结构方程模型来研究代谢指标的中介作用。
多环芳烃和维生素D对肺功能参数有相反的影响[FEV1：β（95%置信区间）= -0.01（-0.02，-0.01）对0.01（0.01，0.04）；FVC：β（95%置信区间）= -0.01（-0.02，0.01）对0.04（0.01，0.06）]以及早期肺功能障碍的风险[比值比（95%置信区间）= 1.22（1.06，1.40）对0.52（0.37，0.73）]。在体重指数（BMI）< 28 kg/m²的受试者中，随着Σ25(OH)D的增加，可观察到ΣOH - PAHs与FEV1、FVC、早期肺功能障碍以及代谢评分 - 内脏脂肪指数（MSV）之间的关联减弱。此外，同时暴露于ΣOH - PAHs和Σ25(OH)D与FEV1、FVC、FEV1/FVC和早期肺功能障碍疾病之间的关联中，分别有2.18%、18.20%、5.70%和4.70%由MSV介导。
我们的研究结果表明，维生素D通过代谢改变拮抗多环芳烃对早期肺功能障碍的有害影响，为识别潜在的高危人群以及采取可行的预防和干预措施以减轻多环芳烃诱导的肺功能障碍提供了新的见解。
