Clinical Pharmacology Research Program, Division of Cardiology, Zuckerberg San Francisco General Hospital, Department of Medicine, University of California, San Francisco, CA, USA.
Center for Tobacco Control Research and Education (CTCRE), University of California, San Francisco, CA, USA.
J Expo Sci Environ Epidemiol. 2021 Mar;31(2):211-223. doi: 10.1038/s41370-019-0159-9. Epub 2019 Aug 12.
It is unclear why Black smokers in the United States have elevated risk of some tobacco-related diseases compared to White smokers. One possible causal mechanism is differential intake of tobacco toxicants, but results across studies are inconsistent. Thus, we examined racial differences in biomarkers of toxic volatile organic compounds (VOCs) present in tobacco smoke.
We analyzed baseline data collected from 182 Black and 184 White adult smokers who participated in a randomized clinical trial in 2013-2014 at 10 sites across the United States. We examined differences in urinary levels of ten VOC metabolites, total nicotine equivalents (TNE), and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), controlling for covariates such as cigarettes per day (CPD), as well as differences in VOCs per TNE to assess the extent to which tobacco exposure, and not metabolic factors, accounted for racial differences.
Concentration of metabolites of acrolein, acrylonitrile, ethylene oxide, and methylating agents were significantly higher in Blacks compared to Whites when controlled for covariates. Other than the metabolite of methylating agents, VOCs per TNE did not differ between Blacks and Whites. Concentrations of TNE/CPD and VOCs/CPD were significantly higher in Blacks. Menthol did not contribute to racial differences in VOC levels.
For a given level of CPD, Black smokers likely take in higher levels of acrolein, acrylonitrile, and ethylene oxide than White smokers. Our findings are consistent with Blacks taking in more nicotine and toxicants per cigarette smoked, which may explain their elevated disease risk relative to other racial groups.
目前尚不清楚与白人吸烟者相比，美国的黑种烟民为何会有一些与烟草相关疾病的风险升高。一种可能的因果机制是烟草毒素的摄入差异，但各研究的结果并不一致。因此，我们研究了存在于烟草烟雾中的有毒挥发性有机化合物（VOC）生物标志物在种族间的差异。
我们分析了 2013 年至 2014 年期间在美国 10 个地点参加一项随机临床试验的 182 名黑种和 184 名白种成年吸烟者的基线数据。我们考察了 10 种 VOC 代谢物、总尼古丁等价物（TNE）和 4-（甲基亚硝氨基）-1-（3-吡啶基）-1-丁醇（NNAL）尿液水平的差异，同时控制了每天香烟数（CPD）等协变量，以及 VOCs/TNE 的差异，以评估烟草暴露而非代谢因素在多大程度上导致了种族差异。
在控制了协变量后，与白人相比，黑人丙烯醛、丙烯腈、环氧乙烷和甲基化剂的代谢物浓度明显更高。除了甲基化剂的代谢物外，黑人与白人之间的 VOCs/TNE 没有差异。TNE/CPD 和 VOCs/CPD 的浓度在黑人中明显更高。薄荷醇并没有导致 VOC 水平的种族差异。
在相同 CPD 水平下，黑种烟民摄入的丙烯醛、丙烯腈和环氧乙烷水平可能高于白种烟民。我们的研究结果与黑种烟民每支烟摄入更多尼古丁和毒素的说法一致，这可能解释了他们与其他种族群体相比，疾病风险更高的原因。
