Chronic Hookah (Waterpipe) Smoking, Vascular Dysfunction, Inflammation and Oxidative Stress

项目摘要 使用水烟筒吸烟在世界范围内迅速流行，特别是在 青年水烟的传播是由未经证实的信念，即烟雾是解毒，因为它促进了吸烟 通过装满水的盆地;大量的水果味烟草产品的营销和美化;以及 缺乏政策监管。因为传统的水烟是唯一一种使用燃烧的烟草产品 除了烟草燃烧产品外，吸烟者还暴露于 木炭燃烧产物包括高水平的一氧化碳（CO），一种有效的血管扩张分子， 显示掩盖了水烟引起的急性内皮功能障碍。众所周知，长期吸烟会导致 内皮和血管功能损害，而香烟和水烟都是烟草的载体， 长期抽水烟的比较效果是未知的。因此，我们现在将注意力转向 阐明水烟对内皮和血管功能的长期健康影响;并确定 长期吸食水烟影响血管健康的有害生物标志物。我们假设在长时间- 术语水烟吸烟，烟草燃烧产物-主要是尼古丁，高浓度的颗粒， 氧化剂和调味剂占主导地位，并推翻了CO的血管舒张作用，导致持续的 内皮和血管功能障碍，从而增加未来动脉粥样硬化和心血管疾病的风险。 疾病我们进一步假设水烟引起的血管功能障碍至少部分是由 增强氧自由基的形成，促进全身血管炎症和氧化 应力为了实现我们的目标，在34名21-49岁的健康慢性水烟吸烟者中， 年龄和性别匹配的34名吸烟者和34名不吸烟者的吸烟者-我们将测量：（a） 内皮功能，通过肱动脉血流介导的扩张;和（B）血管硬度，通过颈动脉-股动脉脉搏 波速度和主动脉扩张指数，作为波反射的量度。炎症的生物学标志物 (high敏感性C反应蛋白、8-异前列腺素F2α、纤维蛋白原）和氧化应激（促氧化剂高， 密度脂蛋白氧化指数和总抗氧化能力）。因为抽水烟 超过了提出循证监管所需的研究，研究结果将：（a）填补我们在这方面的巨大空白。 了解水烟的慢性影响;和（B）为未来的长期研究提供基础 建立生理和全身生物标志物与特定心血管病理学之间的关系， 进程，从而建立科学基础，为目前正在辩论的国家政策决定提供信息， 水烟

Project Summary Tobacco smoking using a hookah (waterpipe) is rapidly increasing in popularity worldwide, particularly among youth. The spread of hookah smoking is promoted by the unsubstantiated belief that smoke is detoxified as it passes through the water filled basin; heavy marketing and glamorization of fruit-flavored tobacco products; and lack of policy regulation. Because traditional hookah is the only form of tobacco product that uses burning charcoal briquettes to heat the tobacco, in addition to tobacco combustion products, smokers are exposed to charcoal combustion products including high levels of carbon monoxide (CO), a potent vasodilator molecule, shown to mask acute hookah-induced endothelial dysfunction. Long-term cigarette smoking is known to cause impairment in endothelial and vascular function, and while both cigarette and hookah are vehicles for tobacco, the comparative effect of long-term hookah smoking is unknown. Accordingly, we now turn our attention to elucidate the long-term health effect of hookah smoking on endothelial and vascular function; and identify biomarkers of harm by which chronic hookah smoking affects vascular health. We hypothesize that with long- term hookah smoking, tobacco combustion products—mainly nicotine, high concentrations of particles, oxidants—and flavorings predominate and override the vasodilator effects of CO, leading to persistent endothelial and vascular dysfunction, thereby increasing the risk of future atherosclerosis and cardiovascular disease. We further hypothesize that the hookah-induced vascular dysfunction is at least in part mediated by enhanced formation of oxygen-derived free radicals, promoting systemic vascular inflammation and oxidative stress. To accomplish our goals, in 34 healthy chronic hookah smokers 21-49 years of age who do not smoke cigarettes—matched for age and sex with 34 cigarette smokers and 34 non-smokers—we will measure: (a) endothelial function, by brachial artery flow-mediated dilation; and (b) vascular stiffness, by carotid-femoral pulse wave velocity and aortic augmentation index, as a measure of wave reflection. Biological markers of inflammation (high sensitivity C-reactive protein, 8-iso-prostaglandin F2α, fibrinogen) and oxidative stress (prooxidant high- density lipoprotein oxidant index and total antioxidant capacity) will be collected. Because hookah smoking has outpaced research needed to propose evidence-based regulation, findings will: (a) fill in large gaps in our understanding of the chronic effects of hookah smoking; and (b) provide a foundation for future long-term studies to establish the relationship between physiological and systemic biomarkers to specific cardiovascular pathologic processes, thereby building a scientific basis to inform the currently debated national policy decisions specific to hookah.