Poudel Remy, Li Shen, Hong Haoyun, Zhao Juan, Srivastava Shweta, Robertson Rose Marie, Hall Jennifer L, Srivastava Sanjay, Hamburg Naomi M, Bhatnagar Aruni, Keith Rachel J
American Heart Association, Dallas, United States.
Department of Medicine, Envirome Institute, University of Louisville, Louisville, United States.
Tob Induc Dis. 2024 Aug 14;22. doi: 10.18332/tid/190687. eCollection 2024.
Smoking elevates catecholamines that increase the risk for cardiovascular disease. Sparse evidence exists about the effects of e-cigarettes and catecholamines. Higher levels of catecholamines could trigger the increased heart rate, blood pressure, and decreased vascular function reported with the use of e-cigarettes. We investigated the difference in urinary catecholamines and their metabolites before and after the use of an e-cigarette containing nicotine or cigarettes compared to no tobacco use.
In our observational cohort exposure study, healthy adults aged 21-45 years who were currently using e-cigarettes, cigarettes, or had never used tobacco, participated in an acute exposure visit using their most common tobacco product. Urine was collected before, 1, and 2 hours after a 3-second puff every 30 seconds for 10 minutes on an e-cigarette or straw or use of 1 cigarette. Urinary catecholamines and their metabolites were measured by ultra-high-performance liquid chromatography. Participants (n=323) were grouped by the product used at the visit. We compared levels of creatinine normalized log-transformed urinary catecholamines and their metabolites across groups using Dunn's test following a Kruskal-Wallis test in unadjusted and demographically adjusted models.
Prior to use, individuals who used cigarettes (n=70) had lower urinary metabolites from epinephrine, serotonin, and norepinephrine. No differences were seen in those who used e-cigarettes (n=171) and those who did not use tobacco (n=82). In fully adjusted models, 1 h after the use of a combustible or e-cigarette, log-transformed urinary metabolites from norepinephrine (β=1.22; 95% CI: 0.39-2.05, p=0.004 and β=1.06; 95% CI: 0.39-1.74, p=0.002), dopamine (β=0.37; 95% CI: 0.24-0.5, p<0.001 and β=0.15; 95% CI: 0.05-0.26, p<0.001), and epinephrine (β=1.89; 95% CI: 0.51-3.27, p=0.008 and β=1.49; 95% CI: 0.38-2.61, p=0.009) were elevated. In fully adjusted models, combustible cigarette use was associated with elevated urinary norepinephrine (β=0.46; 95% CI: 0.13-0.81, p=0.007) and dopamine (β=0.19; 95% CI: 0.06-0.31, p=0.003) 1 h after use.
We found that the use of both e-cigarettes and cigarettes was associated with elevated urinary catecholamines or their metabolites. Catecholamines could be useful as a biomarker of harm for tobacco use and considered by tobacco regulatory scientists in future research.
吸烟会使儿茶酚胺水平升高，从而增加心血管疾病风险。关于电子烟与儿茶酚胺的影响，现有证据较少。较高水平的儿茶酚胺可能会引发使用电子烟时所报告的心率加快、血压升高以及血管功能下降。我们研究了使用含尼古丁电子烟或香烟后与未使用烟草相比，尿儿茶酚胺及其代谢物的差异。
在我们的观察性队列暴露研究中，年龄在21 - 45岁之间、目前正在使用电子烟、香烟或从未使用过烟草的健康成年人，使用他们最常用的烟草产品参加了一次急性暴露访问。在使用电子烟或吸管每30秒吸一口，持续10分钟（共吸20口）或使用1支香烟后的3秒、1小时和2小时收集尿液。通过超高效液相色谱法测量尿儿茶酚胺及其代谢物。参与者（n = 323）根据访问时使用的产品进行分组。在未调整和人口统计学调整模型中，我们使用Kruskal - Wallis检验后的Dunn检验比较了各组中肌酐标准化的对数转换尿儿茶酚胺及其代谢物水平。
在使用前，使用香烟的个体（n = 70）尿中肾上腺素、血清素和去甲肾上腺素的代谢物水平较低。使用电子烟的个体（n = 171）和未使用烟草的个体（n = 82）之间未观察到差异。在完全调整模型中，使用可燃烟草或电子烟1小时后，去甲肾上腺素（β = 1.22；95% CI：0.39 - 2.05，p = 0.004和β = 1.06；95% CI：0.39 - 1.74，p = 0.002）、多巴胺（β = 0.37；95% CI：0.24 - 0.5，p < 0.001和β = 0.15；95% CI：0.05 - 0.26，p < 0.001）和肾上腺素（β = 1.89；95% CI：0.51 - 3.27，p = 0.008和β = 1.49；95% CI：0.38 - 2.61，p = 0.009）的对数转换尿代谢物水平升高。在完全调整模型中，使用可燃香烟1小时后与尿去甲肾上腺素（β = 0.46；95% CI：0.13 - 0.81，p = 0.007）和多巴胺（β = 0.19；95% CI：0.06 - 0.31，p = 0.003）水平升高有关。
我们发现使用电子烟和香烟均与尿儿茶酚胺或其代谢物水平升高有关。儿茶酚胺可用作烟草使用危害的生物标志物，并有待烟草监管科学家在未来研究中加以考虑。
